Response To: Chester B. Stone, Jr.


Dear Chester:

      It is so good to hear from a new friend, or should I say
friends? I need to clarify a few things, so please bear with me.

      First, I do not have ALS.  I have Stealth Virus.  My Stealth
Virus has manifested itself not as ALS as it has with your daughter
Marian, but it is all "STEALTH VIRUS".  The key to getting well is
not treating the symptoms the virus has manifested, but the
underlying infection causing the symptoms.  Why has it manifested as
ALS with your daughter, and not with me, I really can only guess.  My
guess would be genetic predisposition.  We all have genetic
weaknesses, but something often has to trigger them;  or maybe it has
to do with how the particular Stealth Virus has been contracted;  or
maybe it has to do with the particular Stealth Virus that Marian
has.  But the bottom line is this:  TREAT THE STEALTH VIRUS, as
STEALTH VIRUS, and not as "ALS" STEALTH VIRUS.

      Second, the most brilliant physician trying to CURE STEALTH
VIRUS is W. John Martin, M.D., Phd., and he is in charge of your
protocol, and knows best.  And, you can be assured that I am
convinced that "Epione" can and will be a cure for Stealth Viruses.
It has been the thrust of my focus for the past two years, as I was
trying relentlessly to raise the money for the "Epione Project" to
begin.  You can not imagine how happy I am that it finally has, and
how grateful I am that through ALS this most worthy project has
begun.  The suffering of the many ALS patients will not be in vain.

      I am not a Medical Care Professional, my Master's is not in
Medicine, but I am a patient who has been suffering various degrees
of the ravages of this viral condition for a very long time.  I have
had success with my treatment for many reasons.  First I have been
blessed with a truly brilliant Physician who is humble enough to
allow me to experiment, and yet wise enough to guide me.  He has also
taught me to want to get well more than anything, and not to be
afraid.  The combination of these two, wanting to get well and not
being afraid, are very powerful forces.  However, they do not stand
alone.  There needs to be both a gifted Physician, and a disciplined
patient as well.  I happened to have a gifted Physician, and I happen
to have a great deal of discipline.  Here lies the key to my
success.  In addition to all this I have been blessed with knowing
Dr. Martin and his research.  His guidance has always led me closer
to my goal, that of regaining control over my life.  Most of the
treatment that has helped me to regain some degree of control, I
stumbled over. The  rest has been through reading thoroughly Dr.
Martin's work, and trusting and listening carefully to his
suggestions.

      To begin with I would like to present the personal protocol I am
following as twofold:  one is an approach to interfere with how the
Stealth Virus survives, or multiplies;  and the other is to cut off
its food supply or source of stimulation.  Together, it seems to be
working.  I am far from cured, but I monthly see new improvements,
and slowly I am beginning to regain my life.

      I would like to preface my protocol with this, I am on
Cytovene.  It saved my life.  But I did not begin to regain any
control until I began my twofold personal protocol.

I:          The first thing that happened to me that began to change
my life, happened purely by accident, and God's design.  I had put on
50 lbs. from the effects of the virus, and I happened to be listening
to a talk show interview with Dr. Atkin's.  I was not paying too much
attention until I heard him mention "HYPERINSULINISM."  My ears piped
right up.  I had been diagnosed with Hyperinsulinism many, many years
ago, and it was left untreated and finally forgotten. Somehow, I
think by God's grace, my brain made a monumental leap instantaneously
and connected the hyperinsulinism with the Stealth Virus.  It was a
very vague connection, but it was still a connection.  At first I
thought if I could treat the hyperinsulinism, maybe some of my
symptoms would go away.  I was on the level of thinking some of the
symptoms were not Stealth Virus, but rather due to untreated
hyperinsulinism.  But in the back of my mind I knew Stealth Virus
affected the glandular system, particularly the thyroid and adrenals,
and hyperinsulinisn is a disease of the Pancreas, a glandular organ.
But the connection was still vague.  It was not until I put myself on
the Atkin's Low Carbohydrate Diet that the lights went off.  After
only one week on the diet I was feeling much better.  So I went
stricter on the diet, and I got even better.  Again, I went even
stricter, far below what Dr. Atkin's recommends, in an attempt to try
and figure out what exactly was happening to me, and I got even
better. (See:  Dr. Atkin's New Carbohydrate Gram Counter.)

      At this point, I knew I was on to something.  But what?  Dr.
Atkin's attributes the success of his diet to treating
hyperinsulinism.  I was treating my hyperinsulinism with my diet, and
my Stealth Virus symptoms got better.  Therefore, by treating my
hyperinsulinism, I was treating my Stealth Virus.  I began to read
everything I could find on hyperinsulinism, as well as everything Dr.
Atkin's wrote on hyperinsulinism.  All the modalities Dr. Atkin's
recommended to suppress your insulin levels, I tried.  I tried one at
a time, slowly increasing the dosage and documenting everything so I
could properly assess what was attributed to helping my progress.

      The three main nutrient supplements he recommends to
overcome "insulin resistance":  1) L-Carnitine, up to 2,000mg;  2)
Vanadyl Sulfate (Vanadium) up to 100mg;  3) Pantethine, up to 900mg.
These are all daily doses, evenly divided throughout the day.  I have
found maintaining a steady blood level to be critical.  I try to
break everything down to 4 daily doses of each if possible.  If not,
than two dosages at least 10 hours apart.  Zinc and Milkthistle are
also recommended, but they are minor players.  The big hitters are
the top three.  He also recommends between 2 & 3,000mg of  L-
Glutamine because it helps the insulin/sugar balance in such a way
that it helps control your cravings for what is not allowed on the
diet.  It works.  But he also mentions that viral infections deprive
the Immune System of Glutamine, and that Glutamine should be an
essential treatment in all viral syndromes, only with much higher
doses. (See:  "Dr. Atkin's Vita-Nutrient Solution.)  I am presently
taking 2,000mg daily, but soon will try increasing the dose to see if
it helps even more.

      "Insulin Resistance" is defined by Dr. Atkins as a syndrome that
develops due to huge intakes of carbohydrates.  Such an individual
becomes severely unresponsive to the action of insulin because the
carbohydrates are triggering the release of large quantities of
insulin, and the body is incapable of utilizing it efficiently.  The
body's response is to put out even more quantities of insulin, hence
explaining the hyperinsulin state.(See:  Dr. Atkin's New Diet
Revolution.)

      In very difficult cases, Dr. Atkin's recommends a prescription
drug called "Glucophage" to help and lower the insulin levels.(see
p.151, of Dr. Atkin's Vita Nutrient Solution: )
           ''In recent years two drugs have reached the market
            that work on the very pertinent insulin resistance
            problem, thus lowering both the blood sugar and the
            insulin levels...One of these, Glucophage, helps
            lower lipids, and the insulin level and is one of
            the few drugs worth using."
As a footnote to this direct quote, I'd like to clarify that this
drug is not dangerous to reactive hypoglycemia, the type we most
likely all have secondary to the state of hyperinsulinism.  When the
insulin level is reduced, so too is the hypoglycemic state.  My 22
yrs of severe hypoglycemia went completely away.  Glucophage proved
to be most critical because it allowed me to take in slightly more
carbohydrates without the virus becoming more virulent.  Glucophage
is essential because the amount of carbohydrates per day could not
exceed 10grams before taking Glucophage.  Now I maintain around
60grams per day of carbohydrate intake.  The dose for Glucophage will
depend on the individual.  The lowest dose is 500mg. and the highest
2,000mg.  I started with the lowest, and slowly moved up, as each
increase in dosage helped my viral symptoms tremendously.  I am
presently taking 2,000mg per day.  It is important that you maintain
a strict balance between diet, Glucophage, and recommended
supplements.  Taking Glucophage, and or, the supplements without the
diet will not work, nor conversely, can you follow the diet without
at least the recommended supplements.

      You will notice on this regiment I am recommending, that if you
suffer from hypertriglyceridemia (high triglycerides), your
triglyceride levels will become normal or close to normal.  It is
interesting that one of the causes of hypertriglyceridemia can
develop secondary to certain endocrine disorders; such as diabetes,
and hypothyroidism (see p.180-183 "Dr. Atkin's New Diet
Revolution.")  My triglyceride level vacillated between 600-1,000 at
it's worst.  Now it is only abnormal when I am out of the recommended
supplements due to financial constraints.

      The last and final major player found to correct the
hyperinsulinism dilemma is dehydroepiandrosterone, commonly known as
DHEA.  DHEA is an adrenal harmone.  It may be the real key to
unlocking this hyperinsulinism/StealthVirus relationship.  We know
that Stealth Virus directly affects the Adrenal Glands, as it does
the Thyroid.  When this happens, the glands don't produce the proper
amount of harmones.  One of the harmones of the Adrenals known to be
affected is DHEA.  An insufficient amount of DHEA is produced and can
be detected by a simple blood test.  If the DHEA level is low it
causes hyperinsulinism, by impairing the body's response to insulin.
Thus, by supplementing the deficient harmone, the possible cause of
hyperinsulinism may be found and eradicated.  Rather than trying to
increase the body's sensitivity to insulin, or decreasing the level
of the insulin, maybe the answer is to find out why and how the
hyperinsulinism is caused and correct it.  I think the cause has been
found, low levels of DHEA due to Stealth Viral infection; therefore,
the new objective may be balancing the necessary level of DHEA first,
and if still necessary, supplement to enhance insulin sensitivity,
and/or take Glucophage to suppress insulin levels.

      I am hopeful that DHEA may be the missing link.  I have recently
begun to take a very low dose, 5mg per day, of DHEA.  I did not see
results until I ran out of L-Carnitine, as at the time I did not have
the funds to buy it.  I was in a quandary as to what to do.  I get
violent seizures if I go off the diet to any severe degree, or if I
do not take one of the three recommended supplements. (Glucophage is
never missed.)  So in desperation, I decided to experiment with
increasing my dose of DHEA from 5mg once a day, to 5mg twice a day.
I am happy to announce that I still do not have the L-Carnitine and I
have not had one seizure!  However, there are some viral symptoms
worsening to a slight degree.  I will soon be receiving the L-
Carnitine, and I intend to resume it.  I, however will seek
permission to slowly increase the DHEA to see if it can help me to
get even better.  One word of advice, start very slow.  I started at
25mg of DHEA some time ago and got very sick.  I would never have
picked it up again had it not been for the gentle prodding of Dr.
Martin.  He explained that when dealing with hormones, you must start
slow so your body can adjust.  I must admit, I had no intention of
trying it again until I read an article that stated that when there
was a DHEA deficiency, hyperinsulinism resulted.  (article was
written by a Physician affiliated with the Atkin's Center.)

      This theory is my own, that Stealth Virus and Hyperinsulinism
are interrelated.  I have no research to back it up other than my own
trial and error, and phenomenal results.  I am uncertain whether it
is the sugar feeding the virus, or the insulin stimulating it.
Because I rely so heavily on Glucophage, I lean toward the insulin as
the problem.  However, correcting the insulin balances the sugar, and
therefore, it very well could be the sugar.  A member of
TheStealthVirusSupportGroup, Kathy Blanco submitted something very
interesting regarding the relationship of sugar to viruses.  It is
#31 on the message board, entitled, "Sugar increases Polio risk,
Lessons for other Viruses," by Dr. Sandler.  It was written in 1951
during the height of the Polio epidemic.

      For more information on the relationship between Hyperinsulinism
and Stealth Virus:   see the StealthVirusSupportGroup message board:
#'s15,16,18,19,28.

II:           The second leg of my personal protocol has to do with
the Cytokine/Chemokine suppression.  It was hailed by Dr. Martin in
his web site, www.ccid.org as "Hope on Horizon"   The web site now
says that "Epione" is the "hope on the horizon."  I could not agree
more.  I look at the approach in treating Stealth Virus via
Cytokine/Chemokine suppression as an "immediate" hope, and Epione as
the ultimate hope.

      I have tried some of the modalities Dr. Martin recommends to
treat Stealth Virus via Cytokine/Chemokine suppression, and have had
some very promising results.  However, nothing as dramatic as when I
suppressed my insulin levels, until I tried QUERCETIN, a
bioflavonoid.  The results I have had with Quercetin is short of
miraculous.  At the time I decided to try it, my lymphatic system was
showing involvement.  All lymphatic glands in my neck, and under my
arms would swell and turn red, and cause a great deal of pain.  This
would happen each week when my cycle became active.  My viral cycle
is about 3 days more active,  and 4 days less active.  The day I
began Quercetin I noticed results almost immediately.  Each day I
increased the dosage until I got to the level Dr. Martin recommends,
3,000mg in divided dosages.  It was helping so much I asked to exceed
the recommended dose to 4,000mg.  It helped even more.  Within a few
short days, all swollen lymph glands disappeared.  They had been
quite large.  And to date, when my virus becomes more active, I do
not get any swollen lymphatic glands.  Dr. Martin attributes the
success of Quercetin to it's very powerful anti-reverse-transcriptase
property.

      Because of the phenomenal results with Quercetin, I have been
doing some extensive research on Thalidomide because of it's Immune
Modulating capabilities.  If anyone has anything to share regarding
Thalidomide, please send it to me.

With great regards,

H. Lynn Knapp, M.A.
Moderator
TheStealthVirusSupportGroup

No need for alarm over polio shots
By Rita Rubin, USA TODAY

A monkey virus that contaminated polio vaccines given to millions of
people from 1955 through early 1963 has been found in human tumors,
but there is no definitive proof that it actually caused the rare
cancers, a leading researcher said Thursday.

"There's no reason to be alarmed about the polio vaccines,'' said
Janet Butel, head of molecular virology at Baylor College of Medicine
in Houston.

Butel was responding to a story in the (London) Sunday Telegraph that
cited her research in claiming that hundreds of people were dying
yearly from cancers stemming from polio vaccines contaminated with
simian virus 40, or SV40.

SV40 was found in the 1960s in polio vaccine grown in kidney cells
from infected rhesus monkeys. Soon after it was isolated, scientists
discovered SV40 could change normal cells into tumor cells in the
laboratory and induce cancers in hamsters and certain mice, Butel
says. In the past decade, the development of sensitive tests has
enabled scientists in labs around the world to detect SV40 in
childhood brain tumors, bone cancers and a type of malignancy
associated with asbestos exposure.

Butel calls the finding of SV40 in human tumors "very suspicious''
and deserving of further investigation. "We just have to do more work
and figure out in more detail whether we can say it has actually
caused those tumors.''

But that doesn't mean that people are dying of cancer because they
were injected with the Salk vaccine against polio 35 to 40 years ago,
researchers say. In The Journal of the American Medical Association a
year ago, scientists reported that there was no increase in rates of
SV40-associated cancers among people old enough to have received the
contaminated vaccine.

"Some reporters have wanted to make this link between the
contaminated polio vaccine and cancer. That's not right at all,''
Butel says. "People who got the vaccine should not be scared."

As many as 10% of adults born after 1962 carry SV40 antibodies,
suggesting that there must be another source of human infection
besides the contaminated polio vaccine, Butel says. "It's being
transmitted from person to person, and we don't know how.''

NEUROLOGICAL DISEASES CAUSED BY VIRUSES




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Neurological disease is one of the most serious complications of
virus infection.
Clinically, viral neurological disease can be divided into
acute diseases and chronic syndromes.
The pathology may be due either to viral multiplication in the cells
of the brain, or due to the (misdirected) immune response of the
host - post infectious encephalo-myelitis.
Where virus replicates in the brain, virus can usually be isolated
from brain tissue or from cerebrospinal fluid. This is not the case
with the post infectious syndromes.



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Acute neurological syndromes


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Virus may reach the brain either by the blood stream or by spread
along peripheral nerves. Asymptomatic infection of the brain is
common.
There are four main syndromes:

1. Encephalitis
2. Flaccid paralysis
3. Aseptic meningitis
4. Post infectious encephalo-myelitis


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Acute viral encephalitis
Viral replication occurs in the brain tissue itself, causing
destructive lesions in the grey matter. The main symptoms include:
fever, drowsiness, confusion, convulsions and focal neurological
signs. Morbidity and mortality is very high.
Viruses that cause encephalitis include
Herpes Simplex, Rabies and some of the Arboviruses.

The Arboviruses include a miscellaneous group of enveloped, RNA
viruses, that are transmitted from one vertebral host to another via
blood sucking arthropods. The main reservoirs are wild birds and
small mammals. Man may be infected if bitten by the insect vector.
Arboviruses cause two types of disease:


1. Encephalitis, and
2. Fever (often with haemorrhagic manifestations)
Arboviral encephalitis occurs in most parts of the world; but
different agents are responsible for disease in different areas. In
South Africa, there are no endemic arboviruses that specifically
cause encephalitis. Rarely, however, encephalitis may occur as part
of the clinical course of infection with: West Nile virus, Rift
Valley Fever virus, Sinbis virus, Crimean-Congo haemorrhagic fever or
Chickengunya virus. These viruses are endemic in livestock herds in
certain parts of the country and farm workers or vets may
occasionally be infected.

[For more information, see lecture notes on viral haemorrhagic
fevers].



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Flaccid Paralysis
Due to direct infection of motor neurones. Patients present with
fever and flaccid paralysis of a group of muscles. The lower limbs
tend to be involved more commonly than the upper limbs. Signs of
meningitis such as headache and neck stiffness are frequent
accompanying features. The most common aetiological agents include
the polioviruses 1-3, but with the reduction in prevalence of wild
type polio, a number of non-polio enteroviruses have also been
implicated as rare causitive agents.



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Aseptic meningitis
Infection of the meninges. A relatively mild disease with a good
prognosis. Patients present with fever, headache, neck stiffness and
photophobia. Common viral agents include: enteroviruses, mumps virus
and lymphocytic choriomeningitis virus.



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Post infectious encephalomyelitis
This uncommon complication may develop in the convalescent phase of a
number of common virus infections, including: measles, mumps, rubella
and primary varicella-zoster virus infection, as well as following
the administration of certain vaccines, such as: vaccinia virus and
the older neurotissue rabies vaccines. Wide spread demyelinating
lesions develop in the brain and spinal cord, associated with
lymphocytic infiltration and perivascular cuffing of adjacent blood
vessels. Virus cannot be isolated from brain tissue or CSF. The
aetiology is somewhat obscure, but it is believed to be an auto-
immune phenomenon, triggered by exposure to foreign antigens which
are closely related to host proteins normally expressed in brain
tissue (molecular mimicry).



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Gillain Barre syndrome

Poly-neuritis which develops a few days after the acute phase of a
viral infection. The disease is due to demyelination of peripheral
nerves. Patients present with an ascending paralysis, associated with
paraesthesia. Like post infectious encephalomyelitis, it is believed
to be an immunological phenomenon. Patients usually recover
spontaneously over a few weeks or months. There is no specific
treatment.



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Chronic Neurological Conditions:


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A number of viruses and virus-like agents can cause chronic
neurological disaese. Characteristically, these conditions have a
long incubation period followed by slow development of symptoms and a
progressive, uniformly fatal course.


Subacute-sclerosing panencephalitis (SSPE)
Progressive multifocal leuco-encephalopathy (PML)
Retrovirus disease
Spongiform encephalopathies


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Subacute Sclerosing Pan Encephalitis
This is a rare, slowly progressive degenerative disease of the brain
which develops six to eight years following a primary uncomplicated
infection with measles virus. It is due to persistent measles virus
infection in the CNS.

Clinical Features
Patients usually present with personality and behavioural changes
followed by progressive intellectual impairment, convulsions,
myoclonic movements, coma and death.

Pathogenesis
It is thought that the virus gains entry into the CNS during the
viraemia that occurs at the time of the primary infection. The
pathology is due to infection of the brain with a measles virus
mutant that lacks an essential structural gene and cannot therefore
undergo complete cycles of replication. This has two effects:

1.) It enables the virus to establish a persistent infection in the
brain - because there is limited expression of viral antigens on the
surface of infected neurones, an effective immune response cannot be
mounted against the infected cells.

2. ) The disease proceeds very slowly - because, as no infectious
virus particles are released, spread of infection to new cells only
occurs through fusion with adjacent infected cells.

Epidemiology
Occurs in about 1 per million cases of measles. The incidence has
declined sharply since the introduction of vaccination against
measles.

Laboratory diagnosis
Affected individuals have high titres of measles specific antibodies
in their serum and CSF.
Measles virus antigens can be demonstrated in brain tissue



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Progressive multifocal leuco-encephalopathy
There are two members of the Papovavirus family which are known to
infect man, namely JC virus, which replicates in neural tissue and BK
virus which has been isolated from the urinary tract. Neither of them
cause any pathology in healthy people.
JC virus - is associated with progressive multifocal leuco-
encephalopathy

Virology

The Papovavirus family contains two main groups:-

Papilloma viruses (which cause warts), See electronmicrographs
Polyoma viruses,

these are slightly smaller than papilloma viruses, and in animals are
sometimes associated with tumours.
The two known human polyoma viruses are:
JC - Progressive multifocal leuco-encephalopathy
BK - isolated from urine of immunosuppressed patients
dsDNA genome

small icosahedral particles, 42-45 nm

grows in human foetal glial cell cultures (JC) Progressive multifocal
leuco-encephalopathy is a progressive neurological disorder caused by
reactivation of JC virus in the brain. Infection is common, but
neurological disease is rare; it only occurs in immunosuppressed
patients.

Clinical Features
Patients may present with a variety of neurological signs, including:
hemiparesis, dementia, dysphagia, muscular inco-ordination or
impaired vision. The condition is progressive and invariably fatal.

Pathology
Multiple foci of demyelination are found throughout the cerebral
hemispheres and cerebellum. The virus infects oligodendrocytes, which
have a bizzare histological appearance.

Epidemiology
Infection with JC virus is common, but invariably asymptomatic:
Seroprevalence surveys have shown that about 50-60% of adults have
antibodies.



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Spongiform Encephalopathies
(Prion diseases)
A number of transmissable neurological syndromes, caused by
unconventional virus-like agents, have been identified in man and
other animals. These diseases are characterized by the following
features:


Confined to the CNS
Long incubation period
Progressive, uniformly fatal course
Typical brain histology: reactive gliosis, vacuolation of neurones,
deposition of amyloid protein in the brain and the absence of an
inflammatory response.
Infection is believed to be transmitted by means of a novel
infectious protein, termed prion or PrP.

Diseases falling into this category include:

Scrapie - sheep, goats
Bovine spongiform encephalopathy - cattle
Transmissable Mink encephalopathy - mink
Creutzfeldt-Jakob disease - man, sporadic and familial
Gerstmann-Streussler disease - man, familial
Fatal Familial Insomnia - man, familial
Kuru - man, Fore people, New Guinea
Properties of Prions:

1. Infectivity is associated with a novel infectious protein, termed
prion (PrP)
2. Infectious particles are very small - about 20-30 nm in size.
3. No nucleic acid has yet been found to form part of the agent
4. Prions are extremely resistent to inactivation by: ultra-violet
light, formaldehyde and heat.
5. Prions can be transmitted by intra-cerebral or sub-cutaneous
inoculation of material from infected brain.
Pathogenesis of prion diseases
The pathogenesis of prion diseases is still a great mystery. The
pathology appears to be both infectious as well as genetic.

Recent evidence has demonstrated that the prion protein has the same
primary amino acid sequence as a host protein which is normally
present at low levels in healthy brain tissue. The cellular protein
has been termed PrPc. Although the amino acid sequence is the same as
the cellular one, the prion protein, has an abnormal conformation,
due to different post translational modification. Exposure to the
abnormal form triggers a conversion of the cellular isoform to the
infectious form. This is followed by progressive accumulation of the
abnormal form (prion protein) in the brain, which is deposited as
amyloid.



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Scrapie
Scrapie is a neurological disease occurring in sheep and goats. It
was first identified in Britain, but it is now known to occur world
wide. It is the prototype disease of the spongiform encephalopathies;
the scrapie prion is termed PrPsc. The disease is clearly infectious
as it can be transmitted to sheep, mice and hamsters by intra-
cerebral or sub cutaneous inoculation of material from the brains of
infected sheep. Susceptibility to infection appears to be genetically
determined.

Clinical features
The disease is transmitted by contact in flocks of sheep and also
vertically, from ewes to lambs. In natural infection, the incubation
period is 2 to 5 years. Following intra- cerebral inoculation,
however, the incubation is much shorter, only 3 to 24 months.

Affected sheep develop ataxia, tremor and muscular in co-ordination;
the symptoms progress to paralysis and death.



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Bovine Spongiform encephalopathy
Similar disease to scrapie which occurs in cattle. It is believed
that scrapie was introduced into cattle herds fed on feeds containing
scrapie-infected sheep offal. The condition is now epidemic in cattle
herds in England and Wales ("Mad Cow Disease"). There is concern that
the infection may be transmitted to humans, and a report of an
increased number of cases of CJD in young people linked to the
consumption of beef burgers sparked a world wide furore.



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Transmissable Mink encephalopathy

Scrapie has been introduced into minks, bred in captivity through
feeds containing sheep brains.



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Creutzfeldt-Jakob disease (CJD)

In 1920, Creutzfeldt described a progressive dementing illness in a
22 year old woman. The following year, Jakob described four older
patients with a clinically similar presentation and course. Since
then, numerous cases of CJD have been described. CJD occurs world
wide. It is very rare, with an incidence of about 1 case per million
population. While most cases are sporadic, 5-10% are familial. In the
familial form, CJD is inherited as an autosomal dominant condition.

Clinical features
The onset of the disease typically occurs between the ages of 50 and
65 years. There are two main modes of presentation:


1. Chronic dementing illness
2. Progressive cerebellar dysfunction
The condition is relentlessly progressive and patients usually die
within a year of presentation.

Transmission:
The natural route of infection is not known, but CJD has been
accidently transmitted by:
1. Corneal grafts - where the corneas were harvested from cadavers
that died of CJD.
2. Growth hormone preparations, derived from human pituitary glands.
3. In two patients who received grafts of dura mater, prepared from
cadavers, and
4. through electrodes used for electro-encephalography which had
previously been used in a patient with CJD.

The prion detected in the brains of patients with CJD is termed
PrPCJD. The disease has also been experimentally transmitted to
chimpanzees and other primates. Following intracerebral inoculation,
the incubation period is 11-14 months. The disease can also be
transmitted peripherally (IV, intra peritoneal or intramuscular
routes). But transmission is much less efficient and the incubation
period is much longer (many years).

Decontamination procedures:
Prions are extremely resistent to inactivation by ultra-violet light,
forrmaldehyde and heat.


Recommended methods of decontaminating infected material include:
1. Autoclaving for 4.5 hours (121oC, 15 p.s.i)
2. 1N NaOH followed by autoclaving for 1.5 hours


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Gerstmann-Streussler Syndrome

Rare familial neurodegenerative disease which usually manifests in
the third to the seventh decade of life. The condition is both
infectious and genetic: the predisposition is inherited as an
autosomal dominant condition; while, in addition, the disease can be
transmitted to non human primates by intra cerebral inoculation with
brain tissue from cases of GSS.

Recent genetic studies have revealed that affected individuals have a
point mutation in their PrPc gene. The altered amino-acid sequence of
the PrPC protein may make it more susceptible to transformation to
the abnormal conformation.



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Fatal Familial Insomnia

Another rare familial disorder. Predisposed individuals also have a
mutation in their PrPc gene.



----------------------------------------------------------------------
----------
Kuru
This is a transmissable prion disease found only in the Fore people
of New Guinea. It first appeared about 60 years ago and the incidence
increased until the late 1950's. The disease is now known to have
been transmitted through ritual cannibalism: until the late 1950's it
was the practice of women and children to eat the brains and viscera
of dead relatives, including those who had themselves died of Kuru.
Cannibalism stopped in 1957 and the incidence of Kuru has declined
sharply since then.

Clinical features:
The incubation period varied from 4-20 years.
Patients presented with progressive cerebellar dysfunction. Death
usually occurred within a year of initial presentation.

Transmission studies:
Intra-cerebral inoculation of brain tissue from Kuru victims into non
human primates leads to the development of symptoms within two years.




----------------------------------------------------------------------
----------

Retrovirus Disease
Lentivirinae:
Lentiviruses characteristically establish a persistent infection in
the host and cause chronic wasting disorders which are uniformly
fatal. Members of this family that typically cause CNS pathology
include:


Virus Host Clinical Features
Visna-Maedi virus sheep paralysis, wasting, ataxia
Caprine arthritis encephalitis virus (CAEV) goats paralysis, wasting,
ataxia
HIV 1 and 2 humans dementia

Pathology
Inflammatory cell infiltration, perivascular cuffing of blood
vessels, demyelination, necrosis and reactive gliosis.

Pathogenesis
The pathogenesis of the neuropathology is not very clear. Virus is
probably introduced into the CNS by infected monocytes which cross
the blood brain barrier. Differentiation of the infected monocytes
into microglial cells is thought to trigger viral replication. None
of these viruses appear to infect neuro-ectodermal cells directly,
and damage to brain tissue is therefore thought to occur indirectly
by cytokines released during inflammation. It is also thought that
certain viral proteins, such as the gp160 of HIV, may be directly
toxic to neurones.

In addition to the above ( where the neurological damage arises
directly as a result of HIV infection) CNS pathology in patients with
AIDS may also be caused by opportunistic infectious agents such as:
JC virus (PML), HCMV, VZV as well as a number of bacterial and fungal
diseases

Oncovirinae

HTLV 1 - Tropical spastic paraparesis



----------------------------------------------------------------------
----------
RETURN to :
Index of Lecture Notes
Medical Microbiology Homepage


----------------------------------------------------------------------
----------

These notes were prepared by Diana Hardie
for Virology Lectures to 3rd Year Medical Students
in the Department of Medical Microbiology , University of Cape Town.
Illustrations and layout by Linda Stannard, 1999 ©

From:  "Kathy Blanco" <kblanco@m...>
Date:  Mon Mar 12, 2001 10:41pm
Subject:  Fw: [SPCAPV] ABC TV---Monkey Virus, SV-40 and Polio Vaccine


   March 12, 2001    Good Morning America    World News Tonight
20/20    PrimeTime    Nightline    WNN    This Week


GO TO:  Select a Topic GMA World News Tonight 20/20 PrimeTime
Nightline This Week Specials World News Now Sam Donaldson Show
Internet Expose ABCNEWS Store
  HOMEPAGE  WORLD NEWS TONIGHT  FEATURE


Scientists have detected the SV40 virus, which is known to cause
cancer in rhesus monkeys, in humans. How it got there is a mystery.
(ABCNEWS.com)  Mystery Of The Monkey Virus
How Could SV40 Have Infected Humans,
And What Are The Potential Consequences?

By Kevin Newman



March 12 — It is a mystery with enormous implications that has
stumped some of the smartest minds in cancer research: How might a
cancer-causing rhesus monkey virus have wound up in human tumors?



If it is indeed in humans, its role in causing human cancers is
unknown. Scientists say it may play a key part — or possibly no part
at all.
The puzzle began in 1994, when Dr. Michael Carbone, a Loyola
University researcher, found the virus SV40, which had never before
been detected in humans, in 60 percent of the human lung tumors he
was studying.

SV40 is known to create tumors in animals, but how it might have
gotten into humans was unclear.

"I thought there must be something wrong. I must have made a
mistake," he said, remembering the discovery.

Eventually, 60 different labs confirmed the results.

"This finding has been replicated in New Zealand, in China, in
Britain, in France, in Switzerland, in Belgium," Carbone said.

Several labs did not find any evidence of SV40, and some researchers
continue to question Carbone's findings. Efforts in general to
explain the SV40 mystery have been hampered by unusual acrimony among
those studying the problem.

Could It Have Been Transmitted By Polio Vaccine?

If the monkey virus SV40 is indeed in humans, there are several
possible explanations for how it got there, says Janet Butel, a
virologist at Baylor College of Medicine and one of America's leading
virus researchers.

"One is that it has always been there in humans, and no one has
detected it in the past," Butel said.

There is another, much more controversial theory as well, however.

Some researchers contend SV40 was transmitted to humans through the
polio vaccine, which has saved the lives of millions. The vaccine is
made in monkey kidney cells, and from 1955 to 1963 an estimated 20
million Americans were given doses contaminated with SV40.

Still, the virus was not detected in humans until Carbone's 1994
research, possibly because no one had thought to look for it.

In 1961, the Food and Drug Administration ordered the vaccine's
manufacturers to screen out the SV40, which they did.

But a lawyer involved in a recent related polio case has just
published a report claiming contamination continued.

"In certain instances, no [SV40] tests were ever performed," the
lawyer, Stan Kops, wrote about one of the vaccine's manufacturers,
Lederle.


`Every Batch Was Screened,' Insists Vaccine Maker

The company strongly disputes Kops' claim, telling ABCNEWS in a
statement "every batch of the polio virus used to manufacture vaccine
underwent tissue culture testing for SV40."

If that is true, it suggests another possible reason SV40 has been
found in the brain tumors of people born after 1963: transmission
from mother to child.

"I think studies need to be done to figure out precisely what the
role of the virus might be in human cancer," said Butel.

Scientists specializing in SV40 met today in Bethesda, Md., to sort
through some of the controversies.

Some still question whether SV40 truly exists in humans, but the vast
majority of scientists attending the conference believe the role of
SV40 in humans needs urgent attention.

"We need to find out what it's doing there," said Butel. "It will be
a great significance if it's proven to have a role in human cancer
because then … it may be possible to block infection and the
formation of a tumor."

There are as many as six viruses known to be linked to cancer in
humans already, and their discovery has spurred advances in cancer
treatment.



ABCNEWS' Nicholas Regush, whose column Second Opinion appears weekly
on ABCNEWS.com, contributed to this report.


  PRINT THIS PAGE    SEND THIS TO A FRIEND

--- In StealthVirus-Patient@y..., "KokoBaby" <kokobaby@t...> wrote:
Chronic Active Human Herpesvirus-6 (HHV-6) Infection:
A New Disease Paradigm
by Joseph H. Brewer, M.D.
http://www.plazamedicine.com/hhv6/hhv6_1.html

*Hugs*
   ~Anne~

"Write it on your heart that every day is the best day of the
year."
~*~*~*~*~*~*~*~*~*~*~*~*~*~*~*~*~*~
"Gift's By Your's Truly" - President
The Easy Way To Find The Perfect Gift!
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--- End forwarded message ---

Dear
Helen,

3/12/01

       Dr. Martin  called me in August and told me the good news about
the ALS donation to help make Epione a reality..For almost two years,
unsuccessfully, other than to make a lot of contacts for him, I have
tried to raise money to make this research endeavor a reality.

       I have a letter Dr. Martin wrote me in 8/99 entrusting this
endeavor to me.  He asked me to help raise the money that was
necessary to make his research proposal for Epione, the Stealth Virus
inhibitor, a reality.  We independently raced to make it happen.  He,
however, beat me to the goal but I am not done yet.  This e-group I
hope will find many, many, people who have families, who will care
that there is a cure out there and donate to make it a reality.
Ideally I would like my own web site, but I am only 6 months on the
computer...so Yahoo groups is the first step.

       Ultimately, I would like to see a Stealth Virus Foundation set
up that could raise money similar to the way Lyme Foundations and ALS
Foundations do, and thus allocate all the money Dr. Martin needs,
because this is only the beginning of the journey.  The money he
received to begin his Stealth Research from the ALS Foundation is
only the first step in a very long mile.

       I'd like to end with something only you, Dr. Martin and I will
appreciate.  It has to do with our name, Helen, and the name he chose
for the Stealth Virus inhibitor, Epione.

       The day I called Dr. Martin in the summer of 99, I left a
message and signed off with my legal name, Helen, a name I rarely
use.  Only because of the name Helen, he called me back.  It seems he
had been feeling this heavy burden of Epione, knowing this disease
would one day reach epidemic proportions, and he would not have the
inhibitor ready.  And I called. I was "Helen."  If you know the
reason Dr. Martin is calling the Stealth Virus inhibitor, "EPIONE,"
you will understand.  It has something to do with a story in Greek
mythology...it is the story of HELEN OF TROY.  If I understand it
correctly, the beast they were trying to kill, and could not, ended
up being destroyed by Helen of Troy.  Epione is the name of the wife
of the doctor in the story.  She was known for her great kindness and
healing ways.  However, it was HELEN OF TROY who killed the beast,
and who made the impossible, possible.  The beast who could not be
killed, was killed.  The virus that so far evades most medical minds,
and treatments will be eradicated by the development of this
inhibitor, Epione.  And hopefully, this Helen, will have the honor of
playing a role in making Epione happen.  My goal is to see this
research endeavor reach a successful conclusion, and be made
available to all who need it.

      And you my new friend are a "Helen" too.  Maybe we can join
forces, and we two Helen's can make a difference.  At least we can
try.

Sincerely,

H. Lynn Knapp, M.A.
Moderator
The StealthVirusSupportGroup

Helen (Lynn) Knapp!

Sugar Increases Polio Risk -- Lessons For Other Viral Infections

----------------------------------------------------------------------
----------

The following is a chapter from the book Diet Prevents Polio written
by Benjamin P. Sandler, M.D., and published in 1951, at the height of
the polio epidemic.


----------------------------------------------------------------------
----------

Low Blood Sugar And Susceptibility To Polio
During my research I observed a large number of patients who had
symptoms that were caused by low blood sugar.

They complained of the symptoms previously described, namely:


headache
dizziness
weakness
fatigue
abdominal pain
nervousness
palpitation
frequent sweats
occasional fainting spells.

Most of these patients were malnourished, which, physiologically,
meant subnormal liver glycogen storage. Their diet was deficient in
protein and consisted largely of the cheaper starchy foods.

I noted that these patients also had poor resistance to infections
such as colds, sore throat, grippe, influenza, bronchitis, and
pneumonia. By increasing the protein content of their diet and by
reducing the sugar and starch content, they improved considerably.
They became stronger, more vigorous and buoyant, and had fewer
infections.

A few of these patients had had polio in childhood. Observations of
these patients over a long period of time led me to suspect that
their susceptibility to infection was possibly due to their poor diet
with its high sugar and starch content.

Their increased resistance to infection with a better diet confirmed
this suspicion. It then occurred to me that their susceptibility to
polio could be explained on a similar dietary basis.

Specifically, I suspected that children and adults contracted polio
because of low blood sugar brought on by a diet containing sugar and
starch.

I reasoned that the polio virus was able to cross tissue barriers,
reach the brain and spinal cord, invade the nerve cells, damage or
destroy them and cause paralysis. And I further reasoned that if the
blood sugar never fell below 80 mg polio could never result.

I suspected that during a polio epidemic only those children and
adults who experienced periods of low blood sugar would contract the
disease and that those individuals who were in actual contact with
the virus but who maintained normal blood sugar levels would not
contract the disease.

Thus, it remained to prove that low blood sugar could be a factor in
susceptibility to polio. And, after this had been proved, the
following questions had to be answered:


What causes low blood sugar in humans?

How can low blood sugar be prevented?
The prevention of low blood sugar would thus mean the prevention of
polio.

Before describing the experiments performed, I should like to make a
preliminary summary and state without reserve that:


Low blood sugar is a factor of susceptibility to polio.

Low blood sugar occurs frequently in children and adults and is
caused chiefly by a dietary error, namely, the consumption of sugar
and starch

Correction of this dietary error will prevent low blood sugar and
thus prevent polio.
An experimental method to prove that low blood sugar was a factor of
susceptibility to polio was readily available.

In 1938, the only laboratory animal that could contract polio by
experimental inoculation was the monkey.

All other laboratory animals were completely resistant to the polio
virus. The rabbit is one of these resistant animals.

Without knowing the blood sugar range in the monkey and rabbit, it
was suspected that the blood sugar in the monkey reached lower levels
than in the rabbit.

These suspicions were found to have a basis in fact through the
investigations of Drs. Jungeblut and Resnick of Columbia University
who studied blood sugar levels in monkeys, and through the
investigations of Drs. du Vigneaud and Karr of Cornell University who
studied blood sugar levels in rabbits.

In monkeys, blood sugar values as low as 50 mg. were observed,
whereas in the rabbit, values below 100 mg. were never observed. In
numerous determinations made on rabbits I have never obtained values
below 100 mg.

It was therefore concluded that the susceptibility of the monkey to
the polio virus was due to the fact that its blood sugar fell to
subnormal values, and that the resistance of the rabbit might be
associated with the fact that its blood sugar never fell below 100
mg, and that at this concentration cellular oxidation of glucose in
the nervous system and other organs would be maintained at such a
level as to enable the cells to protect themselves against invasion
by the virus.

Physiologists have stated that the normal blood sugar level of 80 mg.
holds true for all mammals.

The next step was to lower the blood sugar of the rabbit to subnormal
values with insulin injections, and then inoculate the rabbit with
polio virus. This was done and it was found that the rabbits became
infected and developed the disease.

The details of these experiments were published in the American
Journal of Pathology, January, 1941.

Some rabbits showed signs of infection 8 to 10 hours after
inoculation. I wish to stress this short period of incubation in the
rabbit because it demonstrates that polio can develop in a short
period of time. This is important, as we shall learn later, when we
discuss the onset of polio in humans within 24 hours after severe
physical exertion.

The rabbit is also resistant to the dog distemper virus. One of the
largest research laboratories has conducted much research with this
virus and when I informed the members of the staff about my success
in inoculating rabbits with polio virus after lowering the blood
sugar, they inoculated rabbits with the dog distemper virus after
insulin and reported to me that they observed signs of infection in
the rabbit for the first time.

This corroborating experiment indicates that low blood sugar may
cause susceptibility to many infections.

I was thus satisfied that low blood sugar was a factor of
susceptibility to the polio virus in monkeys, and that rabbits could
be rendered susceptible after their blood sugar was lowered with
insulin

(Insulin, as you probably know, is the hormone which diabetics inject
into themselves in order to keep their blood sugar within normal
range. It is a quick-acting drug and can lower the blood sugar within
an hour or so after injection).

I concluded that the concept that low blood sugar created
susceptibility to polio in both monkeys and rabbits could be applied
to humans as well.

What Causes Low Blood Sugar in Humans?
The next step in the solution of the polio problem was to find out
the causes of low blood sugar in humans. Fortunately the answer to
this problem was already at hand.

It has been found that the consumption of sugar and starch and foods
containing these substances were the chief causes of low blood sugar.

When patients drank a solution of pure glucose they had a period of
low blood sugar which began one to two hours after the glucose was
taken and which lasted for one to two hours, and longer.

This study of the blood sugar is called the "glucose tolerance test"
and is employed for the detection of hypoglycemia or hyperglycemia.
When they ate a meal containing sugar and starch they also had
periods of low blood sugar which came on an hour or so later and
which lasted for from one to two hours.

The low blood sugar was more marked and lasted for a longer time
after the glucose solution than after a meal containing starch.

It is an established fact that this paradoxic depressant effect on
the blood sugar level is more readily exerted by sugar than it is by
starches. I have observed these results in hundreds of cases and
similar results have been obtained by other investigators.

It is a surprising paradox: the more sugar (and starch) you eat, the
more likely you will develop low blood sugar.

Drs. E. P. McCullagh and C. R. K. Johnston have shown how the glucose
tolerance test is readily influenced by diet. Thus the second
problem: What can cause low blood sugar in the human? was solved.

How Can Low Blood Sugar be Prevented?
The third problem, "How can low blood sugar be prevented?" was the
only one left and this, too, was readily solved.

It had been found by other investigators that a meal consisting of
protein, fat, and carbohydrates, but with no sugar or starch, NEVER
caused low blood sugar.

The addition of sugar and starch to such a meal could readily produce
low blood sugar.

Thus I arrived at a simple formula for preventing polio: eliminate
from the diet sugar and foods containing sugar, and reduce the
consumption of foods containing starch.

Since eating sugar and starch during a meal may cause low blood sugar
after one to three hours, and since elimination of sugar and starch
prevents low blood sugar, the invasion of the body by the polio virus
will be prevented by a diet containing no sugar and no starch.
Protection against polio would thus begin on the very day such a diet
was started and protection would last just as long as such a diet was
adhered to.

I have found that a diet completely free of sugar and starch and
consisting of proteins, fats, and non-starchy vegetables:

May be adhered to for years with beneficial effect and absolutely NO
harmful effect.

There is NO supporting evidence to indicate that sugar and starch are
necessary for health or for energy purposes.

The human is a carnivore and can thrive on protein and fat alone, if
necessary.

The Eskimos thrive well on meat and fish which yield only protein and
fat, and polio is unheard of among them.

American and European explorers in the Arctic regions have lived on
meat and fish for as long as 18 months and have maintained perfect
health all the time on such a diet. Vilhjalmur Stefansson, the Arctic
explorer, has described his existence on such a diet in great detail.
He states that he was in perfect health on such a diet which
consisted of protein and fat alone.



Eskimos who live on meat and fish are not susceptible to infectious
diseases. They do become susceptible when they live amongst white men
and eat the white man's diet with its sugar and starch. It is true
that the Eskimo's fresh contact with the white man exposes him to
infectious diseases to which he (the Eskimo) has not had the
opportunity to become immune.

The presence of sugar and starch in the Eskimo's new diet is of
greater significance. A US public health officer stationed in Alaska
has blamed this dietary factor for the great susceptibility of the
Eskimo to tuberculosis.

A low carbohydrate meal elevates and stabilizes the blood sugar
levels.

This stabilizing effect is important because some of the symptoms of
low blood sugar are due to rapid fall in blood sugar level which
accompany wide fluctuations in blood sugar levels following the
ingestion of sugar and starch.

Diet Prevents Polio, by Benjamin P. Sandler, M.D., and published in
1951 by The Lee Foundation for Nutritional Research, Milwaukee, WI





----------------------------------------------------------------------
----------


DR. MERCOLA'S COMMENT: Wow. This 50 year old article is a real gem,
an absolute classic. It was written a few years before I was born,
and it holds one of the major keys to good health.

Dr. Sandler was generations ahead of his time. He used basic common
sense to provide irrefutable evidence of the importance of severe
restrictions of grains and sugars to avoid polio.

Polio, however, is just one example of a viral infection, and I
assure you that the dietary principles elaborated by Dr. Sandler also
hold true for the other infections that we acquire.

So, by cutting back (hopefully eliminating) the breads, pastas,
sweets and sugars this holiday season and in the future we WILL
absolutely and unequivocally reduce our risk of coming down with the
old winter flus, coughs and colds.

Will following the diet provide absolute protection? Certainly not.
Other factors, such as sleep, stress, exposure to toxins, and
exercise also play a role. But for the most part, you will
practically eliminate your risk of ever getting sick again by
following the diet.

Related Articles:

Mutated Polio From Vaccine

UK Recalls Polio Vaccine Over 'Mad Cow' Fears

Should polio vaccinations be ended?

Lowering Blood Sugar Raises Glutathione and Vitamin E Levels

!!!!

CURRICULUM VITAE

W. John Martin, M.D., Ph.D.


Academic Appointments

• Visiting Scientist and Expert National Cancer Institute, NIH,
Bethesda, MD 1/71?9/72; 2/74?1/76 • Supervisory Medical Officer GS?14
and Head, Oncology Unit, Division of Virology, Bureau of Biologics,
Food and Drug Administration, NIH, Bethesda, MD 1/76?2/81 •
Supervisory Medical Officer GS?15 and Head, Biological Resources
Branch, Biological Response Modifiers Program, National Cancer
Institute, NIH, Bethesda,MD 3/81?1/82 • Associate Professor of
Pathology, Uniformed Services, University of the Health Sciences,
Bethesda, MD 1/826/85 • Professor of Pathology, University of
Southern California School of Medicine 7/85 ? present. Tenured
position with leave granted from 1996.

Clinical Appointments

• Chief of Immunology/Immunopathology Unit, Section of Laboratories
and Pathology, Los Angeles County+University of Southern California
Medical Center, Los Angeles, CA 7/85?6/93. Unit name change to
Immunology/Molecular Pathology 7/88. Director of Flow Cytometry, 6/93
to 10/95 • Director of USC Infectious Diseases Laboratory and of USC
Molecular Pathology Laboratory within the USC Clinical Laboratories,
USC School of Medicine 1/88?10/95

Other Positions

• Founder and Director, Center for Complex Infectious Diseases,
Rosemead, California 91770 (A research and clinical laboratory
testing facility supported by donations and other funding managed by
the National Heritage Foundation)

Board Certification

• Diplomat of the American Board of Medical Laboratory Immunology
1983 • Diplomat of the American Board of Pathology in Anatomic and in
Clinical Pathology 1984 • Special Competence Certification in
Immunopathology, American Board of Pathology, 1984 • Special
Competence Certification in Medical Microbiology, American Board of
Pathology 1985



BIBLIOGRAPHY PEER REVIEWED

1. Martin, W.J.: The cellular basis of immunological tolerance in
newborn animals. Aust. J. Exp. Biol. Med. Sci. 44:605608, 1966.

2. Martin, W.J., and Miller, J.F.A.P.: Site of action of
antilymphocyte globulin. Lancet 2:1285?1287, 1967.

3. Martin, W.J., and Miller, J.F.A.P.: Cell to cell interaction in
the immune response. IV. Site of action of antilymphocyte globulin.
J. Exp. Med. 128:855?874, 1968.

4. Martin, W.J., and Miller, J.F.A.P.: An assay for the
immunosuppressive capacity of antilymphocyte serum based on its
action on thymus?derived cells. Int. Arch. Allergy 35:163178, 1969.

5. Martin, W.J.: Experimental studies relating to the production and
clinical testing of antihuman lymphocyte serum. Med. J. Aust. 2:450?
455, 1969.

6. Martin, W.J.: Assay for the immunosuppressive capacity of
antilymphocyte serum. Evidence for opsonization. J. Immunol. 103:979?
989, 1969.

7. Martin, W.J.: Assay for the immunosuppressive capacity of
antilymphocyte serum. II. Nature and specificity of opsonizing
antibody. J. Immunol. 103:990?999, 1969.

8. Martin, W.J.: Assay for the immunosuppressive capacity of
antilymphocyte serum. III. Opsonizing activity of antihuman
lymphocyte serum. J. Immunol. 103:1999?1005, 1969.

9. Ellman, L., Martin, W.J., Green, I., and Benacerraf, B.: Linkage
between the PLL gene and the locus controlling the major
histocompatibility antigens in strain 2 guinea pigs. Proc. Natl.
Acad. Sci. U.S.A. 66:322?328, 1970.

10. Ellman, L., Green, I., and Martin, W.J.: Histocompatibility
genes, immune responsiveness, and leukemia. Lancet 1:11041006, 1970.

11. Martin, W.J., Ellman, L., Green, I., and Benacerraf, B.:
Histocompatibility type and immune responsiveness in random bred
Hartley strain guinea pigs. J. Exp. Med. 132:125?126, 1970.

12. Martin, W.J., Wunderlich, J.R., Fletcher, F., and Inman, J.K.:
Enhanced immunogenicity of chemically coated tumor cells in syngeneic
mice. Proc. Natl. Acad. Sci. U.S.A. 68:469?472, 1971.


13. Martin, W.J., Maurer, P.H., and Benacerraf, B.: Genetic control
of immune responsiveness to a glutamic acid, alanine, tyrosine
copolymer in mice. Linkage of responsiveness to H?2 genotype. J.
Immunol. 107:715?718, 1971.


14. Martin, W.J., Finerty, J., and Rosenthal, A.: Isolation of
plasmodium berghei (Malaria) organisms by ammonium chloride lysis of
infected erythrocytes. Nature 233:260? 261, 1971.

15. Phillips, S.M., Martin, W.J., Shaw, A., and Wegmann, T.G.: Serum
mediated immunological nonreactivity between histoincompatible cells
in tetraparental mice. Nature 234:146?148, 1971.

16. Miller, J.F.A.P., Sprent, J., Basten, A., Warner, N.L., Breiner,
J.C.S., Rowland, G., Hamilton, J., Silver, M., and Martin, W.J.: Cell
to cell interaction in the immune response. VII. Requirement for
active differentiation of thymus?derived cells. J. Exp. Med. 134:1266?
1284, 1971.

17. Winfred, J.B., Martin, W.J., and Mage, R.G.: Immunization of
neonatal rabbits with bovine serum albumin associated with allogeneic
thymus cells. Int. Arch. Allergy 41:895909. 1971.

18. Martin, W.J., Wunderluch, R.J., and Macdonald, J.: Suppressed
development of cytotoxic lymphoid cells in tumor immunized mice.
Israel J. Med. Sci. 9:324?331, 1973.

19. Wunderlich, J.R., Martin, W.J., and Macdonald, J.: Functional
efficiency of anti?tumor cytotoxic lymphoid cells. Israel J. Med.
Sci. 9:317?323, 1973.

20. Martin, W.J., Esber, E., Cotton, W.M., and Rice, J.M.:
Derepression of alloantigens in malignancy. Evidence for tumor
susceptibility antigens and for possible self?reactivity of lymphoid
cells active in the microcytotoxicity assay. Br. J. Cancer 28 Supp.
1:48?61, 1973.

21. Martin, W.J., and Martin, S.E.: Naturally occurring cytotoxic
antitumor antibodies in sera of congenitally athymic (nude) mice.
Nature 249:564?565, 1974.

22. Martin, W.J.: Immune surveillance directed against derepressed
cellular and viral alloantigens. Cell Immunol. 15:1?10, 1975.

23. Martin, S.E., and Martin, W.J.: Anti?tumor antibodies in normal
mouse sera. Int. J. Cancer 15:658?664, 1975.

24. Martin, S.E., and Martin, W.J.: Interspecies brain antigen
detected by naturally occurring mouse anti?brain autoantibody. Proc.
Natl. Acad. Sci. U.S.A. 72:1036?1040, 1975.

25. Martin, W.J., and Martin, S.E.: Thymus reactive IgM
autoantibodies in normal mouse sera. Nature 254:716?618, 1975.

26. Martin, S.E., and Martin, W.J.: X chromosome linked defect of
CBA/HEN mice in production of tumor reactive naturally occurring IgM
antibodies. J. Immunol. 115:502?507, 1975.


27. Martin, W.J., Esber, E., Cotton, W.G., and Rice, J.M.: Normal
tissue alloantigens and genetic control of susceptibility to tumors.
Microcytotoxicity studies on resistant C3Hf and susceptible (A x
C3Hf) F1 mice inoculated with transplacentally induced C3Hf lung
tumor. J. Immunol. 115:289?295, 1975.

28. Martin, S.E., and Martin, W.J.: Expression by human neuroblastoma
cells of an antigen recognized by naturally occurring mouse anti?
brain anti?antibody. Cancer Res. 35:26092612, 1975.

29. Martin, S.E., and Martin, W.J.: Naturally occurring cytotoxic
tumor reactive antibodies directed against type C viral envelope
antigens. Nature 256:498?499, 1975.

30. Martin, W.J., Gipson, T.G., Martin, S.E., and Rice, J.M.:
Derepressed alloantigen on transplacentally induced tumor coded for
by H?2 linked gene. Science 194:532?533, 1976.

31. Papas, T.S., Renzi, G.R., and Martin, W.J.: Immunological
distinction between ribonuclease H activity of and B forms of avian
myeloblastosis virus (AMY) DNA polymerase. Virology 76:882?885, 1977.

32. Martin, W.J., Gipson T.G., and Rice, J.M.: H?2a?associated
alloantigen expressed by several transplancentally?induced lung
tumors of C3Hf mice. Nature 265:738?739, 1977.

33. Ennis, F.A., Martin, W.J., Verbonitz, M.W., and Butchko, G.M.:
Specificity studies on cytotoxic thymus?derived lymphocytes reactive
with influenza virus?infected cells: Evidence for dual recognition of
H?2 and viral hemagglutinin antigens. Proc. Natl. Acad. Sci. U.S.A.,
74:3005?3010, 1977.

34. Ennis, F.A., Martin, W.J., Verbonitz, M.W.: Hemagglutininspecific
cytotoxic T?cell response during influenza infection. J. Exp. Med.
146:893?898, 1977.

35. Ennis, F.A., Martin, W.J., and Verbonitz, M.W.: Cytotoxic T
lymphocytes induced in mice by inactivated influenza virus vaccine.
Nature 269:418?419, 1977.

36. Ennis, F.A., Martin, W.J., and Verbonitz, M.W.: Distinct
recognition of influenza virus hemagglutinin and H?2 antigens by
cytotoxic thymus? derived lymphocytes. Dev. Biol. Stand. 39:373?378,
1977.

37. Martin, W.J., Gipson, T.G., Conliffe, M.D., Dove, L., Friedman,
R.J., and Rice, J.M.: Common tumor associated transplantation antigen
detected on a proportion of lung tumors induced transplacentally in
several strains of mice. Transplantation 24:294?294, 1977.

38. Gipson, T.G., and Martin, W.J.: In vivo anti?tumor immunity
detected by leukocyte adherence inhibition. Can. Immunol. Immunother.
3:210? 205, 1978.


39. Martin, W.J., Gipson, T.G., Conliffe, M.A., Cotton, W.G., Dove,
L., and Rice, J.M.: Histocompatibility difference between C3HfeB/HeN
and C3H/HeN mice. J. Immunogenet. 5:225?260, 1978.

40. Gipson, T.G., Imamura, M., Conliffe, M.A., and Martin, W.J.: Lung
tumor associated derepressed alloantigen coded for by the K region of
the H?2 major histocompatibility complex. J. Exp. Med. 147:1363?1373,
1978.

41. Butchko, G., Armstrong, R.B., Martin, W.J., and Ennis, F.A.:
Influenza A viruses of the H2N2 subtype are lymphocyte mitogens.
Nature 271:66? 69, 1978.

42. Aulakh, G., Hicks, J.T., Martin, W.J., and Phillips, P.W.: Search
for Type C oncornavirus?related genetic information in tissues from
patients with systemic lupus erythematosus. Arth. Rheum. 21:880?884,
1978.

43. Imamura, M., Gipson, T.G., Bensky, N., Justice, R., and Martin,
W.J.: Lung tumor reactive cytotoxic lymphocytes generated in mixed
lymphocyte reaction between C3HfeB/HeN (N?2kb) and C3H/HeN (H?2k)
strain mice. J. Immunol. 122:1863?1866, 1979.

44. Imamura, M., and Martin, W.J.: Variation in expression and
immunogenicity of an H?2 coded alloantigen on murine tumors. J.
Immunogenet. 7:31?37, 1980.

45. Martin, W.J., and Imamura, M.: Variable expression of
histocompatibility antigens on tumor cells. Clin. Immunol.
Immunother. 8:219, 1980.

46. Pope, B.L., Justice, R., Sarma, C., and Martin, W.J.: Nonspecific
cytotoxic cells generated in vitro in response to a weakly
immunogenic murine adenocarcinoma. In vivo correlations. Int. J.
Cancer 28:77?83, 1981.

47. Martin, W.J., and Imamura, M.: Differential suspectability of
spleen cells from C3H/HeN (H?2k) and C3HfB/NeN (H?2kvl) mouse strains
to cytotoxicity by monoclonal and anti Kk antibody (clone 11?4.1). J.
Immunogenet. 8:73?76, 1981.

48. Pope, B.L., Hapel, A., Martin, W.J., Merchant, B., and Ennis, F.:
An assay for virus specific help. J. Immunol. Methods 40:95?99, 1981.

49. Callahan, G.N., Martin, W.J., and Pardi, D.: Biochemical
comparison of H?2K antigen isolated from C3HfB/HeN mice. Immunogenet.
12:561?568, 1981.

50. Callahan, G.N., Martin, W.J., and Pardi, D.: Biochemical
comparison of H?2K antigen isolated from mutant C3HfB/HeN and parent
C3HeN mice. J. Immunol. 128:2116?2120, 1982.

51. Imamura, M., and Martin, W.J.: Variation in histocompatibility
antigen expression on murine tumors. Differences in expression and
immunogenicity of H?2K region coded unique antigens. J. Immunol.
192:877?881, 1982.


52. Callahan, G.N., Pardi, D., Giedlin, M.A., Allison, J.A., Monzot,
P.M., and Martin, W.J.: Biochemical evidence for expression of a
semi? allogeneic H?2 antigen by a murine adenocarcinoma. J. Immunol.
130:471?479, 1983.

53. Geidlin, M.A., Martin, W.J., and Callahan, G.N.: Immunochemical
characterization of Ia antigens on the murine adenocarcinoma LT?85. J
Natl. Cancer Inst. 71:825?834, 1983.

54. Doyle, A., Martin, W.J., Keiko, F., Gazdar, A., Carney, D.M.,
Martin, S.E., Linnoila, I., Cuttitta, F., Mulshine, J., Bunn, P., and
Minna, J.: Markedly decreased expression of class I
histocompatibility antigens, protein and mRNA in human small?cell
lung cancer. J. Exp. Med. 161:1135?1151, 1985.

55. Shibata, D.K., Arnheim, N. and Martin, W.J.: Detection of human
papilloma virus in paraffin?embedded tissue using the polymerase
chain reaction. J. Exp. Med. 167:225?230, 1988

56. Almoguera, C., Shibata, D., Forrester, K., Martin, W.J., Arnheim,
N. and Perucho, M.: Most human carcinomas of the exocrine pancreas
contain mutant c?K?ras genes. Cell. 53:549? 554, 1988

57. Shibata, D., Yao, S.F., Gupta, J.W., Shah, K.V., Arnheim, N. and
Martin, W.J.: The detection of human papillomavirus in normal and
dysplastic tissue by the polymerase chain reaction. Lab. Invest.
Vol.59:555?559 ,1988

58. Shibata, D., Martin, W.J. and Arnheim, N.:
Molecular "archaeology"; the presence of human papilloma virus in the
late 1940's. Can. Res. 48:4564?4566, 1988

59. Vogel, J.M., Davis, A.C., McKinney, D.M., Macmillan, M., Martin,
W.J. and Goodekow, R.S. Molecular characterization of the C3HfB/HeN H?
2K m2 mutation: Implications for the molecular basis of
alloreactivity. J.Exp. Med. 168: 1781?1800, 1988.

60. Shibata D, Martin WJ, Appleman MD, et al. Detection of
cytomegaloviral DNA in peripheral blood of patients infected with
human immunodeficiency virus. J Infect Dis 158: 1185?1192, 1988.

61. Shibata, D., Cosgrove, M. Arnheim! N., Martin, W.J., and Martln,
S.E. Detection of human papilomavirus in fine needle aspirates of
metastatic cervical carcinomas using the poly merase chain reaction.
Diag. Cytopathol. :540?43, 1989.

62. Kiyabu, M. Shibata, D., Arnheim, N., Martin, W.J., Fitzgibbons,
P.: Detection of human papillomavirus in formalin fixed invasive
squamous carcinomas using the polymerase chain reaction. Am. J. Clin.
Path. :13: 221?224, 1989.

63. McDonnel J.M., Mayr A. and Martin, W.J.: Detection of human
paplllomavlrus type 16 in dysplasias and squamous carcinomas of the
conjunctive. N. Eng. J. Med 320; 1442?1446, 1989.

64. Rao N.A., Atalla 1., Linker?Israeli M., George F.W., Martin W.J.,
Steinman L.: Suppression of experimental uveitis in rats by anti ANTI?
IA antibodies. Invest. Ophthalmol?Vis?Sci 30; 2348?2355, 1989.

65. Vogel J.M., Macmillan M., Martin W.J., and Goodenow R.S.,
Evidence that the derivation of lung adenocarcinoma LT85 predated
establishment of the H?2KmZ mutation in a C3Hf colony of mice.
J.Immunogenet. 164; 363?371, 1989.

66. Mc Donnel J., Mc Donnel P., Martin W.J.: Detection of Human
Papilloma virus type 16 in a recurrent squamous carcinoma of the eye
lid. Arch. Ophthalmol. 107; 1631?1634, 1989.

67. Greenspoon JS, Martin WJ, Greenspoon RL, McNamara BT. Necessity
for routine screening for hepatitis B surface antigen. J. Reproduct.
Med. 34; 655?8, 1989.

68. George F., Law J., Rich K., Martin W.J: Identification of a T
cell epitope on the circumsporozoite protein of plasmodium vivax.
Infection and Immunity. 58; 575?78, 1990.

69. Rich KA, George FW, Law J. Martin WJ.: Cell adhesive motif in the
circumspozoite (CS) gene of malaria. Science 249; 1574?1576, 1990.

70. Mohabeer A, Hiti A, Martin WJ.: Non?radioactive detection of
single strand conformation polymorphism (SSCP) using the Pharmacia
Phast System. Nuc. Acids Res. 19; 3154, 1991.

71. Sullivan SM, Gieseler RKH, Lenzner S. Ruppert J. Gabrysiak TG,
Peters JH, Cox G. Richer L, Martin WJ, Scolaro MJ. Inhibition of
human immunodeficiency virus?1 proliferation by liposome?encapsulated
sense DNA to the 5' TAT spliceacceptor site. Antisense Res. Develop.
2; 187?197 1992.

72. Biswas J. Mayr AJ, Martin WJ, Rao NA. Detection of human
cytomegalovirus in ocular tissue by polymerase chain reaction and in
situ hybridization. Graefes Arch Clin Exp Opthal 231: 66?70 (1993)

73. Martin WJ, Zeng LC, Ahmed K, Roy M. Cytomegalovirus?related
sequences in an atypical cytopathic virus repeatedly isolated from a
patient with the chronic fatigue syndrome. Am. J. Path. 145: 441?452,
1994.

74. Martin WJ. Stealth virus isolated from an autistic child. J. Aut.
Dev. Dis. 25:223?224,1995

75. Martin WJ, Ahmed KN, Zeng LC, Olsen J?C, Seward JG, Seehrai JS.
African green monkey origin of the atypical cytopathic 'stealth
virus' isolated from a patient with chronic fatigue syndrome. Clin.
Diag. Virol. 4: 93?103, 1995.

76. Martin WJ, Glass RT. Acute encephalopathy induced in cats with a
stealth virus isolated from a patient with chronic fatigue syndrome.
Pathobiology 63: 115?118, 1995.

77. Gollard RP, Mayr A, Rice DA, Martin WJ. Herpesvirus?related
sequences in salivary gland tumors. J. Exp. Clin. Can. Res. 15: 1?4,
1996.

78. Martin WJ. Genetic instability and fragmentation of a stealth
viral genome. Pathobiology 64:9?17, 1996.

79. Martin WJ. Severe stealth virus encephalopathy following chronic
fatigue syndrome?like illness: Clinical and histopathological
features. Pathobiology 64:1?8, 1996.

80. Martin WJ. Stealth viral encephalopathy: Report of a fatal case
complicated by cerebral vasculitis. Pathobiology 64:59?63, 1996.

81. Martin WJ. Simian cytomegalovirus?related stealth virus isolated
from the cerebrospinal fluid of a patient with bipolar psychosis and
acute encephalopathy. Pathobiology 64:64?66, 1996.

82. Martin WJ, Anderson D: Stealth virus epidemic in the Mohave
Valley. Initial report of viral isolation. Pathobiology 65:51-56,
1997.

83. Martin WJ. Cellular sequences in stealth viruses. Patobiology
66:53-58, 1998.

84. Magyarosy E, Martin WJ, Chu EW, Martin SE. Differential
diagnostic significance of the paucity of HLA-I antigens on
metastatic breast carcinoma cells in effusions. Pathol Oncol Res 5:32-
5, 1999

85. Martin WJ. Bacteria related sequences in a simian cytomegalovirus-
derived stealth virus culture. Exp Mol Path. 66: 8-14, 1999.

86. Martin WJ. Stealth adaptation of an African green monkey simian
cytomegalovirus. Exp Mol Path. 66:3-7, 1999.

87. Martin WJ. Melanoma Growth stimulatory activity (MGSA/GRO-alpha)
chemokine genes incorporated into an African green monkey simian
cytomegalovirus (SCMV)-derived stealth virus. Exp Mol Path. 66: 15-
18,1999.

88. Martin WJ, Anderson D. Stealth Virus Epidemic in the Mohave
Valley: Severe Vacuolating Encephalopathy in a Child Presenting with
a Behavioral Disorder. Exp Mol Pathol. 66:19-30 1999.

89. Martin WJ. Chemokine receptor-related sequences in an African
green monkey simian cytomegalovirus (SCMV)-derived stealth virus.
(Exp Mol Path. (in press)




NON?PEER REVIEWED (conference proceedings, partial listing)

1. Martin, W.J., and Miller, J.F.A.P.: Assay for the opsonizing
activity of anti?lymphocyte serum. In Propriates Immu no?depressive
Et Mechanisme D' action Du Serum Antilymphocytaire. Collog. Int. Du
Centre National de la Researche Scientifique 1190:111?120, 1971.

2. Martin, W.J., Esber, E., and Wunderlich, J.R.: Evidence for the
suppression of the development of cytotoxic lymphoid cells in tumor
immunized mice. Fed. Proc. 32:173?179, 1973.

3. Martin, W.J., and Wunderlich, J.R.: Immune response of mice to
concanavalin A?coated El?4 leukemia. National Cancer Institute
Monograph No. 35: U.S. Dept. of Health, Education, and Welfare,
Public Health Service, Washington, D.C., U.S. Govt. Printing Office,
1972, pp.295?299.

4. Wunderlich, J., Martin, W.J., Macdonald, J., and Fletcher, F.:
Functional capacity of cytotoxic lymphoid cells. National Cancer
Institute Monograph No. 35: U.S. Dept. of Health, Education, and
Welfare, Public Health Service, Washington, D.C., U.S. Govt. Printing
Office, 1972, pp. 243?249.

5. Esber, E., Martin, S.E., and Martin, W.J.: Nerve and tumor
specific antigens in mouse and human neuroblastoma cells. Proc. Int.
Symp. Neuroblastoma, Genoa, Italy, Gaslini 11:157?164, 1979.

6. Martin, W.J., Martin, S.E., and Rice, J.M.: Cross?reactive tumor
associated antigens detected on murine tumors by naturally occurring
antibodies ln mouse sera. Proc. Third. Intl., Symp. Detection and
Prevention of Cancer. Marcel Decker Ind. , New York,

7. Martin, W.J.: Report of workshop on natural tumor immunity and
surveillance. Progress in Immunology III. Proceedings of the Third
International Congress of Immunology. Sydney, Australia. Ed. T.E.
Mandell, et al. North Holland Publish ing Co., New York, pp. 827?828,
1978.

8. Martin, W.J., and Esber, E.E.: Enhanced immunogenicity of
concanavalin coated tumor cells. Proc. Intl. Conf. Xenogenization of
Tumor Cells, Sapporo, Japan, 1978, GANN, Monoraph on Cancer Res.
23:111, 1978

9. Immura, M., and Martin, W.J.: Variation in expression of H? 2
histocompatibility antigens on tumor cells. Transplant Proc. 12:77?
79, 1980.

10. Hapel, A.J., Cole, G.A., Pope, B., and Martin, W.J.: Microvesicle
induced antigen transfer to target cell membranes. Transplant Proc.
12:91?94, 1980.

11. Martin, W.J.: MHC coded unique alloantigens and anti?tumor
immunity. Transplant Proc. 13:1837?1840, 1981.

12. Martin, W.J.: Structural and functional alterations of MHC coded
antigens on tumor cells. Transplant Proc. 15:2097?3000, 1983.

13. Martin, W.J., and George, F.W.: Potential mode of action of
adjuvants used for malarial vaccines. in Proceedings of First Asian
and Pacific Conference on Malaria. Uni. Hawaii Press 1985

14. Martin, W.J.: An overview of FDA requirements for vaccine
development. in Proceedings of First Asian and PacificConference on
Malaria Uni. Hawaii Press 1985

15. Martin W.J. Detection of viral related sequences in CFS patients
using the polymerase chain reaction.in "The Clinical and Scientific
Basis of Myalgic Encephalomyelitis Chronic Fatigue Syndrome." Byron
M. Hyde Editor. Nightingdale Research Foundation Press. Ottawa Canada
pp 278?283, 1992.

16. Martin W.J. Viral infection in CFS patients. in "The Clinical and
Scientific Basis of Myalgic Encephalomyelitis Chronic Fatigue
Syndrome." Byron M. Hyde Editor. Nightingdale Research Foundation
Press. Ottawa Canada pp 325?327, 1992.

17. Martin W.J. Chronic fatigue syndrome (letter). Science 255: 663,
1992.

18. Martin W.J. Stealth viruses as neuropathogens. CAP Today 8 67?70,
1994

19. Martin WJ. Viteria: Bacterial Sequences in Animal and Human
Viruses. J Degenerative Dis. 1:1999

20. Martin WJ Brain damage in stealth virus infected children. The
Mind of a Child Conf. Proc. 1; 17-24, 1999



BOOK REVIEWS

1. Neuroblastoma. Clinical and Biologic Manifestations. Ed. Carl
Pochedly, 1982. Reviewed for New England Journal of Medicine, 1983.

2. Immunodiagnosis for Clinicians: Interpretations for Immunoassays.
Eds. M.H. Grieco and D.K. Meriney, 1983. Reviewed for New England
Journal of Medicine, 1983.

3. Molecular Immunology. A Textbook. Eds. M.Z. Atassi, C.J.Van Oss,
and D.R. Absolom, 1984. Reviewed for New England Journal of Medicine,
311:925?926, 1984

4. Sandritter's Color Atlas and Textbook of Histopathology. Eds. C.
Thomas and G.W. Richter.VII Edition, 1984. Re viewed for New England
Journal of Medicine, 312:798, 1985.

CHAPTERS

1. Green, I., Ellman, L., Martin, W.J., and Benacerraf, B.: Genetic
control of immuni responsiveness in guinea pigs. In: Cellular
Interactions in the Immune Response. (Eds. Z. Cohen, G. Cudkowicz,
and R.T. McCluskey), pp. 148?156.

2. Martin, W.J., Wunderlich, R.R., and MacDonald, J.: Suppressed
development of cytotoxic lymphoid cells in tumor?immunized mice In
Immunoligical Parametes of Host Tumor Relationships. Vol. 2. Ed.
David W. Weiss, Academic Press, New York, pp. 120?127, 1974

3. Wunderlich, J.R., Martin, W.J., and MacDonald, J.: Functional
efficiency of antitumor cytotoxic lymphoid cells In: Immunological
Parameters of Host Tumor Relationships. Vol. 2 (Ed. by David W.
Weiss) Academic Press, New York. pp. 113?119, 1974.

4. Martin, W.J.: Use of concanavalin A to enhance immunogenicity of
tumors antigens. In: Concanavalin A as a Tool. (Ed. H. Brittinger)
Academic Press. Chapter 54, pp. 363?571, 1981.

5. Martin, W.J.: Tumor Immunology ? Overview In: Comprehensive
Textbook of Oncology 2nd Edition. Williams & Wilkins, Baltimore MD.
Moossa AR, Schimpff SC and Robson MC, Editors. pp 101?103, 1991.

6. Martin, W.J.: Polymerase Chain Reaction: A tool for the modern
pathologist. In: Molecular Diagnostics in Pathology United States and
Canadian Academy of Pathology Inc. series "Techniques in Diagnostic
Pathology" CM. Fenoglio?Preiser and CL. Willman, Editors pp 21?46,
1991

7. Martin, W.J.: Infectious Disease Testing in The Polymerase Chain
Reaction Birkhauser, Boston MA. K.B. Mullis, F. Ferre and R.A. Gibbs,
Editors. 1994








----------------------------------------------------------------------
----------

Last changed: March 08, 2001

Victoria Hall, RN< BSN,CCRN, will be joining us.  I spoke to her
regarding the enclosed.  The man who wrote it has passed away.



ThisRe: Stealth Virus
From: victoria@...
Date: 07 Jul 2000
Time: 11:22:10


Comments
I too am interested in learning more about this study. I received
this email a week or two ago - hopefully the format will remain
intact. Victoria.

Dear PALS,

I enclose for your information the introducing of the ALS group study
and the study update from the 24th June.

I have myself sent in a blood sample. As you will read 'at least 13
people have sent in their blood samples and have tested positive for
stealth adapted viruses'. I think that Dr. Martin may be on the right
track and I suggest you send a blood sample too.

Please forward this message to fellow PALS.

Best regards, Lars

Date: 25 June 2000 07:01 Subject: Private ALS Group Study Update

June 24, 2000

Hello Again!

We are making progress! At least 13 people have sent in their blood
samples and have tested positive for stealth adapted viruses.
Providing their clinicians agree to try the suggested protocol, these
patients will be included in the study. We need to have more ALS
patients submit their blood in order to have a larger data base. Dr.
Martin is excited about the positive culture results obtained so far,
and with more participants will be able proceed with the study. The
sooner we get started, the sooner we will have some concrete
information, and as promised, we will keep everyone in the study
informed.

1. How do I send my blood sample in?

Follow the instructions included in the introductory e-mail and send
the 10 ml sample in a "yellow Topped (ACD) tube" by overnight Federal
Express or Express mail to Dr. Martin, CCID, 3328 Stevens Avenue,
Rosemead, CA 91770 . Please e-mail us after you have mailed the
sample with the tracking number so that we will know to expect the
sample and can track if it does not arrive. If you send in your blood
sample you will automatically be included in the study and informed
as to the results of the study.

2. Tell us more about Dr. Martin, the ALS stealth virus, and the
treatment protocol.

Dr. Martin has a web-site at ccidlab@... , or www.ccid.org .
The suggested protocol is being discussed with several knowledgeable
physicians and pharmacists. In addition the protocol and supporting
data will be submitted to an Institutional Review Board (IRB). Dr.
Martin is primarily a virologist working towards understanding how
viruses can potentially cause diseases, such as ALS, without evoking
and anti-viral inflammatory reaction. He coined the term "stealth-
adapted" viruses to describe such viruses and has learned how to
detect the viruses using tissue culture methods. Dr. Martin is an
experienced, well published investigator. At the request of several
people, a copy of his Curriculum Vitae is attached.

Dr. Martin in conjunction with his medical colleagues is planning to
recommend a protocol to clinicians caring for culture positive ALS
patients. The decision to treat will be the responsibility of the
clinician, along with the consent of the patient. Each participant
will need to give their clinician authorization to discuss their case
with Dr. Martin and/or his colleagues regarding the suitability of
the patient for receiving the suggested protocol. Dr. Martin DOES NOT
(in order to preserve the "blinded study" aspect) want to know which
participants have elected to be treated, but as a requirement for
participation, each participant will need to send a blood sample
prior to, and one week following the decision to either treat or not.
Treated patients should stay on the therapy for 3 weeks, even if the
one week result has shown no improvement in the level of virus
activity. A third blood sample will be required from all
participants, whether treated or not. The medications chosen for the
initial study are based on their known chemokine and viral inhibitory
activity. They are widely prescribed and relatively non-toxic. By
using a cocktail, rather than using single drugs, additive effects
may be achieved.

By monitoring the viral activity levels, the potential for long term
benefits of continued treatments can be discerned.

In more basic research studies, Dr. Martin also hopes to gain
sequence data on some of the isolates from ALS patients. There is
also a molecular inhibitor that accumulates in the cultures, and he
believes that this inhibitor holds the best promise for suppressing
stealth virus infection.

3. What is the cost of the ALS Study, and is there a Non-profit
Foundation associated with CCID?

From the very beginning, we have been sensitive to the issue of cost.
Dr. Martin is associated with a Non-profit Foundation for the Center
for Complex Infectious Diseases organized under the

National Heritage Foundation, 6218 Beachway Drive, Box 1776, Falls
Church VA 22041 800-986-4483. Fax 703 820-5100.

The President of the Foundation is Dr. John T. Houk.

To date, all donations have gone to a stealth virus trust account,
and all contributions for this study may be sent to the foundation.
The cost is currently anticipated to be $1,000 per participant. Each
culture assay is between $250 and $400 and each participant requires
three cultures. Lab fees, IRB fees, and other direct costs associated
with the study make up the difference. No one involved with this
study is in any way individually monetarily benefiting from this
study. Several of you have already so generously offered to
contribute, we need to prevail upon your kind generosity to help fund
the study. If you or your organization has any questions regarding
the foundation or the use of the funds, please do not hesitate to
ask.

We have had some wonderful support from PALS, CALS, and various
organizations such as Hope for ALS. Please contact your fellow ALS
friends, acquaintances, and e-mail buddies and let them know about
the study. We have the possibility to affect the lives of countless
individuals with the positive results of this study. Let us know if
you have any questions and we will endeavor to respond.

Best Regards and may God bless you all.

Helen Mouat

Response  to Jeff Kelly @ StealthVirus-Patient   3/9/01
Re: Relationship between Stealth Virus and Hyperinsulinism

From:  H. Lynn Knapp, M.A.
Moderator
TheStealthVirusSupportGroup


Dear Jeff:

           First, I'd like to invite you to join us at
TheStealthVirusSupportGroup.  You have a lot to offer.

           Second, I'd like to address some of your questions and
misconceptions.  Please do not mistake the messenger with the
message!  Get your focus off Atkins and on to any low carbohydrate
diet that works for you.

           Again, I will be sharing from my own experience:  When I
stumbled over this phenomenon of insulin affecting Stealth Virus,
(and again I say it may not be the insulin, but the sugar that
stimulates the virus), as it was only my opinion that it is the
insulin, I had no one to answer my questions, nor to guide me, as
this phenomenon was thought to be unique to me.  Since I had no
guide, I had no recourse but to rely on the Atkins Diet, carbohydrate
counter, and book called, "Dr. Atkins' Vita-Nutrient Solution." These
resources served me well only as long as I temporarily threw out all
my previous preconceived notions re: my food allergies, etc.  I was
in so much pain, the focus was emergency intervention, and then later
balance with food allergies etc.  Remember, due to my critical
condition, this is what "I" had to do, it does not mean you will have
to be so severe.

           I began by not taking in any more than 20 carbohydrates a
day, as Atkin's recommends for losing weight.  I instantly saw
dramatic improvement in my viral symptoms.  I didn't understand, no
one did.  But I asked permission of my M.D. to drop to only 10
carbohydrates a day to see if it really was the low carbohydrate
level.  To my great surprise, my symptoms improved even more
dramatically!  Each time I tried to increase my carbohydrate intake,
my symptoms flared up with a vengeance.  Some of my symptoms are very
severe and can not be easily mistaken to be something else wrong.
One example is my Tetany.  The contortions are so severe, that
without immediate help, the contractions could, and would brake my
bones.  The other severe symptom is CHF.  I have a myriad of other
symptoms, but since these are objective, able to be documented and
witnessed; I use them as my guide.


           I found myself finally having control over THE BEAST THAT
DWELLS WITHIN by simply containing my carbohydrate count to 10 or
below grams per day.  It did not matter which carbohydrate I ate, as
long as the daily count was 10 or below.  When it became evident that
this was truly giving some of my life back, thought had to be given
as to how to increase my carbohydrate intake without setting off the
virus.  I tried again to increase the carbohydrates slowly to only
achieve the same result, a virulently active virus.  It was as though
I had starved the virus, and as soon as I gave it what it needed to
live, it came on with a renewed vengeance, stronger than before I cut
the carbohydrates.  It soon became obvious that I could not live on
10 grams of Carbohydrate a day.  So I once again turned to Atkins.  I
read everything he wrote and discovered he had a protocol he followed
with the low carbohydrate diet for hypoglycemics, diabetics, and
those suffering from hyperinsulinism and high triglycerides.  The
protocols are fairly similar for each of the three sugar related
illnesses.  I tried each and every one and documented its effects,
trying one at a time.

           The first thing I found to be a necessity so I could
increase my carbohydrates slightly, was Glucophage.  Glucophage is
used in type I and type ll diabetes to lower insulin.  It lowers the
insulin by helping to stabilize the sugar.  It is the sugar that
raises the insulin.  We started slowly because I had very severe
hypoglycemia  and it was feared Glucophage may lower my sugar.  My
first surprise was that it not only did not lower my sugar, but it
stabilized my hypoglycemia.  My hypoglycemia was being caused by
hyperinsulinism.  It was reacting to the hyperinsulinism.  So by
controlling the insulin, we completely got rid my hypoglycemia!

           We started on a low dose of Glucophage, and slowly moved up
as we saw how much it was helping to control the virulence of my
viral symptoms.  But around 4:00 am, I would awaken screaming with an
attack of severe Tetany.  It was realized that I needed a steady
blood level of Glucophage, and the maximum dose was given, divided
into 4 dosing times, of 500mg each for a daily total of 2,000mg.

          This, however, was not enough, as I needed more to constrain
my insulin levels as I tried to increase slightly my carbohydrate
intake.  I once again turned to Dr. Atkins.  I read and reread; I
experimented and re-experimented with everything he suggested that
would help in lowering insulin and triglyceride levels.  I believe he
is correct that high insulin causes high triglycerides because
everything I tried to lower my insulin, also lowered dramatically my
triglyceride levels.  The book that helped me the most is  "Atkin's
Vita-Nutrient Solution".

              For myself, I found four things to be essential:   The
first is the Glucophage.  The second is Vanadyl Sulfate.  Be sure to
start low and build up till you get results.  Also be sure to start
one at a time for two reasons:  First to allow your body to adjust,
and second, so you can discern which it is you are taking that is
helping or not helping.  I need 25mg of Vanadyl Sulfate 4 times a
day.  Each individual may vary.  Remember not to go up too fast…be
patient and document everything, doses and results.  This is truly
critical to get a sure and accurate protocol for yourself.  The Third
is Pantethine, not Pantethenic acid, Pantethine is stronger.  I found
Mega Pantethine produced by Atkin's to help me the most.  I take 450
twice a day.  And finally, L-Carnitine.  I take 500mg 4 times a day.
I try to keep steady blood levels with everything I take.  If at any
time I run out of any of the above, I first experience violent Tetany
and then I begin to elicit increased pulmonary edema.  An example is
this week.  I ran out of Mega Pantethine and the muscle seizures
began.  Then I ran out of L-Carnitine.  Both were backordered.  The
first day I was out of both I experienced the most violent Tetany I
ever had.  It took 6, 5mg Valium's, administered every 15 minutes
before I stopped screaming.  At least I know these four are essential!

           The last and final key supplement that may really help
Stealth Virus via helping insulin is DHEA.  This nutrient fits in a
class all it's own when it comes to helping insulin.  The other four
I mention help to either lower insulin and thus triglycerides, or
lower triglycerides and thus insulin.  DHEA does not lower insulin or
triglycerides at all, it helps to prevent it from happening in the
first place.  It may be the reason Stealth Patients suffer from
hyperinsulism.  If your DHEA level is low, as it is with most Stealth
Patients (any Dr. can draw DHEA levels, and the lab clearly
interprets the result), then you develop insulin resistance, which in
turn becomes hyperinsulism.   DHEA is an adrenal harmone, and we all
know the adrenals are directly affected by Stealth Virus.  It is too
early for me to comment fully on the effect of DHEA on hyperinsulism,
but my early experimentation looks good.  I had begun with a low dose
of 5mg daily so my body could adjust.  But when I ran out of
Carnitine and Pantethine, and the attacks of Tetany would not let up
and Valium was my only recourse, I increased my dose of DHEA to 5mg 2
times a day.  The results are interesting.  The attacks are less
frequent and less severe, and very little Valium has been needed.
Please note I always divide my doses.  I have found a steady blood
level seems to work best in controlling the virus.  When back on the
Pantethine and Carnitine, the attacks will cease and the Valium will
be shelved.

            However, I must remain on a strict low carbohydrate diet.
When my virus is active I must stay on a 60gram of Carbohydrate diet
per day.  When my virus is less active, then I can increase 20-40mg
of carbohydrates a day.  But not more!  My virus cycles, four days
active, and three days somewhat dormant.

            Dr. Atkin's recommends a few other things to lower
insulin, but my experience has been none of them are critical like
the ones I have already listed.  He recommends Milkthistle to lower
insulin, but it is not high on his list, nor mine in importance
regarding lowering insulin.  I take it anyway.  But I must admit, I
can not discern how much, if any, it is helping to lower insulin.

             I would like to mention one thing I've discovered with
myself.  When deciding to increase some degree of carbohydrates, try
to stay away from direct sugars, like fruit or sweets.  I can not
tell you how severe your reaction will be once you have deprived the
virus.  On my birthday  I ate one piece of chocolate fudge cake.
Within the hour I was screaming with acute Tetany, and it lasted all
through the night.  Yesterday I ate a grapefruit and the Tetany
attacks lasted all day and night.  The pain was excruciating.  I have
found increasing carbohydrates with vegetables, nuts and complex
carbohydrates in moderation is better  .Dr. Atkin's also recommends
taking L-Glutamine to control your cravings.  It really does help.  I
take 500mg 4 times a day.

           Finally, I'd like to add how wonderful it is having some
degree of control over THE MONSTER WITHIN.  I'm no longer in a
hospital bed;  I'm  down to a very low liter flow of O2;  I'm on less
than half the diuretics I used to need;  I no longer need Ativan or
Phenobarbital;  my HGB is higher and more stable;  my white count is
higher;  my thyroid is responding to Synthroid when prior it would
not respond at all;  my Tetany only occurs now if I run out of one of
the "FOUR", or if I go off the low carbohydrate diet;  my cold sweats
are markedly better, and so are my fevers;  I no longer wear my
corporal tunnel braces;  nor do I sleep with my mouth brace for TMJ;
my vision is much less blurred; and cognitive impairment is less
evident;  joint pain is at a minimum and so is my fibromyralgia;  my
cyanosis is less severe;  and my hair is starting to grow in very
faintly, enough though that I have a new hairline.

           I have to add that this is a very delicate balance.  My
immune system is severely impaired.  I have hypogammaglobulinemia.
This too has gotten better, however not enough to protect me from
picking up secondary infections.  If and when I pick up a secondary
illness, the Stealth comes on like a monster coming out of
hibernation, and I get very, very ill.

           It is also important to note I am on Cytovene, and taking
modalities to suppress   Cytokine/Chemokine activity.  I am taking
500mg of Quercetin 4 times daily because of its powerful anti-reverse
transcriptase  activity.  I is very powerful, one of the most
powerful things I have witnessed to date.  When active, My whole
lymphatic system would swell;  under arms, back of neck, under neck,
groin, etc.  I also have a face lesion that would grow and burn.  I
was scheduled for lymphatic and facial bx's.  I began Quercetin,
500mg daily at first, but when I saw my lumps going down and my
faciel lesion shrinking, I began to increase the dose.  Finally I
reached the maximun recommended, 500mg 4 times a day, totaling
2,000mg.  Since I began Quercetin, I have not elicited any lymphatic
involvement, and my face lesion has stopped growing and has lightened
in color.  And I cancelled the lymphatic and facial lesion bx.

           Please note that the reason I can be so definite as to how
and why these modalities are working is this:   I have a very severe
autoimmune problem, and therefore can not take most things.  Anything
that helps my immune system, hurts me because my immune system
attacks me.  Thus I can only take modalities that directly interfere
in the virus's growth process, like Quecertin; and modalities that
help to suppress the virus by interfering with either what feeds it,
or what stimulates it, ie, insulin suppressing modalities.

           This is only my personal experience from personal
experimentation.  I am not a healthcare professional, just a fellow
sufferer of this virulent disease.  I have been sick 22yrs, and only
now do I have some degree of control.  I can not tell you how great
that feeling is, it is indescribable.  I wish this all for you.  I
hope I have stumbled upon something that will help you all.

God be with you,

H. Lynn Knapp, M.A
Moderator
TheStealthVirusSupportGroup

PROPOSAL

Title:  STEALTH VIRUS INHIBITOR  (EPIONE):  Request for tax-exempt
support for the initial studies required to develop an anti-stealth
viral agent for potential therapy of patients, a shockingly
increasing number of whom present with physical and neurological
symptoms consistent with chronic fatigue syndrome, fibromyalgia, viral
encephalitis, Gulf War syndrome, autism, Lyme disease, and
neuropsychiatric diseases.


Submitted by:  W. John Martin, M.D., Ph.D.  (626) 572-7288
		  CENTER  FOR COMPLEX  INFECTIOUS DISEASES
		  3328 Stevens Avenue, Rosemead, CA   91770


		 I have used both tissue culture and molecular
techniques to search for a viral origin of  complex neurological
diseases in adults and in children.  This work has led to the
identification of a novel class of cytopathic viruses that have been
designated "stealth viruses" because they can induce disease without
evoking an inflammatory response.  The prototype stealth virus has
been derived from African green monkey simian cytomegalovirus (SCMV)
by a process of gene deletions, gene acquisitions and mutations.
Significantly, there is loss of genes coding for the major
antigenic components in SCMV that would ordinarily evoke an
inflammatory reaction.  The infected individual, therefore, cannot
use his immune system to combat and eliminate the virus.  Rather, it
is necessary to develop an alternative approach to treatment.

		 Positive blood cultures for stealth virus (and in
some patients, positive cultures from brain tissue and from the
cerebrospinal fluid surrounding the brain) have been obtained from
patients with a variety of illnesses, many of which share a common
symptomology.  Stealth viruses also induced neurological diseases
when inoculated into cats.  Some of the severely ill patients (as
well as some of the cats) have shown improvement over time in the
absence of any pharmacological intervention.  These findings support
the underlying hypothesis that some form of viral inhibition can
occur.

		 I have also observed an inhibitor in the tissue
culture fluid of stealth viral cultures grown in certain cell lines.
I believe this inhibitor represents a genetically-mutated viral
product which can interfere with stealth viral replication. It has
been tentatively termed "Epione" after the wife of Asculpius, the
Greek "Father of Medicine",  who was known for her ability to soothe
pain.  My first goal is to purify this compound from the tissue
culture fluid and determine its composition.  The second goal is to
define, by genetic sequencing,  the gene which codes for Epione and
the genes that are affected by this compound.  I have cloned the
genome of an SCMV-derived stealth virus, and should have a source of
a small quantity of genetically-produced material.  Using this
material, my third goal is to request FDA approval of its use in a
few severely ill, stealth virus-infected patients.  Objective
clinical improvement would help validate the hypothesis that the
stealth virus infection was the primary cause of the patient's
illness.  Larger quantities of the compound will then be produced,
probably in conjunction with a pharmaceutical company, for the final
goal:  to undertake a large-scale double blind
study.

		 These biochemical, genetic and therapeutic studies
offer real hope for a major breakthrough in our understanding of many
neurological and neuropsychiatric diseases in both adults and
children.   Financial assistance through the tax-exempt National
Heritage Foundation is urgently needed so that the project can be
initiated, and the first two goals met.  The planned studies will
cost approximately $250.000.00, as detailed in the attached budget.
The work can begin immediately.



BUDGET

1. Purification and Chemical Identification of the Stealth Virus
Inhibitor:

Salary for a technician to perform studies $20,000.00
Media and plasticware supplies  $10,000.00
Filtration and fractionation of fluid  $20,000.00
Testing of anti-viral activity 	 $20,000.00
Composition studies of purified inhibitor $20,000.00
Testing of clones for inhibitor coding gene $10,000.00
					           __________
					           $100,000.00

2. Production of Small Quantity of Inhibitor for Possible
Clinical Use:

Salary for technicians to perform studies $40,000.00
Production of inhibitor for clinical use $50,000.00
General safety testing as required by FDA $10,000.00
In vitro toxicity tests 		 $10,000.00
Animal toxicity studies 	 $20,000.00
Animal efficacy tests 		 $20,000.00
					           __________
					           $150,000.00


REFERENCES

1.        Martin WJ,  Zeng LC, Ahmed K, Roy M.   Cytomegalovirus-
Related Sequences In an Atypical Cytopathic Virus Repeatedly Isolated
from a Patient with the Chronic Fatigue Syndrome.   Am. J. Path. 145:
441-452, 1994.

2.         Martin  WJ,   Stealth Virus Isolated from an Autistic
Child. J. Aut. Dev. Dis. 25:223-224, 1995.

3.         Martin WJ,  Ahned KN, Zeng LC, Olsen J-C, Seward JG,
Seehrai JS.  African Green Monkey Origin of the Atypical
Cytopathic "Stealth Virus" Isolated From A Patient with Chronic
Fatigue Syndrome.  Clin. Diag. Virol. 4: 93-103, 1995.

4.        Martin WJ,  Glass RT.   Acute Encephalopathy Induced in
Cats with a Stealth Virus Isolated from a Patient with Chronic
Fatigue Syndrome. Pathobiology 63:115-118,1995.

5.        Gollard RP, Mayr A, Rice DA, Martin WJ.   Herpervirus-
related Sequences in Salivary Gland  Tumors.  J. Exp. Clin. Can. Res.
15: 1-4, 1996.

6.        Martin WJ.   Genetic Instability and Fragmentation of a
Stealth Virus Genome.  Pathobiology   64: 9-17, 1996.

7.        Martin WJ.   Severe Stealth Virus Encephalopathy Following
Chronic Fatigue Syndrome-like  Illness:   Clinical and
Histopathological Features.  Pathobiology 64: 1-8,1996.

8.        Martin WJ.   Stealth Viral Encephalopathy: Report of a
Fatal Case Complicated by Cerebral  Vasculitis.  Pathobiology  64: 50-
63, 1996.

9.       Martin WJ.   Simian Cytomegalovirus-related Stealth Virus
Isolated from the Cerebrospinal  Fluid of a Patient with Bipolar
Psychosis and Acute Encephalopathy.  Pathobiology 64: 64- 66, 1996.


Cara Jaffe
Director of Marketing
626.572.7288 vox
626.572.9288 fax

See Message March 9, 2001, "Research Program", W. John Martin, M.D.,
Phd.

Dear List member,

           As some of you know, I have been in Australia since early January
caring for my 81 year old mother. This experience has been personally quite
gratifying and I am pleased to report that she has begun the road to
recovery.  She was determined to live and refused repeated offers of a
painless passage from the ward to the morgue.

           I am now ready to return to the US and to resume efforts on behalf
of those infected with stealth-adapted viruses. The major focus will be the
development of a stealth virus inhibitor termed Epione. Funding was received
last October to biochemically characterize Epione and to produce sufficient
material for preclinical testing. Hopefully, these goals will be achievable
within the next few months. Another task to be completed is to compile the
extensive DNA sequencing data available on a prototype stealth-adapted
virus. This virus was unequivocally derived from an African green monkey
cytomegalovirus, and by inference, entered into humans as a contaminant of a
live polio virus vaccine. The compiled sequence data should provide the
irrefutable scientific proof necessary to convince reluctant Public Health
officials of the reality of vaccine-derived stealth-adapted viruses.

           The sequence data have also provided important insights into the
replication of this virus via an RNA intermediate, and into the capacity of
stealth viruses to capture, amplify and mutate additional genetic sequences
of both cellular and bacterial origins.  Unfortunately, for those infected
with stealth-adapted viruses, the potential capturing of cancer-related
cellular sequences (oncogenes) underscores the need to move quickly with
inhibitor-based research.

           The finding of bacterial sequences is also of major biological
concern since it implies breaching of the prokaryote (bacterial) : eukaryote
(plant and animal cells) barrier. On a practical level, viruses with
incorporated bacterial sequences (which I have termed viteria) can explain
why many stealth virus infected patients can be easily misdiagnosed as
having a true bacterial infection such as might be due to Mycoplasma,
Chlamydia, Borrelia (the spirochete that causes classic Lyme disease),
Ehrlichia (a rickettsia bacterium), etc.

           Another major finding from the sequence studies is the retention,
and indeed marked expansion of chemokine and of chemokine receptor coding
viral genes. Many viruses, including HIV, use chemokine receptors to gain
entry into cells. These receptors also stimulate aspects of cellular
functions that promote virus replication, including the production of
message molecules called cytokines. It was not too surprising, therefore,
that many of the drugs successfully used by clinicians to treat illnesses,
now known to be potentially caused by stealth-adapted viruses, act to
suppress chemokine/cytokine pathways. These agents include widely used
antibiotics, such as clarithromycin (Biaxin); disease modifying
anti-rheumatic drugs, various hormones and a wide range of nutraceutical and
anti-oxidant compounds. By combining relatively low doses of various
chemokine inhibitors, it has been possible to achieve marked reductions in
stealth virus culture activity in several repeatedly tested individuals.
Until a stealth virus inhibitor is available, clinical trials employing
various combinations of chemokine inhibitors in patients monitored by
stealth virus cultures, need to be performed. Combination treatments, along
with specific therapies for stealth virus induced alterations in particular
organ and system functions, have now helped a number of patients. The
favorable outcomes of several of these patients will be described in detail
in a forthcoming book by Dr. George Lewis of CCID. Additional information
regarding the anti-chemokine approach to stealth virus therapy is available
at www.ccid.org

           Finally, I would like to thank those who sent well wishes for my
mother. I can well understand how serious illness can reset one’s
priorities. I also appreciate the hope that many of you have placed in
stealth virus research. I will try to move things along as fast as possible
and to cut through the muddled and politically influenced thinking that has
impeded the understanding and acceptance of stealth-adapted viruses as the
cause of serious diseases among all age groups.


                     Kind regards, W. John Martin, M.D., Ph.D.


_________________________________________________________________
Get your FREE download of MSN Explorer at http://explorer.msn.com

You can forward this to Dr William Philpott, to see what he thinks?

Yes, my son almost died from his DPT (also a bad lot pertussis).  All other
children as well got vaccines, except we thought the P in DPT was the bad
guy so they got the DT.  I have a daughter with high functioning autism as
well.  MMR sinks kids into autism too :(  The problem with our family is
thusly:
1.  We have a complement system problem on our HLA called C4b.  This gene
handles virals toxins and fungals.  My husband and I have zero complement on
C4b which was fully expressed in our autistic children, therefore, they
SHOULD HAVE NEVER GOTTEN A VACCINE.  Of course this information is new or
could have been related to me with a simple immune panel BEFORE vaccinations
(and yes, I am suing).   Things would be markers are things such as
deficient secretory IGA, or High scores on viral titres to these childhood
illnesses.  I am going to sue for breach of consent becuase I was not
informed of this status and if I was, we would obviously hold off on
vaccinations or seperate them out.
2.  HHV6 titres are high in my chidren with autism, high in my mother with
multiple myeloma, high in me, and I also have EBV chronically (low level but
there).  I also had MONO while carrying my son which is the EBV virus, but
also have learned that proteins homogolous to EBV can do something to an in
utero babe who's myelin sheath is not fully formed.  Well....what does
vaccines do?  They attack myelin and the gut (epilethial fatty coverings on
all the body really).  Mercury or Thimersol in vaccines also attack the gut
and myelin, so if you don't have VIABLE of either of those, watch the baby
regress into autism.  Flouride also does this, so what are we given to give
our babies?  Flouride tablets and vaccines, damn, what a conspiracy of caca.
(it makes the GA-GTP which attacks the thyroid too).  Also babies who have
problems with mercury usually do not have efficient bile flow in order for
the body to detox mercury properly...gee I wonder why we all rushed out and
did secretin infusions?  Secretin makes bile flow better, more of
it......hmmm?
3.  The Chromosome 6 gene they believe is the gene that has this complement
on it.  It produces a protein and if you don't have this protein you don't
handle virals, toxins and fungals well.  This gene also is seen in dyslexia,
auditory processing problems and ADD.  BADA BING, that describes my BROTHERS
to a TTTTT.  And yes, they had obvious sequale after vaccinations
too.....wishing that my mother remembered a little more clearly about this
connection, I probably would have been more cautious with vaccinations after
hearing their stories.  But, you have to remember, my mom has had the
stealth virus for some time, she clearly has ADD, problems with memory etc.
Kathy
-----Original Message-----
From: Jennifer Walton <jwalton@...>
To: TheStealthVirusSupportGroup@yahoogroups.com
<TheStealthVirusSupportGroup@yahoogroups.com>
Date: Monday, March 05, 2001 9:21 PM
Subject: Re: [TheStealthVirusSupportGroup] Epstein-Barr Virus Linked to
Breast Cancer and Lymphoma, healthmall.com


>Kathy,
>
>Did your son receive vaccinations as well?ie: polio. MMR DPT? They can also
>cause autism in children that have other health weaknesses.
>I have been interviewing medical professionals in re: to chronic illnesses
>and viral infection.  For quite sometime I have been following the work of
>Dr. William Philpott whom I believe has a great viral inhibitor which works
>for all teh tough viruses like ebv. cytomegalo, HHV6 and many others
>including stealth....it is a  specific high-tech magnetic treatment.  It
>sounds simple and others are using magnets, but not anything like he is.
He
>is a neuro-pyschiatrist with a double PhD, a genius, 87 years old and has
>years of studies and case histories about successful treatment of
everything
>from CFS, Tourettes, Autism,  to schitzophrenia and psychosis.  We will
have
>audio interviews on our site emergingworlds.com after March 31st with him
>and other medical professionals with a variety of new treatment
>possibilities.as they emerge.  More later-we are on deadline schedules
until
>after Mar. 31st.
>Kind regards,
>
>Jennifer
>----- Original Message -----
>From: "Jim Blanco" <kblanco@...>
>To: <TheStealthVirusSupportGroup@yahoogroups.com>
>Sent: Monday, March 05, 2001 1:58 PM
>Subject: Re: [TheStealthVirusSupportGroup] Epstein-Barr Virus Linked to
>Breast Cancer and Lymphoma, healthmall.com
>
>
>> Well, that explains it...while I was carrying my autistic son, I had mono
>> Kathy
>> -----Original Message-----
>> From: Lynn Knapp <lynnknapp@...>
>> To: TheStealthVirusSupportGroup@yahoogroups.com
>> <TheStealthVirusSupportGroup@yahoogroups.com>
>> Date: Monday, March 05, 2001 1:08 PM
>> Subject: [TheStealthVirusSupportGroup] Epstein-Barr Virus Linked to
Breast
>> Cancer and Lymphoma, healthmall.com
>>
>>
>> >Epstein-Barr Virus Linked to Breast Cancer and Lymphoma
>> >
>> >Scientists in the University of Michigan Medical School have found a
>> >molecular link between aggressive breast and lymphatic cancers and the
>> >Epstein-Barr virus, which causes infectious mononucleosis.
>> >
>> >In a paper published in the March 2001 issue of Nature Medicine, U-M
>> >scientists show how the Epstein-Barr virus alters the function of a
>> >cellular
>> >protein that normally suppresses the movement of malignant cells.
>> >When this
>> >natural brake on cell migration is disabled by the virus, cancerous
>> >breast
>> >and lymphatic cells are free to metastasize or spread.
>> >
>> >"This is the first evidence of a human virus associated with the
>> >development
>> >of cancerous tumors targeting a cellular protein to promote the
>> >migration of
>> >malignant cells," says Erle S. Robertson, Ph.D., who directed the
>> >study.
>> >Robertson is an assistant professor of microbiology and immunology in
>> >the
>> >U-M Medical School and a researcher in the U-M's Comprehensive Cancer
>> >Center.
>> >
>> >"The Epstein-Barr virus is associated with many human cancers --
>> >including
>> >Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease and
>> >invasive
>> >breast cancer," Robertson says.
>> >The virus is very common. More than 90 percent of adults show signs of
>> >previous viral infection. Adolescents infected with the acute phase
>> >of the
>> >virus can develop infectious mononucleosis, but usually the body's
>> >natural
>> >immune response forces the virus to revert to its latent phase --
>> >where it
>> >hides inside the nucleus of immune cells called lymphocytes without
>> >producing any symptoms.
>> >
>> >Even though the virus is endemic in humans, Robertson emphasizes that
>> >most
>> >cells infected by the virus may never become malignant. Additional
>> >genetic
>> >factors are required to trigger development of cancer. Should cancer
>> >develop, however, Robertson says the risk of metastasis may be higher
>> >in
>> >individuals previously exposed to the virus.
>> >
>> >"People with aggressive forms of cancer are most vulnerable and
>> >should be
>> >checked to determine the status of previous viral exposure when
>> >physicians
>> >are choosing the most appropriate treatment for them," Robertson
>> >says. "It
>> >also would be wise to closely monitor people with a history of active
>> >Epstein-Barr viral infection for early signs of cancer."
>> >
>> >In the study, Chitra Subramanian, Ph.D., a U-M research fellow, and
>> >Murray
>> >A. Cotter II, a U-M graduate student, investigated a gene from the
>> >Epstein-Barr virus called EBNA-3C, and the protein produced by
>> >infected
>> >lymphocytes when this gene is expressed. The EBNA-3C protein was
>> >found in
>> >all EBV-infected cancerous lymphocytes in the breast cancer and
>> >lymphoma
>> >cell lines analyzed in the study.
>> >
>> >U-M researchers discovered that the EBNA-3C protein binds to a human
>> >metastatic suppressor protein called Nm23-H1, which is found in all
>> >human
>> >cells. "The interaction between the two proteins disables Nm23-H1's
>> >natural
>> >ability to keep malignant cells in their original location thereby
>> >promoting
>> >metastasis," explains Robertson.
>> >
>> >"We have mapped the binding site to one region of the viral protein
>> >EBNA-3C
>> >and hope in future research to identify the exact location on the
>> >targeted
>> >protein," Robertson says. "Our goal is to find the binding site and
>> >discover
>> >how to block the interaction between these two proteins.
>> >
>> >"If we succeed, physicians could one day be able to treat primary
>> >breast and
>> >lymphatic cancers, as well as other cancers associated with the
>> >Epstein-Barr
>> >virus, without worrying about malignant cells spreading to other
>> >parts of
>> >the body."
>> >
>> >
>> >
>> >
>> >
>> >
>> >
>> >
>> >
>> >
>> >Your use of Yahoo! Groups is subject to
http://docs.yahoo.com/info/terms/
>> >
>> >
>>
>>
>>
>>
>>
>> Your use of Yahoo! Groups is subject to http://docs.yahoo.com/info/terms/
>>
>>
>
>
>
>
>
>Your use of Yahoo! Groups is subject to http://docs.yahoo.com/info/terms/
>
>

Kathy,

Did your son receive vaccinations as well?ie: polio. MMR DPT? They can also
cause autism in children that have other health weaknesses.
I have been interviewing medical professionals in re: to chronic illnesses
and viral infection.  For quite sometime I have been following the work of
Dr. William Philpott whom I believe has a great viral inhibitor which works
for all teh tough viruses like ebv. cytomegalo, HHV6 and many others
including stealth....it is a  specific high-tech magnetic treatment.  It
sounds simple and others are using magnets, but not anything like he is.  He
is a neuro-pyschiatrist with a double PhD, a genius, 87 years old and has
years of studies and case histories about successful treatment of everything
from CFS, Tourettes, Autism,  to schitzophrenia and psychosis.  We will have
audio interviews on our site emergingworlds.com after March 31st with him
and other medical professionals with a variety of new treatment
possibilities.as they emerge.  More later-we are on deadline schedules until
after Mar. 31st.
Kind regards,

Jennifer
----- Original Message -----
From: "Jim Blanco" <kblanco@...>
To: <TheStealthVirusSupportGroup@yahoogroups.com>
Sent: Monday, March 05, 2001 1:58 PM
Subject: Re: [TheStealthVirusSupportGroup] Epstein-Barr Virus Linked to
Breast Cancer and Lymphoma, healthmall.com


> Well, that explains it...while I was carrying my autistic son, I had mono
> Kathy
> -----Original Message-----
> From: Lynn Knapp <lynnknapp@...>
> To: TheStealthVirusSupportGroup@yahoogroups.com
> <TheStealthVirusSupportGroup@yahoogroups.com>
> Date: Monday, March 05, 2001 1:08 PM
> Subject: [TheStealthVirusSupportGroup] Epstein-Barr Virus Linked to Breast
> Cancer and Lymphoma, healthmall.com
>
>
> >Epstein-Barr Virus Linked to Breast Cancer and Lymphoma
> >
> >Scientists in the University of Michigan Medical School have found a
> >molecular link between aggressive breast and lymphatic cancers and the
> >Epstein-Barr virus, which causes infectious mononucleosis.
> >
> >In a paper published in the March 2001 issue of Nature Medicine, U-M
> >scientists show how the Epstein-Barr virus alters the function of a
> >cellular
> >protein that normally suppresses the movement of malignant cells.
> >When this
> >natural brake on cell migration is disabled by the virus, cancerous
> >breast
> >and lymphatic cells are free to metastasize or spread.
> >
> >"This is the first evidence of a human virus associated with the
> >development
> >of cancerous tumors targeting a cellular protein to promote the
> >migration of
> >malignant cells," says Erle S. Robertson, Ph.D., who directed the
> >study.
> >Robertson is an assistant professor of microbiology and immunology in
> >the
> >U-M Medical School and a researcher in the U-M's Comprehensive Cancer
> >Center.
> >
> >"The Epstein-Barr virus is associated with many human cancers --
> >including
> >Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease and
> >invasive
> >breast cancer," Robertson says.
> >The virus is very common. More than 90 percent of adults show signs of
> >previous viral infection. Adolescents infected with the acute phase
> >of the
> >virus can develop infectious mononucleosis, but usually the body's
> >natural
> >immune response forces the virus to revert to its latent phase --
> >where it
> >hides inside the nucleus of immune cells called lymphocytes without
> >producing any symptoms.
> >
> >Even though the virus is endemic in humans, Robertson emphasizes that
> >most
> >cells infected by the virus may never become malignant. Additional
> >genetic
> >factors are required to trigger development of cancer. Should cancer
> >develop, however, Robertson says the risk of metastasis may be higher
> >in
> >individuals previously exposed to the virus.
> >
> >"People with aggressive forms of cancer are most vulnerable and
> >should be
> >checked to determine the status of previous viral exposure when
> >physicians
> >are choosing the most appropriate treatment for them," Robertson
> >says. "It
> >also would be wise to closely monitor people with a history of active
> >Epstein-Barr viral infection for early signs of cancer."
> >
> >In the study, Chitra Subramanian, Ph.D., a U-M research fellow, and
> >Murray
> >A. Cotter II, a U-M graduate student, investigated a gene from the
> >Epstein-Barr virus called EBNA-3C, and the protein produced by
> >infected
> >lymphocytes when this gene is expressed. The EBNA-3C protein was
> >found in
> >all EBV-infected cancerous lymphocytes in the breast cancer and
> >lymphoma
> >cell lines analyzed in the study.
> >
> >U-M researchers discovered that the EBNA-3C protein binds to a human
> >metastatic suppressor protein called Nm23-H1, which is found in all
> >human
> >cells. "The interaction between the two proteins disables Nm23-H1's
> >natural
> >ability to keep malignant cells in their original location thereby
> >promoting
> >metastasis," explains Robertson.
> >
> >"We have mapped the binding site to one region of the viral protein
> >EBNA-3C
> >and hope in future research to identify the exact location on the
> >targeted
> >protein," Robertson says. "Our goal is to find the binding site and
> >discover
> >how to block the interaction between these two proteins.
> >
> >"If we succeed, physicians could one day be able to treat primary
> >breast and
> >lymphatic cancers, as well as other cancers associated with the
> >Epstein-Barr
> >virus, without worrying about malignant cells spreading to other
> >parts of
> >the body."
> >
> >
> >
> >
> >
> >
> >
> >
> >
> >
> >Your use of Yahoo! Groups is subject to http://docs.yahoo.com/info/terms/
> >
> >
>
>
>
>
>
> Your use of Yahoo! Groups is subject to http://docs.yahoo.com/info/terms/
>
>

Carolyn:
I strongly recommend reading Atkin's "The Vita Nutrient Solution."
It will tell you all you need re: taking Glucophage, Pantethine,
Vanadyl Sulfate, and L-Carnitine, as well as DHEA to lower insulin
levels.

It is just my personal theory that Stealth Virus causes
hyperinsulinism, and the hyperinsulinism causes high triglycerides.
This theory comes from my personal experience.  The experience was
that I suddenly was able to have control over the monster that lives
within me.  If I denied it the sugar and subsequent insulin, it
seemed to weaken dramatically.  I do not know if I was denying it
it's food, ie, the sugar; or what stimulated it, ie, the insulin.

How I know those first three supplements, and the one medication are
critical to continued success is that each time I tried to
discontinue one of them I experienced violent tetany and a continued
worsening of all my viral symptoms.  It is too soon to comment on the
success of DHEA in this regard.

I must add though that none of the above will help without remaining
on a very strict low carbohydrate diet.

Good luck!
H. Lynn Knapp, M.A.

Hi Lynn,

I had a similar experience with the Atkins diet. I went on it
because I had adrenal insufficiency, low blood sugar and
high insulin levels. I noticed that after I was on the
Atkins diet for a while that my energy level improved
and I wasn't as viral as often as I had been and when I
was I wasn't quite as bad as I used to be. But I hadn't read
about taking Vanadyl Sulfate. In fact, I have never heard of
that. Can you tell me what it is and where I can get it?
Also the Mega Pantethine.

Thanks,

Carolyn

At 10:06 PM 3/5/2001 +0000, Lynn Knapp wrote:

>In the summer, I stumbled over something not prior associated with
>Stealth. (Dr.Martin was fully apprised)  I put myself on a very
>strict high protein diet, the Atkins Diet, because since the onset on
>the virus I had gained 50lbs.
>
>Instantly I noticed that when I went active, my symptoms were less
>severe.  I cut the carbs more, and with even better results. Finally,
>I began to read thoroughly on the Atkins Diet trying to find the
>connection.  I discovered that the success of his diet is based on
>one simple thing, correcting hyperinsulinism.  I remembered, I was
>diagnosed with hyperinsulinism years ago and suffered from severe
>hypoglycemia.
>
>I presented this info to my Dr. and also presented Atkins
>recommendation to take Glucophage if the hyperinsulimism is severe.
>Needless to say, we began Glucophage with trepidation, as I had low
>blood sugar.  But to amazement, it did not lower my sugar at all,
>only my insulin level and high triglycerides, (high triglycerides go
>with hyperinsulinism). As my Stealth symptoms lessened in severity,
>and were markedly improved, we would try more Glucophage until we
>obtained the desired results.
>
>According to Atkins, taking Vanadyl Sulfate (I take 25mg), L-Carnitine
>(I take 2,000) and Mega Pantethine,(I take 900mg),(all doses above
>taken daily), helps dramatically in lowering insulin levels and
>triglycerides.  (Read "Dr Atkins Vita Nutrient Solution").
>
>Since this discovery that the virus either is stimulated by insulin,
>or feeds on carbohydrates, my virus is much more controllable.  My
>HGB has been stable around 11; my pulmonary edema has markedly
>improved with much less O2 needed and much less diuretic necessary.
>I am completely off Phenobarbital, and Ativan.  The Tetany now only
>occurs if I go off the low carb diet, or if I fail to take any of the
>following:  Glucophage, L-Carnitine, Vanadyl Sulfate, or Pantethine.
>
>Atkins also thinks there is a link between low DHEA levels and
>hyperinsulinism.  My DHEA levels are very low, and we are slowly
>adding 5mg DHEA to my regiment.  It is too early to tell.  Hope some
>of this helps.  Feel free to ask Dr. Martin.
>
>regards, Lynn
>
>
>
>
>
>Your use of Yahoo! Groups is subject to http://docs.yahoo.com/info/terms/

interestingly, my son has a CARBOHYDRATE METABOLISM PROBLEM, hmmm?
Kathy
-----Original Message-----
From: Lynn Knapp <lynnknapp@...>
To: TheStealthVirusSupportGroup@yahoogroups.com
<TheStealthVirusSupportGroup@yahoogroups.com>
Date: Monday, March 05, 2001 2:07 PM
Subject: [TheStealthVirusSupportGroup] Re: The relationship between
Hyperinsulinism and Stealth Virus


>Kathy:
>
>Re: the kids muscle spasms, are they protracted spasms that cause
>screaming, and I mean screaming, multiple very protracted spasms as
>never seen before?  That is called Tetany.  It has been the worst
>symptom of my Stealth Virus.  Prior to treatment, they happened all
>night and day.  My nursing aids would try to message them out to no
>avail.  Finally valium was resorted to in an attempt to treat the
>violent spasms.  Every 15 minutes we would take a 5mg valium until
>they subsided, or until they arrested before the #6th Valium.
>
>With treatment, this was my first symptom to improve dramatically.
>It would only happen when my virus went active.  My virus cycles 3-4
>days on and 2-3 off.
>
>In the summer, I stumbled over something not prior associated with
>Stealth. (Dr.Martin was fully apprised)  I put myself on a very
>strict high protein diet, the Atkins Diet, because since the onset on
>the virus I had gained 50lbs.
>
>Instantly I noticed that when I went active, my symptoms were less
>severe.  I cut the carbs more, and with even better results. Finally,
>I began to read thoroughly on the Atkins Diet trying to find the
>connection.  I discovered that the success of his diet is based on
>one simple thing, correcting hyperinsulinism.  I remembered, I was
>diagnosed with hyperinsulinism years ago and suffered from severe
>hypoglycemia.
>
>I presented this info to my Dr. and also presented Atkins
>recommendation to take Glucophage if the hyperinsulimism is severe.
>Needless to say, we began Glucophage with trepidation, as I had low
>blood sugar.  But to amazement, it did not lower my sugar at all,
>only my insulin level and high triglycerides, (high triglycerides go
>with hyperinsulinism). As my Stealth symptoms lessened in severity,
>and were markedly improved, we would try more Glucophage until we
>obtained the desired results.
>
>According to Atkins, taking Vanadyl Sulfate (I take 25mg), L-Carnitine
>(I take 2,000) and Mega Pantethine,(I take 900mg),(all doses above
>taken daily), helps dramatically in lowering insulin levels and
>triglycerides.  (Read "Dr Atkins Vita Nutrient Solution").
>
>Since this discovery that the virus either is stimulated by insulin,
>or feeds on carbohydrates, my virus is much more controllable.  My
>HGB has been stable around 11; my pulmonary edema has markedly
>improved with much less O2 needed and much less diuretic necessary.
>I am completely off Phenobarbital, and Ativan.  The Tetany now only
>occurs if I go off the low carb diet, or if I fail to take any of the
>following:  Glucophage, L-Carnitine, Vanadyl Sulfate, or Pantethine.
>
>Atkins also thinks there is a link between low DHEA levels and
>hyperinsulinism.  My DHEA levels are very low, and we are slowly
>adding 5mg DHEA to my regiment.  It is too early to tell.  Hope some
>of this helps.  Feel free to ask Dr. Martin.
>
>regards, Lynn
>
>
>
>
>
>Your use of Yahoo! Groups is subject to http://docs.yahoo.com/info/terms/
>
>

Kathy:

Re: the kids muscle spasms, are they protracted spasms that cause
screaming, and I mean screaming, multiple very protracted spasms as
never seen before?  That is called Tetany.  It has been the worst
symptom of my Stealth Virus.  Prior to treatment, they happened all
night and day.  My nursing aids would try to message them out to no
avail.  Finally valium was resorted to in an attempt to treat the
violent spasms.  Every 15 minutes we would take a 5mg valium until
they subsided, or until they arrested before the #6th Valium.

With treatment, this was my first symptom to improve dramatically.
It would only happen when my virus went active.  My virus cycles 3-4
days on and 2-3 off.

In the summer, I stumbled over something not prior associated with
Stealth. (Dr.Martin was fully apprised)  I put myself on a very
strict high protein diet, the Atkins Diet, because since the onset on
the virus I had gained 50lbs.

Instantly I noticed that when I went active, my symptoms were less
severe.  I cut the carbs more, and with even better results. Finally,
I began to read thoroughly on the Atkins Diet trying to find the
connection.  I discovered that the success of his diet is based on
one simple thing, correcting hyperinsulinism.  I remembered, I was
diagnosed with hyperinsulinism years ago and suffered from severe
hypoglycemia.

I presented this info to my Dr. and also presented Atkins
recommendation to take Glucophage if the hyperinsulimism is severe.
Needless to say, we began Glucophage with trepidation, as I had low
blood sugar.  But to amazement, it did not lower my sugar at all,
only my insulin level and high triglycerides, (high triglycerides go
with hyperinsulinism). As my Stealth symptoms lessened in severity,
and were markedly improved, we would try more Glucophage until we
obtained the desired results.

According to Atkins, taking Vanadyl Sulfate (I take 25mg), L-Carnitine
(I take 2,000) and Mega Pantethine,(I take 900mg),(all doses above
taken daily), helps dramatically in lowering insulin levels and
triglycerides.  (Read "Dr Atkins Vita Nutrient Solution").

Since this discovery that the virus either is stimulated by insulin,
or feeds on carbohydrates, my virus is much more controllable.  My
HGB has been stable around 11; my pulmonary edema has markedly
improved with much less O2 needed and much less diuretic necessary.
I am completely off Phenobarbital, and Ativan.  The Tetany now only
occurs if I go off the low carb diet, or if I fail to take any of the
following:  Glucophage, L-Carnitine, Vanadyl Sulfate, or Pantethine.

Atkins also thinks there is a link between low DHEA levels and
hyperinsulinism.  My DHEA levels are very low, and we are slowly
adding 5mg DHEA to my regiment.  It is too early to tell.  Hope some
of this helps.  Feel free to ask Dr. Martin.

regards, Lynn

Epstein-Barr Virus Linked to Breast Cancer and Lymphoma

Scientists in the University of Michigan Medical School have found a
molecular link between aggressive breast and lymphatic cancers and the
Epstein-Barr virus, which causes infectious mononucleosis.

In a paper published in the March 2001 issue of Nature Medicine, U-M
scientists show how the Epstein-Barr virus alters the function of a
cellular
protein that normally suppresses the movement of malignant cells.
When this
natural brake on cell migration is disabled by the virus, cancerous
breast
and lymphatic cells are free to metastasize or spread.

"This is the first evidence of a human virus associated with the
development
of cancerous tumors targeting a cellular protein to promote the
migration of
malignant cells," says Erle S. Robertson, Ph.D., who directed the
study.
Robertson is an assistant professor of microbiology and immunology in
the
U-M Medical School and a researcher in the U-M's Comprehensive Cancer
Center.

"The Epstein-Barr virus is associated with many human cancers --
including
Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease and
invasive
breast cancer," Robertson says.
The virus is very common. More than 90 percent of adults show signs of
previous viral infection. Adolescents infected with the acute phase
of the
virus can develop infectious mononucleosis, but usually the body's
natural
immune response forces the virus to revert to its latent phase --
where it
hides inside the nucleus of immune cells called lymphocytes without
producing any symptoms.

Even though the virus is endemic in humans, Robertson emphasizes that
most
cells infected by the virus may never become malignant. Additional
genetic
factors are required to trigger development of cancer. Should cancer
develop, however, Robertson says the risk of metastasis may be higher
in
individuals previously exposed to the virus.

"People with aggressive forms of cancer are most vulnerable and
should be
checked to determine the status of previous viral exposure when
physicians
are choosing the most appropriate treatment for them," Robertson
says. "It
also would be wise to closely monitor people with a history of active
Epstein-Barr viral infection for early signs of cancer."

In the study, Chitra Subramanian, Ph.D., a U-M research fellow, and
Murray
A. Cotter II, a U-M graduate student, investigated a gene from the
Epstein-Barr virus called EBNA-3C, and the protein produced by
infected
lymphocytes when this gene is expressed. The EBNA-3C protein was
found in
all EBV-infected cancerous lymphocytes in the breast cancer and
lymphoma
cell lines analyzed in the study.

U-M researchers discovered that the EBNA-3C protein binds to a human
metastatic suppressor protein called Nm23-H1, which is found in all
human
cells. "The interaction between the two proteins disables Nm23-H1's
natural
ability to keep malignant cells in their original location thereby
promoting
metastasis," explains Robertson.

"We have mapped the binding site to one region of the viral protein
EBNA-3C
and hope in future research to identify the exact location on the
targeted
protein," Robertson says. "Our goal is to find the binding site and
discover
how to block the interaction between these two proteins.

"If we succeed, physicians could one day be able to treat primary
breast and
lymphatic cancers, as well as other cancers associated with the
Epstein-Barr
virus, without worrying about malignant cells spreading to other
parts of
the body."

If anyone has any information regarding Stealth Viruses; such as
medical journal articles, publications, presentations, or interviews,
please feel free to post.  I'd like to see this message board become
a resource center, and not a chat room.

      Also, I would like to maintain a focus on Stealth Virus related
issues, without puting emphasis on any one illness caused by the
Virus.

      Finally, I'd like to know if you want the posted messages sent
to you personally when posted, as it is presently set, or to only
view them when at the site.

      Any input would be greatly appreciated.  Thank you.

                                          Sincerewly,

                                          H. Lynn Knapp, M.A.
                                          TheStealthVirusSupportGroup
                                          Moderator

From:  "Jim Blanco" <kblanco@m...>Date:  Tue Jan 30, 2001
4:05pmSubject:  Things to take for stealth virus, from multiple
myeloma to autism
Therapeutic Approaches Aimed at Suppression of Cytokine/Chemokine
MediatedStealth Virus InfectionTherapeutic agent Reference to its
effect on cytokine/chemokine mediated activitiesAnti-oxidantsVitamin
CVitamin EN-acetyl-cysteineAlpha-lipoic acidCoenzyme Q10Butylated
hydroxytoluene BHT Vlahopoulos S, et.al. Blood 1999;94:1878-89Wu D,
et.al. Atherosclerosis. 1999; 7:297-307.Gosset P, et.al. Eur Respir J
1999;14:98-105Suzuki YJ, et.al. Biochem Biophys Res Commun
1992;189:1709-15Hodges S, et.al. Biofactors 1999;9:365-70Hulten LM,
et al. Transplantation 1998;66(3):364-9Diet and Nutritional
SupplementsAsparagus cochinchinensisGamma linoleic acidOmega-3
lipidsFish oilFlaxseed oilPalm oilFiberButyrateYogurtL-GlycineL-
ArginineZincInosineTaurine chloramineS-adenosylmethionineDHEA Kim H,
et al. Int J Immunopharmacol 1998;20(4-5):153-62Dirks J, et.al.
Prostaglandins Leukot Essent Fatty Acids 1998;59:273-7Venkatraman JT
andChu WC . J Am Coll Nutr 1999;18:602-13James MJ, et al. Am J Clin
Nutr 2000;71(1 Suppl):343S-8SJames MJ, et al. Am J Clin Nutr 2000;71
(1 Suppl):343S-8SEngelberts I, et.al. Br J Nutr 1993;69:159-67Andoh
A, et.al. JPEN J Parenter Enteral Nutr 1999;23(5 Suppl):S70-3Andoh A
et al. Clin Exp Immunol 1999;118:23-9Ha CL, et.al. J Food Prot
1999;62:181-8Spittler A, et al. FASEB J 1999 ;13:563-71Haberstroh U,
et al. J Am Soc Nephrol 1998 ;9:203-10.Connell P, et al. J Am Coll
Nutr 1997 ;16:411-7Hasko G, et al. J Immunol 2000;164:1013-9Kontny E,
et al. Arthritis Rheum 1999;42:2552-60Watson WH, et al. Biochem J
1999;342 ( Pt 1):21-5Araghi-Niknam M, et al. Proc Soc Exp Biol Med
1997 ;216:386-91Herbal MedicinesBindaritCapsaicinCurcuminChongmyung-
TangEpigallocatechin gallateCimicifuga rhizomaGenisteinGinkgo
bilobaHymenialdisineOren-gedoku-toPolygala tenuifoliaRosmarinus
officinalis LinnGlucosidorum Tripterygii tororumQuercetinRehmannia
glutinosaGallic acid esters (red wine)SanguinarineSesquiterpene
lactone helenalinSilymarinUrtica dioicaZingiberaceae Zoja C, et al.
Kidney Int 1998 ;53:726-34Yu R, et al. Int J Vitam Nutr Res
1998;68:114-9Jobin C, et al.. J Immunol 1999;163:3474-83Kim HM, et
al. J Ethnopharmacol 1999;66:295-300Yang F, et al. J Nutr
1998;128:2334-40Hirabayashi T, et al.. Planta Med 1995;61:221-6Tabary
O, et al. Am J Pathol 1999;155:473-81Wei Z, et al.. Gen Pharmacol
1999;33:369-75Breton JJ, et al. J Pharmacol Exp Ther 1997;282:459-
66Wang LM,et al.. J Pharm Pharmacol 1997;49:102-4Kim HM, et al.. J
Ethnopharmacol 1998;61:201-8al-Sereiti MR, et al. Indian J Exp Biol
1999;37:124-30Wang ZG. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih
1997;17:348-50Ishikawa Y, et al. J Am Soc Nephrol 1999;10:2290-6Kim
HM,. et al. Pharmacol Res 1999;40:171-6Murase T, et al. Arterioscler
Thromb Vasc Biol 1999;19:1412-20Chaturvedi MM, et al. J Biol Chem
1997 28;272:30129-34Lyss G, et al. J Biol Chem 1998 11;273:33508-
16Saliou C, et al. FEBS Lett 1998 27;440:8-12Riehemann K, et al. FEBS
Lett 1999; 8;442:89-94Surh Y. Mutat Res 1999;428:305-27Anti-
leukotriene medicationsMontelukastZileuton Denizot Y, et al. Cytokine
1999;11:606-10Aoki Y, et al. Am J Physiol 1998;274:L1030-9Over the
Counter anti-ulcer medicationsSulglycotideRebamipidePolaprezinc
Slomiany BL, Piotrowski J, Slomiany A.Aihara M, et al.. Dig Dis Sci
1998;43(9 Suppl):174S-180SShimada T, et al.. J Pharmacol Exp Ther
1999;291:345-52Over the Counter anti-rheumatic
medicationsAspirinIbuprofenSodium salicylateNimesulideDiclofenac Shi
X, et al. Mol Cell Biochem 1999;199:93-102.Stuhlmeier KM, et al.
Biochem Pharmacol 1999 1;57:313-20Lemay S, et al. Clin Diagn Lab
Immunol 1999;6:567-72Azab A, et al. J. Life Sci 1998;63: 323-
7Henrotin YE, et al. Clin Exp Rheumatol 1999;17:151-60Prescription
ani-rheumatic drugs*ChloroquineSulfasalazineD-
penicillamineGoldGlucocorticoidsMethotrexateBucillamineQuinineQuinacri
neThalidomide Zhu X, et al.. Immunology 1993;80:122-6Deleuran B, et
al. Cytokine 1992;4:403-9Deleuran B, et al. Cytokine 1992;4:403-
9Yoshida S, et al. Int Immunol 1999;11:151-8Bourke E, and Moynagh PN.
J Immunol 1999;163:2113-9.Boiardi L, et al. Clin Exp Rheumatol
1999;17:419-25Matsuno H, et al.. Int J Immunopharmacol 1998;20:295-
304Maruyama N, et al. Am J Respir Cell Mol Biol 1994;10:514-
20Bondeson J, and Sundler R. Gen Pharmacol 1998;30:357-66Dunzendorfer
S, et al. Immunopharmacology 1999;43:59-64Antibiotics that suppress
chemokines*ClarithromycinRoxithromycinErythromycinDoxycyclineMinocycli
ne Matsuoka N, et al. Clin Exp Immunol 1996;104:501-8Nonaka M, et al.
Acta Otolaryngol Suppl 1998;539:71-5Takizawa H, et al. J. Am J Respir
Crit Care Med 1997;156:266-71Attur MG, et al. J Immunol 1999
15;162:3160-7Attur MG, et al. J Immunol 1999 15;162:3160-7Other Drugs
that can suppress chemokines*ACE Inhibitors+HMG-CoA reductase#
inhibitorsNitric oxide synthase inhibitorsCa(2+)-channel blockersPGE
(2) including agentsNucloside
analogueDesferrioxaminePentoxifyllineFurosemideThyroxineVitamin
B3Vitamin B6Vitamin B12Vitamin DProgesteroneEstrogensBile
acidsKetamineMorphineLevodopaSelegilineSertralineTrazadoneHaloperidol
Gullestad L, et al. J Am Coll Cardiol 1999;34:2061-7Ortego M, et al.
J. Atherosclerosis 1999;147:253-61Lane TE,et al. J Neurovirol
1999;5:48-54Rodler S, et al. J Mol Cell Cardiol 1995;27:2295-
302Kunkel SL, et al. J Biol Chem 1988 15;263:5380-4Zidek Z, et al.
Eur J Pharmacol 1999 2;376:91-100Martelius T, et al. Transplantation
1999 15;68:1753-61Neuner P, et al. Immunology 1994 ;83:262-
7Yuengsrigul A, et al. Ann Allergy Asthma Immunol 1999;83:559-
66Rittenhouse PA, and Redei E. Endocrinology 1997 ;138:1434-9Pero RW,
et al. Mol Cell Biochem 1999;193:119-25Roubenoff R,et al. Arthritis
Rheum 1995;38:105-9Buccellato FR, et al. . FASEB J 1999;13:297-
304Harant H, et al.. Eur J Biochem 1997 15;250:63-71Vassiliadou N, et
al. J Immunol 1999;15;162:7510-8Inadera H, et al. Endocrinology
2000;141:50-9Saitoh O, et al. J Gastroenterol Hepatol 1998;13:1212-
7Kawasaki T, et al. Anesth Analg 1999;89:665-9Grimm MC, et al. Ann N
Y Acad Sci 1998 1;840:9-20Bessler H, et al. Biomed Pharmacother
1999;53:141-5Muller T, J Neural Transm Suppl 1998;52:321-8.Maes M, et
al. Neuropsychopharmacology 1999;20:370-9Maes M, et al.
Neuropsychopharmacology 1999;20:370-9Moots RJ, et al. Ann Rheumatic
Dis 1999;58:585-7Chemokine and chemokine receptor blocking
agentsHeparin*ChondroitinMannansPeptide T Ramdin L, et al. Clin Exp
Allergy 1998;28:616-24Kuschert GS et al. Biochemistry 1999;38:12959-
68Mbemba E, et al. Virology 1999;265:354-64Redwine LS, et al. Clin
Immunol 1999;93:124-31Legend to the Table* The use of these
medications solely for stealth virus infections is notbeing
suggested. This does not, however, preclude an assessment of
theirpotential anti-stealth virus activity in patients in whom the
use of themedication is medically indicated.+ ACE Angiotension
converting enzyme# Cholesterol lowering<!--See my SuperSig:
http://proxy.supersig.com/sig?45002326_45002140--
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Spiroplasma & Transmissible Spongiform Encephalopathies
By Ed Gehrman
Introduction
Transmissible Spongiform Encephalopathy (TSE) is identified by the
plaques
of mutated amyloid protein that form within the brain tissue and
destroy
synapses and neurotransmitter functions and take on a characteristic
sponge
or Swiss cheese appearance. CJD, Scrapie and Kuru are all members of
this
degenerative disease family, afflictions known about for over two
hundred
years but not studied intently until the early sixties when they were
found
to be transmissible.

Dr. Carleton Gajdusek was a young researcher looking for unusual
diseases
when he visited the Fore Peoples of Papau, New Guinea during the late
1950s.
The Papuans of those years were suffering from a population density
that put
a strain on very limited resources. They practiced female infanticide
and
cannibalism and were in a constant state of warfare with their
neighbors
over land and pigs. Severe limitations on normal heterosexual
relations were
imposed; the men spent most of their time at the men1s clubhouse
where they
prepared for war and engaged in homosexual relations with the young
boys.
This homosexual activity was all part of an elaborate bonding thought
needed
to ensure macho warriors and dependable compatriots. The warfare was
brutal,
often hand-to-hand; capture meant being tortured and killed.
Solidarity was
essential and achieved through the sharing of semen. The females of
the
group were disrespected and often abused because they were thought to
steal
the men1s strength and resolve in battle as well as their vital
semen. The
malnourishment of females and young children was part of this intense
process; they supplemented their diet by eating anything that
3crawled or
crept~. Midwives ate placentas of the new born and women dug up the
partly
decomposed bodies of relatives and ate and shared with young children
the
flesh, brains and the accumulations of maggots and mites. This was
not a
religious ceremony but an attempt to fend off malnutrition. (1)
Gajdusek
observed that some of the Fore women and a few children died from
symptoms
indicating a neurological disorder: dementia, frenzied behavior,
blindness
and eventual agonizing death. He studied the tribal dynamics and soon
hypothesized that the condition, known as Kuru, came from their habit
of
eating the brains of dead relatives; he brought some diseased brain
tissue
back to the USA. Gajdusek soon discovered that when he made a broth
from the
Kuru tissue and injected this mixture into lab animals, they too
exhibited
the Kuru symptoms. He then processed Kuru diseased lab animals1
brains and
injected the mixture into other lab animals. They also died the same
excruciating deaths. This meant that the condition could be
transmitted from
organism to organism and was therefore transmissible, hence
Transmissible
Spongiform Encephalopathy (TSE). Gajdusek and his colleagues at the
National
Institute of Health were never able to isolate or positivly identify
the
agent that causes the TSE even though they1ve been trying since the
early
sixties. Scrapie and CJD were also studied and found to be
transmissible.
All this was well known underground medical information; many doctors
refused to autopsy CJD victims. For years the NIH conjectured that the
infective culprit was a slow virus. Nothing seemed to distroy the
agent; not
heat, cold, or any of the normal chemical disinfectants. Nor could
they find
a trace of its chemical or mocular identity. Furthermore, the virus
didn1t
cause inflamation so antibodies failed to leave a calling card. Some
completely new agent was essential.
Bastian's work

Another tenacious TSE researcher is Dr. Frank O. Bastian, MD, a
professor of
pathology and director of neuropathology at the University of South
Alabama,
Mobile. He has published numerous research articles relating to the
etiology
of Creutzfeldt-Jakob Disease and also edited a book entitled
Creutzfeldt-Jakob Disease and Other Transmissible Spongiform
Encephalopathies. (2)

In 1976,Bastian examined a brain biopsy from a patient with CJD using
electron microscopy. He saw a spiral structure foreign to the tissue.
It had
features of the newly reported spiroplasmas (Spiroplasmas were only
discovered in 1976). In 1981, a team in New York reported finding a
fibril
protein in scrapie-infected brain tissue. This scrapie-associated
fibril
(SAF) protein was 4 nm in diameter and 200 nm long. In 1983, the team
looked
at various tissues of CJD and Kuru and demonstrated scrapie-associated
fibrils consistently in these diseases but not in control tissues.
These SAF
were identical morphologically to the internal fibrils of
spiroplasmas.

Moreover, antibodies to SAF react with internal fibrillar proteins
from
Spiroplasma and digested brain material from people with CJD,
suggesting
that these proteins essentially are the same. This similarity
solidified in
Bastian's mind the link between spiroplasmas and CJD.

Dr. Bastian has postulated that Spiroplasma bacteria causes CJD and
other
TSE. His twenty years of research indicates a role for Spiroplasma.
The
evidence includes the following: spiroplasma-like inclusions were
seen in
brain biopsies from patients with CJD (Arch Pathol Lab Med.
1979;103:665-669); spiroplasma internal fibril proteins are identical
morphologically to those seen in TSEs; the spiroplasma proteins show
immunological cross reactivity with the TSE proteins (J Clin Biol.
1987;25:2430-2431); and spiroplasma, when inoculated into rodents,
produces
a similar neuropathology (Amer J Pathol. 1984;114:496-514).

Spiroplasmas
Spiroplasmas, are present in the hemolymph of almost all insects;
there
probably are several million strains. They can also cause diseases in
plants
but are usually associated with a vector. For example, a leaf hopper
carries
a spiroplasma that infects orange trees.

Spiroplasmas are similar to mycoplasmas. They do not have a cell wall
(cell
wall deficient) and have among the smallest genomes of any living
organism.
Mycoplasma, are the smallest and perhaps the oldest life forms. These
bacteria, one cause of "walking pneumonia", are thought by many to be
rather
fragile, but nothing could be further from the truth. They tolerate
extreme
fluctuations in temperature, lay dormant in the soil for generations
and
survive the harshest elements; only drano-like chemicals kill them
effectively outside the body. Under normal circumstances our immune
system
efficiently deals with this complicated, membrane enclosed piece of
DNA .

Spiroplasmas as the cause of CJD
A common phenomenon among the mycoplasmas is that the organisms bind
host
proteins that often are of identical molecular weight to their surface
proteins and, therefore, are looked at by the immune system as being
the
same as the host. The spiralin protein on the surface of spiroplasmas
shows
a migration pattern on gel electrophoresis with a molecular weight of
27,000
Da to 30,000 Da, similar to that of the prion protein. This
biochemical
similarity is compatible with spiroplasma etiology.

Bastian was able to show that spiroplasmas were neurotropic. When
inoculated
peripherally into suckling rats, they will eventually localize to the
brain
tissues. The organisms will produce a persistent infection and
produce a
spongy change in the brain tissue of these animals. The
neuropathologic
changes are similar to those seen in CJD.

Spiroplasmas are also within the size range of the agent that
transmits CJD
and other transmissible Spongiform encephalopathies. Spiroplasmas
will pass
through a 50 nm-pore filter. The transmissible agent's size has been
determined to be 42 nm.

The obvious way to look for an agent directly is by electron
microscopy, but
this method may not be appropriate for spiroplasmas. Spiroplasmas are
similar to mycoplasmas, and it is a well-known phenomenon that
mycoplasmas
are able to blend with cell membranes. What happens, possibly, is that
spiroplasmas essentially fuse with host-cell organelle membranes,
thereby
blending with the background, so you would not see it unless you had a
marker to label it. Developing such as marker has been difficult
because
spiroplasmas are very fastidious (difficult to cultivate)organisms.

Bastian also inoculated suckling rats with spiroplasmas, and examined
their
brain tissues by electron microscopy early in the infection process;
he
documented the organisms in the tissues. They appeared as membrane-
bound
forms, except for the one instance where he observed the spiral form.
Later
in infection, when he knew that the tissues were infectious by broth
culture, he couldn't find any evidence of spiroplasmas by looking at
the
tissues extensively with electron microscopy.

Bastian insists that the infection-related protein that most
researchers
refer to as a "prion" is produced by the host in response to the
infection
and is not the causative agent. Prions are thought to be self-
replicating
proteins. Some researchers believe prions are the cause of CJD and
related
illnesses because they have found prions in brain tissue from people
with
CJD and sheep with scrapie but not in normal brain tissue. Bastian
states
that a shortcoming in the prion theory is that CJD and scrapie can be
transmitted without prions.

Brain material from which the prion has been removed with antibodies
can
still infect animals. Moreover, the prion has been found in unrelated
disease processes, such as Kawsaski syndrome and inclusion body
myositis.
Prion researchers have jumped to conclusions and have not considered
any
other possibility. It is quite possible that spiroplasmas may be
inducing
the formation of the prion protein to protect itself from the immune
system.

The immune system is very important in the pathogenesis of CJD. The
agent
replicates in the spleen and lymph nodes and occasionally causes an
immunologic reaction. Auto-antibodies are characteristically seen in
the
late stages of experimental and naturally occurring disease. The gene
for
the host protein is located on the chromosome in the region of the
major
histocompatibility complex (MHC) in the mouse. "Occasionally, you see
elevation of immuno globulins; there are morphological alterations of
the
leukocytes; there is leukopenia," Bastian explains, "and auto
antibodies are
characteristically seen in the late stages of both experimental and
naturally occurring infection. There is partial MHC restriction in
both
human and animal disease." "The immune reaction seen in these
Spongiform
diseases can be explained by super antigen activity, Bastian says. He
notes
that, normally, an antigen is presented to the cell surface in the
MHC and
interacts with the T-cell receptor--the antigen lying in a groove in
the
T-cell-MHC sets in motion the standard reaction. A super antigen, on
the
other hand, binds outside the groove of the T-cell and interacts with
the
MHC. This results in some immunoglobulin production, but only
transiently.
The major effect is clonal deletion of T cells, resulting in a state
of
immune tolerance. Autoantibodies can also form. In Spongiform
diseases, PrP
presumably acts as a super antigen. It is noteworthy that inclusion
body
myositis, a condition in which prions are seen, is an established
super
antigen disease."

Dr. Bastian also notes that investigators have reported transmitting
a TSE
to mice from hay mites gathered from farms in Iceland where scrapie is
endemic (Lancet. 1996;347:1114). He is virtually certain that these
hay
mites contain spiroplasma, noting that the investigators have not so
far
found PrP in the mites.

If hay mites can cause TSE, why couldn't the same be true for the
maggots
and mites on the Fore corpses? (3) Could Gajdusek have overlooked the
main
factor connecting Kuru to the Fore women and children? Was the
initial cause
of Kuru the ingesting of large quantities of maggots and mites by
protein
famished women and children? We know that the maggots and mites
contain
spiroplasma. By eating the brains of the Papuans that died from Kuru,
the
disease(Spiroplasma) was retransmitted to those remaining, in a deadly
cycle. Transmissible Spongiform Encephalopathies will continue to be
misunderstood unless we begin to study and understand these simple
connections.

ENDNOTES
(1) This information comes from several sources. It is well known to
anthropologists that these conditions existed among the Fore peoples
and
many other New Guinea tribes like the Sambia. I know it's hard to
believe in
these modern times but we must if we are to understand the world in
which we
live. My main source is Our Kind by Marvin Harris; Harper & Row;
1989. He
took much of his information from Shirley Lindenbaum, Kuru Sorcery:
Disease
and Danger in the New Guinea Highlands; 1979; Mayfield

(2) JAMA August 14, 1996 DC Capital Conference spring 1996 A
dissenting view
on the cause of mad cow disease Bastian regards the prion theory as a
red
herring. The cause of transmissible Spongiform encephalopathies
(TSEs), he
says, is a conventional microorganism--a mollicute or, more
specifically, a
spiroplasma. "The infection-related protein is produced by the host in
response to the infection,".

[Infectious Disease News Homepage] (June 1996) Spiroplasma may cause
Creutzfeldt-Jakob Disease An interview with a leading expert in
infectious
diseases, Frank O. Bastian, MD,. In 1992, Bastian arranged an
international
symposium on bovine Spongiform Encephalopathy.

I used information, quotes, and descriptions from the above article
and
interview to weave together Dr Bastian's ideas, knowledge and words,
with my
own research and interviews. I edited and rearranged both words and
sequence
for coherence sake. I did the best I could to convey this important
message.

I've had three phone conversations with Dr Bastian. He was
cooperative and
helpful at first and sent me much useful information which I have
included.
But he cut a scheduled interview short when I began to suggest that
biowarfare research might inadvertently help to spread the TSE agent.
I
called one more time and he refused to talk. He has refused to answer
a long
letter I wrote. I thought it both rude and arrogant, but even with
that
nonsense, I still believe Bastian's elegant hypothesis is far more
rational
than any I've studied.

(3)Common arthropods occuring on dead bodies: The Acari, or mites as
they
also are called, are small organisms, usually less than a mm in
lenght.
Mites occur under the dead body in the soil, during the later stages
of
decay. Many mites are transported to the body via other insects, such
as
flies or beetles. Other mites are soil dwelling forms which can be
predators, fungus feeders or detritus feeders. Most species will be
found in
soil samples from seepage area under the body. Sarchophagidae Among
the
Sarcophagids we find the large flesh-flies with red eyes and a
grey-checkered abdomen. These flies does not deposit eggs, but larvae
on the
corpse. They are, together with the Calliphorids, among the first
insects to
arrive at the corpse. The larvae are predators on blowfly larvae, as
well as
carrion feeders. Many Sarcophagids are feeding on snails and
earthworms.

Return to index page <welcome.htm>

Stealth Viruses
By Gussie Fauntleroy  For The New Mexican,
The New Mexican - 1/29/2001


Jamie Sams, 49, walks like an old woman. She shuffles, hunched over,
and sometimes forgets what she came into a room for. Off and on for
11 of the past 30 years she's been bedridden with an illness that has
been misnamed and renamed many times, but generally is referred to as
chronic fatigue syndrome.

Yet in spite of constant exhaustion, pain, 80-hour headaches and a
long list of other health problems, Sams is driven to help others who
suffer from similar symptoms. Her mission is to raise awareness about
what she sees as one of the most misunderstood, least known and
sometimes openly denied medical theories of our time: that chronic
fatigue, certain cancers, autism, attention-deficit disorder,
multiple sclerosis and a host of other serious and often life-
threatening diseases originate as viral infections.

These viruses, Sams and others believe, often are introduced into the
body by way of vaccinations. And some are contagious even while they
remain latent and almost undetectable in the body for many years. In
particular, a newly discovered category of virus, called stealth
viruses, are so small they are detectable only by electron microscope.

Stealth viruses behave in ways that previously were believed to be
impossible, and are the hidden culprit behind many diseases, Sams
believes.

Sams, a Santa Fe resident for the past 14 years, is co-author of
Medicine Cards and author of a number of other books on American
Indian spirituality and related topics. (Her own heritage is Seneca,
Cherokee and French.)

In the past few years she has been immersed in reading and research
on what she believes to be the source of her lifelong health
problems. She has amassed volumes of studies, documents, books and
Web sites dealing with the question of viral infections, and is in
regular communication with a number of physicians and scientists
actively involved in the issue.

It is a subject that soon will break into the public's attention,
Sams predicts. So she and others working with her are setting up what
she calls "information grand central," a Web site where doctors,
nurses, scientists, care givers and the general public can have
access to worldwide networking and the newest studies and resources
on chronic disease and stealth viruses.

The Emerging Worlds Web site (www.emergingworlds.com) is scheduled to
be up by the end of March. It is being established under the umbrella
of the Children of Earth Foundation, which Sams founded a number of
years ago to fund a variety of programs for American Indian youth,
artists, elders and others.

The site will include a secure, private discussion forum where
researchers, doctors and nurses around the world can share
information and exchange ideas. Another secure chat room will be
available for patient to patient exchanges.

Among the research studies and articles posted on the site will be
audio interviews with scientists and physicians working on these
issues. There will be information on alternative treatments for
chronic illness, and innumerable links to related sites.

Sams sees a need for this type of resource in part because most
medical Web sites are owned by pharmaceutical companies, and on many
sites medical researchers feel inhibited about discussing
unconventional theories and treatments. Sams and her colleagues hope
to provide a centralized, independent resource for the immense volume
of new information available.

"I think there needs to be a free spot on the bingo card so any
researcher who knows something can come forth with it. Our motto
is 'check your ego and your preconceptions at the (chat room) door.'
We're trying to create a way for doctors in the field in third world
countries to get involved in the dialogue and link up with the latest
research, not just on viral illness, but for any chronic illness,"
she said.

Discussion of stealth viruses, in particular, runs up against long-
held beliefs within the established medical system, Sams said. Dr. W.
John Martin, at the Center for Complex Infectious Diseases in
Rosemead, Calif., has been studying the link between stealth viruses
and chronic fatigue, multiple sclerosis and other chronic diseases
that up till now have not been considered contagious.

According to Martin's research, stealth viruses have the previously
unknown capacity to mimic other strains of virus within their
species. Martin believes they can even mutate to the extent that they
jump species and become a completely different form of virus. And as
the name implies, they are able live undetected in a body for years
without killing the host, thus increasing the chances of spreading
latent and undiagnosed disease.

Having mutated or adapted from well known viruses, stealth viruses
become transmittable through saliva, sexual intercourse, mother's
milk and blood transfusions, Martin believes. As a result, babies can
be born with viral infections that lead to serious illnesses, even
though their mothers may be asymptomatic. Without the patient
exhibiting symptoms of common viral infections, most doctors don't
know to look for viruses in the body.

A number of researchers now believe one of the primary ways many
viruses have been, and continue to be introduced into the population
is through vaccines and forced inoculations. Some vaccines, such as
those for polio and rubella, contain live human viruses to which Sams
believes no one should be exposed. Other vaccines are "contaminated"
with wild animal viruses that can wreck havoc in the human body.

"A live virus going into a human body can be deadly, and viral
medicine is in its infancy, in my opinion, when it comes to
understanding the long term effects of these things," Sams said. She
added that even attenuated vaccines, those made without live viruses,
are not necessarily safe. Attenuated vaccines are created by
injecting a live virus into substances such as animal organs or
chicken eggs, and then producing a vaccine with the antibodies
created by this process.

However, it recently was discovered that some batches of oral polio
vaccine in England were made with antibodies grown in bovine cells
from cows infected with mad cow disease. As a result, children
receiving the vaccine are in danger of manifesting the deadly viral
infection that causes a variation of mad cow disease in humans, Sams
said.

In another case, a large number of children in Norway were diagnosed
with autism within a very short time of being inoculated with the
measles/mumps/rubella vaccine that included a live rubella virus. A
class action lawsuit currently is ongoing, brought by parents of
those children.

Many people also believe the source of the debilitating Gulf War
Syndrome was forced inoculations of military personnel with vaccines
containing dangerous combinations of animal and human viruses, Sams
said.

Central to all such cases is the fact that there is no required
testing of vaccines, a situation Sams and others see as
unconscionable.

"We have to be real clear on the fact that there have been major
scientific blunders with attenuated and live vaccines. All vaccines
need to be tested. We have to have a way of knowing that vaccines on
the market are safe. As it is now, it's a matter of Russian roulette
of which (batch) your doctor gets," she said.

If testing of vaccines had been required since the introduction of
the first polio vaccines in the 1950s, Sams believes her own life
would have been very different. An athletic young child growing up in
Waco, Texas, she suddenly passed out several times in the eighth
grade, and has had continually more serious chronic health problems
since then.

In college she collapsed for a year and a half with what was
diagnosed as mononucleosis. From age 16 to 28 she underwent eight
surgeries on her abdomen, ovaries, uterus and other organs. Now her
condition is called chronic fatigue, the current name for a general
set of symptoms she shares with some 12 million Americans.

"Chronic fatigue syndrome is a real weird label. It includes people
with environmental illness, heavy metal toxins and candida. I think
there are five different kinds of CFS. But in every case the person
is waylaid, and even if they're doing well they may have 50 percent
of the energy level they used to have. And you never know, if you
overdo things, when it'll come back with a vengeance. It's scary as
the dickens," she said.

"They keep misnaming this disease. They called it the Yuppie flu,
then chronic Epstein-Barr virus, but they never talk about the fact
that there are many other viruses involved."

She added that the majority of doctors still consider chronic fatigue
a "phantom disease," claiming the patient's symptoms are "all in the
head." Contributing to this is the fact that most doctors do not test
such patients for latent viral infections. Stealth viruses show up in
blood cultures only when viewed under an electron microscope or by
PCR (polymer chain reaction) machine, which detects latent viruses in
DNA.

Sams said she has tested positive for 23 active and latent strains of
easily detectable viruses, as well as several stealth viruses. She is
convinced at least some of these entered her body through
inoculations with the original polio vaccines, which contained a
simian (wild monkey) virus. The vaccine was made with live kidney
cells from monkeys that had viral infections, she said.

In her case, the stew of viruses in her body has produced a type of
cerebral encephalopathy, or eating away of brain cells, as well as
chronic hemorrhaging of the brain and other organs, and viral
meningitis.

Sams uses a combination of Western drugs and alternative treatments
to keep herself as functional as possible. Some viral inhibitors are
available, and Dr. Martin currently is working on developing an
inhibitor for stealth viruses.

Everyone, Sams says, should follow preventative measures such as safe
sex and not sharing food, drinking glasses or utensils. She also
strongly believes laws must be put into place to require testing of
all vaccines for contamination by animal viruses, and all blood banks
should be tested for contamination by stealth viruses.

"People need to bind together and put pressure on the FDA and on
senators and congressmen to stop forced vaccinations and to test all
vaccines," Sams said. "There's a multibillion-dollar link (between
the FDA and drug companies) where they don't have to have vaccines
tested. It's all about money and the bottom line, instead of human
health."

The Emerging Worlds Web site (www.emergingworlds.com) being set up by
Jamie Sams and others is scheduled to be online by late March. In the
meantime, for information on support groups and current medical
research on chronic fatigue syndrome and other chronic illnesses,
here is a list of Web sites, books and resources suggested by Sams.

· Chronic Ill Net, www.chronicillnet.org

· Chenney Medical Center, www.fnmedcenter.com

· Center for Complex Infectious Diseases - stealth virus research,

www.ccid.org/stealth/svresearch.html

· Australian research - Newcastle University biology department and

links to CFS researchers worldwide: www.ahmf.org/links

· www.cfids.net

· www.chronicfatigue.org/index.html

· The CFIDS Association of America, 800-442-3437

· National Vaccine Information Center, 800-909-SHOT, or
www.909shot.com

· Books: Osler's Web: Inside the Labyrinth of the Chronic Fatigue
Syndrome Epidemic, by Hillary Johnson

· The Virus Within: A Coming Epidemic - How Medical Detectives are
Tracking a Terrifying Virus that Hides in Almost all of Us, by
Nicholas Regush

· 50 More Things you Should Know About CFIDS and its Link to AIDS
by
Neeya Ostrum (www.chronicillnet.org/book/ostrum)











Your use of Yahoo! Groups is subject to http://docs.yahoo.com/info/terms/

Lynn, Check this out! Sincerely, Jamie Sams


Spiroplasma & Transmissible Spongiform Encephalopathies
By Ed Gehrman
Introduction
Transmissible Spongiform Encephalopathy (TSE) is identified by the plaques
of mutated amyloid protein that form within the brain tissue and destroy
synapses and neurotransmitter functions and take on a characteristic sponge
or Swiss cheese appearance. CJD, Scrapie and Kuru are all members of this
degenerative disease family, afflictions known about for over two hundred
years but not studied intently until the early sixties when they were found
to be transmissible.

Dr. Carleton Gajdusek was a young researcher looking for unusual diseases
when he visited the Fore Peoples of Papau, New Guinea during the late 1950s.
The Papuans of those years were suffering from a population density that put
a strain on very limited resources. They practiced female infanticide and
cannibalism and were in a constant state of warfare with their neighbors
over land and pigs. Severe limitations on normal heterosexual relations were
imposed; the men spent most of their time at the men1s clubhouse where they
prepared for war and engaged in homosexual relations with the young boys.
This homosexual activity was all part of an elaborate bonding thought needed
to ensure macho warriors and dependable compatriots. The warfare was brutal,
often hand-to-hand; capture meant being tortured and killed. Solidarity was
essential and achieved through the sharing of semen. The females of the
group were disrespected and often abused because they were thought to steal
the men1s strength and resolve in battle as well as their vital semen. The
malnourishment of females and young children was part of this intense
process; they supplemented their diet by eating anything that 3crawled or
crept~. Midwives ate placentas of the new born and women dug up the partly
decomposed bodies of relatives and ate and shared with young children the
flesh, brains and the accumulations of maggots and mites. This was not a
religious ceremony but an attempt to fend off malnutrition. (1) Gajdusek
observed that some of the Fore women and a few children died from symptoms
indicating a neurological disorder: dementia, frenzied behavior, blindness
and eventual agonizing death. He studied the tribal dynamics and soon
hypothesized that the condition, known as Kuru, came from their habit of
eating the brains of dead relatives; he brought some diseased brain tissue
back to the USA. Gajdusek soon discovered that when he made a broth from the
Kuru tissue and injected this mixture into lab animals, they too exhibited
the Kuru symptoms. He then processed Kuru diseased lab animals1 brains and
injected the mixture into other lab animals. They also died the same
excruciating deaths. This meant that the condition could be transmitted from
organism to organism and was therefore transmissible, hence Transmissible
Spongiform Encephalopathy (TSE). Gajdusek and his colleagues at the National
Institute of Health were never able to isolate or positivly identify the
agent that causes the TSE even though they1ve been trying since the early
sixties. Scrapie and CJD were also studied and found to be transmissible.
All this was well known underground medical information; many doctors
refused to autopsy CJD victims. For years the NIH conjectured that the
infective culprit was a slow virus. Nothing seemed to distroy the agent; not
heat, cold, or any of the normal chemical disinfectants. Nor could they find
a trace of its chemical or mocular identity. Furthermore, the virus didn1t
cause inflamation so antibodies failed to leave a calling card. Some
completely new agent was essential.
Bastian's work

Another tenacious TSE researcher is Dr. Frank O. Bastian, MD, a professor of
pathology and director of neuropathology at the University of South Alabama,
Mobile. He has published numerous research articles relating to the etiology
of Creutzfeldt-Jakob Disease and also edited a book entitled
Creutzfeldt-Jakob Disease and Other Transmissible Spongiform
Encephalopathies. (2)

In 1976,Bastian examined a brain biopsy from a patient with CJD using
electron microscopy. He saw a spiral structure foreign to the tissue. It had
features of the newly reported spiroplasmas (Spiroplasmas were only
discovered in 1976). In 1981, a team in New York reported finding a fibril
protein in scrapie-infected brain tissue. This scrapie-associated fibril
(SAF) protein was 4 nm in diameter and 200 nm long. In 1983, the team looked
at various tissues of CJD and Kuru and demonstrated scrapie-associated
fibrils consistently in these diseases but not in control tissues. These SAF
were identical morphologically to the internal fibrils of spiroplasmas.

Moreover, antibodies to SAF react with internal fibrillar proteins from
Spiroplasma and digested brain material from people with CJD, suggesting
that these proteins essentially are the same. This similarity solidified in
Bastian's mind the link between spiroplasmas and CJD.

Dr. Bastian has postulated that Spiroplasma bacteria causes CJD and other
TSE. His twenty years of research indicates a role for Spiroplasma. The
evidence includes the following: spiroplasma-like inclusions were seen in
brain biopsies from patients with CJD (Arch Pathol Lab Med.
1979;103:665-669); spiroplasma internal fibril proteins are identical
morphologically to those seen in TSEs; the spiroplasma proteins show
immunological cross reactivity with the TSE proteins (J Clin Biol.
1987;25:2430-2431); and spiroplasma, when inoculated into rodents, produces
a similar neuropathology (Amer J Pathol. 1984;114:496-514).

Spiroplasmas
Spiroplasmas, are present in the hemolymph of almost all insects; there
probably are several million strains. They can also cause diseases in plants
but are usually associated with a vector. For example, a leaf hopper carries
a spiroplasma that infects orange trees.

Spiroplasmas are similar to mycoplasmas. They do not have a cell wall (cell
wall deficient) and have among the smallest genomes of any living organism.
Mycoplasma, are the smallest and perhaps the oldest life forms. These
bacteria, one cause of "walking pneumonia", are thought by many to be rather
fragile, but nothing could be further from the truth. They tolerate extreme
fluctuations in temperature, lay dormant in the soil for generations and
survive the harshest elements; only drano-like chemicals kill them
effectively outside the body. Under normal circumstances our immune system
efficiently deals with this complicated, membrane enclosed piece of DNA .

Spiroplasmas as the cause of CJD
A common phenomenon among the mycoplasmas is that the organisms bind host
proteins that often are of identical molecular weight to their surface
proteins and, therefore, are looked at by the immune system as being the
same as the host. The spiralin protein on the surface of spiroplasmas shows
a migration pattern on gel electrophoresis with a molecular weight of 27,000
Da to 30,000 Da, similar to that of the prion protein. This biochemical
similarity is compatible with spiroplasma etiology.

Bastian was able to show that spiroplasmas were neurotropic. When inoculated
peripherally into suckling rats, they will eventually localize to the brain
tissues. The organisms will produce a persistent infection and produce a
spongy change in the brain tissue of these animals. The neuropathologic
changes are similar to those seen in CJD.

Spiroplasmas are also within the size range of the agent that transmits CJD
and other transmissible Spongiform encephalopathies. Spiroplasmas will pass
through a 50 nm-pore filter. The transmissible agent's size has been
determined to be 42 nm.

The obvious way to look for an agent directly is by electron microscopy, but
this method may not be appropriate for spiroplasmas. Spiroplasmas are
similar to mycoplasmas, and it is a well-known phenomenon that mycoplasmas
are able to blend with cell membranes. What happens, possibly, is that
spiroplasmas essentially fuse with host-cell organelle membranes, thereby
blending with the background, so you would not see it unless you had a
marker to label it. Developing such as marker has been difficult because
spiroplasmas are very fastidious (difficult to cultivate)organisms.

Bastian also inoculated suckling rats with spiroplasmas, and examined their
brain tissues by electron microscopy early in the infection process; he
documented the organisms in the tissues. They appeared as membrane-bound
forms, except for the one instance where he observed the spiral form. Later
in infection, when he knew that the tissues were infectious by broth
culture, he couldn't find any evidence of spiroplasmas by looking at the
tissues extensively with electron microscopy.

Bastian insists that the infection-related protein that most researchers
refer to as a "prion" is produced by the host in response to the infection
and is not the causative agent. Prions are thought to be self-replicating
proteins. Some researchers believe prions are the cause of CJD and related
illnesses because they have found prions in brain tissue from people with
CJD and sheep with scrapie but not in normal brain tissue. Bastian states
that a shortcoming in the prion theory is that CJD and scrapie can be
transmitted without prions.

Brain material from which the prion has been removed with antibodies can
still infect animals. Moreover, the prion has been found in unrelated
disease processes, such as Kawsaski syndrome and inclusion body myositis.
Prion researchers have jumped to conclusions and have not considered any
other possibility. It is quite possible that spiroplasmas may be inducing
the formation of the prion protein to protect itself from the immune system.

The immune system is very important in the pathogenesis of CJD. The agent
replicates in the spleen and lymph nodes and occasionally causes an
immunologic reaction. Auto-antibodies are characteristically seen in the
late stages of experimental and naturally occurring disease. The gene for
the host protein is located on the chromosome in the region of the major
histocompatibility complex (MHC) in the mouse. "Occasionally, you see
elevation of immuno globulins; there are morphological alterations of the
leukocytes; there is leukopenia," Bastian explains, "and auto antibodies are
characteristically seen in the late stages of both experimental and
naturally occurring infection. There is partial MHC restriction in both
human and animal disease." "The immune reaction seen in these Spongiform
diseases can be explained by super antigen activity, Bastian says. He notes
that, normally, an antigen is presented to the cell surface in the MHC and
interacts with the T-cell receptor--the antigen lying in a groove in the
T-cell-MHC sets in motion the standard reaction. A super antigen, on the
other hand, binds outside the groove of the T-cell and interacts with the
MHC. This results in some immunoglobulin production, but only transiently.
The major effect is clonal deletion of T cells, resulting in a state of
immune tolerance. Autoantibodies can also form. In Spongiform diseases, PrP
presumably acts as a super antigen. It is noteworthy that inclusion body
myositis, a condition in which prions are seen, is an established super
antigen disease."

Dr. Bastian also notes that investigators have reported transmitting a TSE
to mice from hay mites gathered from farms in Iceland where scrapie is
endemic (Lancet. 1996;347:1114). He is virtually certain that these hay
mites contain spiroplasma, noting that the investigators have not so far
found PrP in the mites.

If hay mites can cause TSE, why couldn't the same be true for the maggots
and mites on the Fore corpses? (3) Could Gajdusek have overlooked the main
factor connecting Kuru to the Fore women and children? Was the initial cause
of Kuru the ingesting of large quantities of maggots and mites by protein
famished women and children? We know that the maggots and mites contain
spiroplasma. By eating the brains of the Papuans that died from Kuru, the
disease(Spiroplasma) was retransmitted to those remaining, in a deadly
cycle. Transmissible Spongiform Encephalopathies will continue to be
misunderstood unless we begin to study and understand these simple
connections.

ENDNOTES
(1) This information comes from several sources. It is well known to
anthropologists that these conditions existed among the Fore peoples and
many other New Guinea tribes like the Sambia. I know it's hard to believe in
these modern times but we must if we are to understand the world in which we
live. My main source is Our Kind by Marvin Harris; Harper & Row; 1989. He
took much of his information from Shirley Lindenbaum, Kuru Sorcery: Disease
and Danger in the New Guinea Highlands; 1979; Mayfield

(2) JAMA August 14, 1996 DC Capital Conference spring 1996 A dissenting view
on the cause of mad cow disease Bastian regards the prion theory as a red
herring. The cause of transmissible Spongiform encephalopathies (TSEs), he
says, is a conventional microorganism--a mollicute or, more specifically, a
spiroplasma. "The infection-related protein is produced by the host in
response to the infection,".

[Infectious Disease News Homepage] (June 1996) Spiroplasma may cause
Creutzfeldt-Jakob Disease An interview with a leading expert in infectious
diseases, Frank O. Bastian, MD,. In 1992, Bastian arranged an international
symposium on bovine Spongiform Encephalopathy.

I used information, quotes, and descriptions from the above article and
interview to weave together Dr Bastian's ideas, knowledge and words, with my
own research and interviews. I edited and rearranged both words and sequence
for coherence sake. I did the best I could to convey this important message.

I've had three phone conversations with Dr Bastian. He was cooperative and
helpful at first and sent me much useful information which I have included.
But he cut a scheduled interview short when I began to suggest that
biowarfare research might inadvertently help to spread the TSE agent. I
called one more time and he refused to talk. He has refused to answer a long
letter I wrote. I thought it both rude and arrogant, but even with that
nonsense, I still believe Bastian's elegant hypothesis is far more rational
than any I've studied.

(3)Common arthropods occuring on dead bodies: The Acari, or mites as they
also are called, are small organisms, usually less than a mm in lenght.
Mites occur under the dead body in the soil, during the later stages of
decay. Many mites are transported to the body via other insects, such as
flies or beetles. Other mites are soil dwelling forms which can be
predators, fungus feeders or detritus feeders. Most species will be found in
soil samples from seepage area under the body. Sarchophagidae Among the
Sarcophagids we find the large flesh-flies with red eyes and a
grey-checkered abdomen. These flies does not deposit eggs, but larvae on the
corpse. They are, together with the Calliphorids, among the first insects to
arrive at the corpse. The larvae are predators on blowfly larvae, as well as
carrion feeders. Many Sarcophagids are feeding on snails and earthworms.

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Stealth Viruses
By Gussie Fauntleroy  For The New Mexican,
The New Mexican - 1/29/2001


Jamie Sams, 49, walks like an old woman. She shuffles, hunched over,
and sometimes forgets what she came into a room for. Off and on for
11 of the past 30 years she's been bedridden with an illness that has
been misnamed and renamed many times, but generally is referred to as
chronic fatigue syndrome.

Yet in spite of constant exhaustion, pain, 80-hour headaches and a
long list of other health problems, Sams is driven to help others who
suffer from similar symptoms. Her mission is to raise awareness about
what she sees as one of the most misunderstood, least known and
sometimes openly denied medical theories of our time: that chronic
fatigue, certain cancers, autism, attention-deficit disorder,
multiple sclerosis and a host of other serious and often life-
threatening diseases originate as viral infections.

These viruses, Sams and others believe, often are introduced into the
body by way of vaccinations. And some are contagious even while they
remain latent and almost undetectable in the body for many years. In
particular, a newly discovered category of virus, called stealth
viruses, are so small they are detectable only by electron microscope.

Stealth viruses behave in ways that previously were believed to be
impossible, and are the hidden culprit behind many diseases, Sams
believes.

Sams, a Santa Fe resident for the past 14 years, is co-author of
Medicine Cards and author of a number of other books on American
Indian spirituality and related topics. (Her own heritage is Seneca,
Cherokee and French.)

In the past few years she has been immersed in reading and research
on what she believes to be the source of her lifelong health
problems. She has amassed volumes of studies, documents, books and
Web sites dealing with the question of viral infections, and is in
regular communication with a number of physicians and scientists
actively involved in the issue.

It is a subject that soon will break into the public's attention,
Sams predicts. So she and others working with her are setting up what
she calls "information grand central," a Web site where doctors,
nurses, scientists, care givers and the general public can have
access to worldwide networking and the newest studies and resources
on chronic disease and stealth viruses.

The Emerging Worlds Web site (www.emergingworlds.com) is scheduled to
be up by the end of March. It is being established under the umbrella
of the Children of Earth Foundation, which Sams founded a number of
years ago to fund a variety of programs for American Indian youth,
artists, elders and others.

The site will include a secure, private discussion forum where
researchers, doctors and nurses around the world can share
information and exchange ideas. Another secure chat room will be
available for patient to patient exchanges.

Among the research studies and articles posted on the site will be
audio interviews with scientists and physicians working on these
issues. There will be information on alternative treatments for
chronic illness, and innumerable links to related sites.

Sams sees a need for this type of resource in part because most
medical Web sites are owned by pharmaceutical companies, and on many
sites medical researchers feel inhibited about discussing
unconventional theories and treatments. Sams and her colleagues hope
to provide a centralized, independent resource for the immense volume
of new information available.

"I think there needs to be a free spot on the bingo card so any
researcher who knows something can come forth with it. Our motto
is 'check your ego and your preconceptions at the (chat room) door.'
We're trying to create a way for doctors in the field in third world
countries to get involved in the dialogue and link up with the latest
research, not just on viral illness, but for any chronic illness,"
she said.

Discussion of stealth viruses, in particular, runs up against long-
held beliefs within the established medical system, Sams said. Dr. W.
John Martin, at the Center for Complex Infectious Diseases in
Rosemead, Calif., has been studying the link between stealth viruses
and chronic fatigue, multiple sclerosis and other chronic diseases
that up till now have not been considered contagious.

According to Martin's research, stealth viruses have the previously
unknown capacity to mimic other strains of virus within their
species. Martin believes they can even mutate to the extent that they
jump species and become a completely different form of virus. And as
the name implies, they are able live undetected in a body for years
without killing the host, thus increasing the chances of spreading
latent and undiagnosed disease.

Having mutated or adapted from well known viruses, stealth viruses
become transmittable through saliva, sexual intercourse, mother's
milk and blood transfusions, Martin believes. As a result, babies can
be born with viral infections that lead to serious illnesses, even
though their mothers may be asymptomatic. Without the patient
exhibiting symptoms of common viral infections, most doctors don't
know to look for viruses in the body.

A number of researchers now believe one of the primary ways many
viruses have been, and continue to be introduced into the population
is through vaccines and forced inoculations. Some vaccines, such as
those for polio and rubella, contain live human viruses to which Sams
believes no one should be exposed. Other vaccines are "contaminated"
with wild animal viruses that can wreck havoc in the human body.

"A live virus going into a human body can be deadly, and viral
medicine is in its infancy, in my opinion, when it comes to
understanding the long term effects of these things," Sams said. She
added that even attenuated vaccines, those made without live viruses,
are not necessarily safe. Attenuated vaccines are created by
injecting a live virus into substances such as animal organs or
chicken eggs, and then producing a vaccine with the antibodies
created by this process.

However, it recently was discovered that some batches of oral polio
vaccine in England were made with antibodies grown in bovine cells
from cows infected with mad cow disease. As a result, children
receiving the vaccine are in danger of manifesting the deadly viral
infection that causes a variation of mad cow disease in humans, Sams
said.

In another case, a large number of children in Norway were diagnosed
with autism within a very short time of being inoculated with the
measles/mumps/rubella vaccine that included a live rubella virus. A
class action lawsuit currently is ongoing, brought by parents of
those children.

Many people also believe the source of the debilitating Gulf War
Syndrome was forced inoculations of military personnel with vaccines
containing dangerous combinations of animal and human viruses, Sams
said.

Central to all such cases is the fact that there is no required
testing of vaccines, a situation Sams and others see as
unconscionable.

"We have to be real clear on the fact that there have been major
scientific blunders with attenuated and live vaccines. All vaccines
need to be tested. We have to have a way of knowing that vaccines on
the market are safe. As it is now, it's a matter of Russian roulette
of which (batch) your doctor gets," she said.

If testing of vaccines had been required since the introduction of
the first polio vaccines in the 1950s, Sams believes her own life
would have been very different. An athletic young child growing up in
Waco, Texas, she suddenly passed out several times in the eighth
grade, and has had continually more serious chronic health problems
since then.

In college she collapsed for a year and a half with what was
diagnosed as mononucleosis. From age 16 to 28 she underwent eight
surgeries on her abdomen, ovaries, uterus and other organs. Now her
condition is called chronic fatigue, the current name for a general
set of symptoms she shares with some 12 million Americans.

"Chronic fatigue syndrome is a real weird label. It includes people
with environmental illness, heavy metal toxins and candida. I think
there are five different kinds of CFS. But in every case the person
is waylaid, and even if they're doing well they may have 50 percent
of the energy level they used to have. And you never know, if you
overdo things, when it'll come back with a vengeance. It's scary as
the dickens," she said.

"They keep misnaming this disease. They called it the Yuppie flu,
then chronic Epstein-Barr virus, but they never talk about the fact
that there are many other viruses involved."

She added that the majority of doctors still consider chronic fatigue
a "phantom disease," claiming the patient's symptoms are "all in the
head." Contributing to this is the fact that most doctors do not test
such patients for latent viral infections. Stealth viruses show up in
blood cultures only when viewed under an electron microscope or by
PCR (polymer chain reaction) machine, which detects latent viruses in
DNA.

Sams said she has tested positive for 23 active and latent strains of
easily detectable viruses, as well as several stealth viruses. She is
convinced at least some of these entered her body through
inoculations with the original polio vaccines, which contained a
simian (wild monkey) virus. The vaccine was made with live kidney
cells from monkeys that had viral infections, she said.

In her case, the stew of viruses in her body has produced a type of
cerebral encephalopathy, or eating away of brain cells, as well as
chronic hemorrhaging of the brain and other organs, and viral
meningitis.

Sams uses a combination of Western drugs and alternative treatments
to keep herself as functional as possible. Some viral inhibitors are
available, and Dr. Martin currently is working on developing an
inhibitor for stealth viruses.

Everyone, Sams says, should follow preventative measures such as safe
sex and not sharing food, drinking glasses or utensils. She also
strongly believes laws must be put into place to require testing of
all vaccines for contamination by animal viruses, and all blood banks
should be tested for contamination by stealth viruses.

"People need to bind together and put pressure on the FDA and on
senators and congressmen to stop forced vaccinations and to test all
vaccines," Sams said. "There's a multibillion-dollar link (between
the FDA and drug companies) where they don't have to have vaccines
tested. It's all about money and the bottom line, instead of human
health."

The Emerging Worlds Web site (www.emergingworlds.com) being set up by
Jamie Sams and others is scheduled to be online by late March. In the
meantime, for information on support groups and current medical
research on chronic fatigue syndrome and other chronic illnesses,
here is a list of Web sites, books and resources suggested by Sams.

· Chronic Ill Net, www.chronicillnet.org

· Chenney Medical Center, www.fnmedcenter.com

· Center for Complex Infectious Diseases - stealth virus research,

www.ccid.org/stealth/svresearch.html

· Australian research - Newcastle University biology department and

links to CFS researchers worldwide: www.ahmf.org/links

· www.cfids.net

· www.chronicfatigue.org/index.html

· The CFIDS Association of America, 800-442-3437

· National Vaccine Information Center, 800-909-SHOT, or
www.909shot.com

· Books: Osler's Web: Inside the Labyrinth of the Chronic Fatigue
Syndrome Epidemic, by Hillary Johnson

· The Virus Within: A Coming Epidemic - How Medical Detectives are
Tracking a Terrifying Virus that Hides in Almost all of Us, by
Nicholas Regush

· 50 More Things you Should Know About CFIDS and its Link to AIDS
by
Neeya Ostrum (www.chronicillnet.org/book/ostrum)

Lynn, Check this out! Sincerely, Jamie Sams


Spiroplasma & Transmissible Spongiform Encephalopathies
By Ed Gehrman
Introduction
Transmissible Spongiform Encephalopathy (TSE) is identified by the plaques
of mutated amyloid protein that form within the brain tissue and destroy
synapses and neurotransmitter functions and take on a characteristic sponge
or Swiss cheese appearance. CJD, Scrapie and Kuru are all members of this
degenerative disease family, afflictions known about for over two hundred
years but not studied intently until the early sixties when they were found
to be transmissible.

Dr. Carleton Gajdusek was a young researcher looking for unusual diseases
when he visited the Fore Peoples of Papau, New Guinea during the late 1950s.
The Papuans of those years were suffering from a population density that put
a strain on very limited resources. They practiced female infanticide and
cannibalism and were in a constant state of warfare with their neighbors
over land and pigs. Severe limitations on normal heterosexual relations were
imposed; the men spent most of their time at the men1s clubhouse where they
prepared for war and engaged in homosexual relations with the young boys.
This homosexual activity was all part of an elaborate bonding thought needed
to ensure macho warriors and dependable compatriots. The warfare was brutal,
often hand-to-hand; capture meant being tortured and killed. Solidarity was
essential and achieved through the sharing of semen. The females of the
group were disrespected and often abused because they were thought to steal
the men1s strength and resolve in battle as well as their vital semen. The
malnourishment of females and young children was part of this intense
process; they supplemented their diet by eating anything that 3crawled or
crept~. Midwives ate placentas of the new born and women dug up the partly
decomposed bodies of relatives and ate and shared with young children the
flesh, brains and the accumulations of maggots and mites. This was not a
religious ceremony but an attempt to fend off malnutrition. (1) Gajdusek
observed that some of the Fore women and a few children died from symptoms
indicating a neurological disorder: dementia, frenzied behavior, blindness
and eventual agonizing death. He studied the tribal dynamics and soon
hypothesized that the condition, known as Kuru, came from their habit of
eating the brains of dead relatives; he brought some diseased brain tissue
back to the USA. Gajdusek soon discovered that when he made a broth from the
Kuru tissue and injected this mixture into lab animals, they too exhibited
the Kuru symptoms. He then processed Kuru diseased lab animals1 brains and
injected the mixture into other lab animals. They also died the same
excruciating deaths. This meant that the condition could be transmitted from
organism to organism and was therefore transmissible, hence Transmissible
Spongiform Encephalopathy (TSE). Gajdusek and his colleagues at the National
Institute of Health were never able to isolate or positivly identify the
agent that causes the TSE even though they1ve been trying since the early
sixties. Scrapie and CJD were also studied and found to be transmissible.
All this was well known underground medical information; many doctors
refused to autopsy CJD victims. For years the NIH conjectured that the
infective culprit was a slow virus. Nothing seemed to distroy the agent; not
heat, cold, or any of the normal chemical disinfectants. Nor could they find
a trace of its chemical or mocular identity. Furthermore, the virus didn1t
cause inflamation so antibodies failed to leave a calling card. Some
completely new agent was essential.
Bastian's work

Another tenacious TSE researcher is Dr. Frank O. Bastian, MD, a professor of
pathology and director of neuropathology at the University of South Alabama,
Mobile. He has published numerous research articles relating to the etiology
of Creutzfeldt-Jakob Disease and also edited a book entitled
Creutzfeldt-Jakob Disease and Other Transmissible Spongiform
Encephalopathies. (2)

In 1976,Bastian examined a brain biopsy from a patient with CJD using
electron microscopy. He saw a spiral structure foreign to the tissue. It had
features of the newly reported spiroplasmas (Spiroplasmas were only
discovered in 1976). In 1981, a team in New York reported finding a fibril
protein in scrapie-infected brain tissue. This scrapie-associated fibril
(SAF) protein was 4 nm in diameter and 200 nm long. In 1983, the team looked
at various tissues of CJD and Kuru and demonstrated scrapie-associated
fibrils consistently in these diseases but not in control tissues. These SAF
were identical morphologically to the internal fibrils of spiroplasmas.

Moreover, antibodies to SAF react with internal fibrillar proteins from
Spiroplasma and digested brain material from people with CJD, suggesting
that these proteins essentially are the same. This similarity solidified in
Bastian's mind the link between spiroplasmas and CJD.

Dr. Bastian has postulated that Spiroplasma bacteria causes CJD and other
TSE. His twenty years of research indicates a role for Spiroplasma. The
evidence includes the following: spiroplasma-like inclusions were seen in
brain biopsies from patients with CJD (Arch Pathol Lab Med.
1979;103:665-669); spiroplasma internal fibril proteins are identical
morphologically to those seen in TSEs; the spiroplasma proteins show
immunological cross reactivity with the TSE proteins (J Clin Biol.
1987;25:2430-2431); and spiroplasma, when inoculated into rodents, produces
a similar neuropathology (Amer J Pathol. 1984;114:496-514).

Spiroplasmas
Spiroplasmas, are present in the hemolymph of almost all insects; there
probably are several million strains. They can also cause diseases in plants
but are usually associated with a vector. For example, a leaf hopper carries
a spiroplasma that infects orange trees.

Spiroplasmas are similar to mycoplasmas. They do not have a cell wall (cell
wall deficient) and have among the smallest genomes of any living organism.
Mycoplasma, are the smallest and perhaps the oldest life forms. These
bacteria, one cause of "walking pneumonia", are thought by many to be rather
fragile, but nothing could be further from the truth. They tolerate extreme
fluctuations in temperature, lay dormant in the soil for generations and
survive the harshest elements; only drano-like chemicals kill them
effectively outside the body. Under normal circumstances our immune system
efficiently deals with this complicated, membrane enclosed piece of DNA .

Spiroplasmas as the cause of CJD
A common phenomenon among the mycoplasmas is that the organisms bind host
proteins that often are of identical molecular weight to their surface
proteins and, therefore, are looked at by the immune system as being the
same as the host. The spiralin protein on the surface of spiroplasmas shows
a migration pattern on gel electrophoresis with a molecular weight of 27,000
Da to 30,000 Da, similar to that of the prion protein. This biochemical
similarity is compatible with spiroplasma etiology.

Bastian was able to show that spiroplasmas were neurotropic. When inoculated
peripherally into suckling rats, they will eventually localize to the brain
tissues. The organisms will produce a persistent infection and produce a
spongy change in the brain tissue of these animals. The neuropathologic
changes are similar to those seen in CJD.

Spiroplasmas are also within the size range of the agent that transmits CJD
and other transmissible Spongiform encephalopathies. Spiroplasmas will pass
through a 50 nm-pore filter. The transmissible agent's size has been
determined to be 42 nm.

The obvious way to look for an agent directly is by electron microscopy, but
this method may not be appropriate for spiroplasmas. Spiroplasmas are
similar to mycoplasmas, and it is a well-known phenomenon that mycoplasmas
are able to blend with cell membranes. What happens, possibly, is that
spiroplasmas essentially fuse with host-cell organelle membranes, thereby
blending with the background, so you would not see it unless you had a
marker to label it. Developing such as marker has been difficult because
spiroplasmas are very fastidious (difficult to cultivate)organisms.

Bastian also inoculated suckling rats with spiroplasmas, and examined their
brain tissues by electron microscopy early in the infection process; he
documented the organisms in the tissues. They appeared as membrane-bound
forms, except for the one instance where he observed the spiral form. Later
in infection, when he knew that the tissues were infectious by broth
culture, he couldn't find any evidence of spiroplasmas by looking at the
tissues extensively with electron microscopy.

Bastian insists that the infection-related protein that most researchers
refer to as a "prion" is produced by the host in response to the infection
and is not the causative agent. Prions are thought to be self-replicating
proteins. Some researchers believe prions are the cause of CJD and related
illnesses because they have found prions in brain tissue from people with
CJD and sheep with scrapie but not in normal brain tissue. Bastian states
that a shortcoming in the prion theory is that CJD and scrapie can be
transmitted without prions.

Brain material from which the prion has been removed with antibodies can
still infect animals. Moreover, the prion has been found in unrelated
disease processes, such as Kawsaski syndrome and inclusion body myositis.
Prion researchers have jumped to conclusions and have not considered any
other possibility. It is quite possible that spiroplasmas may be inducing
the formation of the prion protein to protect itself from the immune system.

The immune system is very important in the pathogenesis of CJD. The agent
replicates in the spleen and lymph nodes and occasionally causes an
immunologic reaction. Auto-antibodies are characteristically seen in the
late stages of experimental and naturally occurring disease. The gene for
the host protein is located on the chromosome in the region of the major
histocompatibility complex (MHC) in the mouse. "Occasionally, you see
elevation of immuno globulins; there are morphological alterations of the
leukocytes; there is leukopenia," Bastian explains, "and auto antibodies are
characteristically seen in the late stages of both experimental and
naturally occurring infection. There is partial MHC restriction in both
human and animal disease." "The immune reaction seen in these Spongiform
diseases can be explained by super antigen activity, Bastian says. He notes
that, normally, an antigen is presented to the cell surface in the MHC and
interacts with the T-cell receptor--the antigen lying in a groove in the
T-cell-MHC sets in motion the standard reaction. A super antigen, on the
other hand, binds outside the groove of the T-cell and interacts with the
MHC. This results in some immunoglobulin production, but only transiently.
The major effect is clonal deletion of T cells, resulting in a state of
immune tolerance. Autoantibodies can also form. In Spongiform diseases, PrP
presumably acts as a super antigen. It is noteworthy that inclusion body
myositis, a condition in which prions are seen, is an established super
antigen disease."

Dr. Bastian also notes that investigators have reported transmitting a TSE
to mice from hay mites gathered from farms in Iceland where scrapie is
endemic (Lancet. 1996;347:1114). He is virtually certain that these hay
mites contain spiroplasma, noting that the investigators have not so far
found PrP in the mites.

If hay mites can cause TSE, why couldn't the same be true for the maggots
and mites on the Fore corpses? (3) Could Gajdusek have overlooked the main
factor connecting Kuru to the Fore women and children? Was the initial cause
of Kuru the ingesting of large quantities of maggots and mites by protein
famished women and children? We know that the maggots and mites contain
spiroplasma. By eating the brains of the Papuans that died from Kuru, the
disease(Spiroplasma) was retransmitted to those remaining, in a deadly
cycle. Transmissible Spongiform Encephalopathies will continue to be
misunderstood unless we begin to study and understand these simple
connections.

ENDNOTES
(1) This information comes from several sources. It is well known to
anthropologists that these conditions existed among the Fore peoples and
many other New Guinea tribes like the Sambia. I know it's hard to believe in
these modern times but we must if we are to understand the world in which we
live. My main source is Our Kind by Marvin Harris; Harper & Row; 1989. He
took much of his information from Shirley Lindenbaum, Kuru Sorcery: Disease
and Danger in the New Guinea Highlands; 1979; Mayfield

(2) JAMA August 14, 1996 DC Capital Conference spring 1996 A dissenting view
on the cause of mad cow disease Bastian regards the prion theory as a red
herring. The cause of transmissible Spongiform encephalopathies (TSEs), he
says, is a conventional microorganism--a mollicute or, more specifically, a
spiroplasma. "The infection-related protein is produced by the host in
response to the infection,".

[Infectious Disease News Homepage] (June 1996) Spiroplasma may cause
Creutzfeldt-Jakob Disease An interview with a leading expert in infectious
diseases, Frank O. Bastian, MD,. In 1992, Bastian arranged an international
symposium on bovine Spongiform Encephalopathy.

I used information, quotes, and descriptions from the above article and
interview to weave together Dr Bastian's ideas, knowledge and words, with my
own research and interviews. I edited and rearranged both words and sequence
for coherence sake. I did the best I could to convey this important message.

I've had three phone conversations with Dr Bastian. He was cooperative and
helpful at first and sent me much useful information which I have included.
But he cut a scheduled interview short when I began to suggest that
biowarfare research might inadvertently help to spread the TSE agent. I
called one more time and he refused to talk. He has refused to answer a long
letter I wrote. I thought it both rude and arrogant, but even with that
nonsense, I still believe Bastian's elegant hypothesis is far more rational
than any I've studied.

(3)Common arthropods occuring on dead bodies: The Acari, or mites as they
also are called, are small organisms, usually less than a mm in lenght.
Mites occur under the dead body in the soil, during the later stages of
decay. Many mites are transported to the body via other insects, such as
flies or beetles. Other mites are soil dwelling forms which can be
predators, fungus feeders or detritus feeders. Most species will be found in
soil samples from seepage area under the body. Sarchophagidae Among the
Sarcophagids we find the large flesh-flies with red eyes and a
grey-checkered abdomen. These flies does not deposit eggs, but larvae on the
corpse. They are, together with the Calliphorids, among the first insects to
arrive at the corpse. The larvae are predators on blowfly larvae, as well as
carrion feeders. Many Sarcophagids are feeding on snails and earthworms.

Return to index page <welcome.htm>
If you wish to contact Ed Gehrman, he is available at egehrman@...

Date:  Fri Feb 16, 2001 2:23pm
Subject:  Re: [StealthVirus-Patient] New mouse stealth virus


Mouse Birth Control Experiments Spark Fears of Bioterrorism
-----------------------------------------------------------
[A report in "New Scientist" magazine states that] Australian
scientists,
who have accidently created a deadly version of mouse smallpox in the
laboratory, say lethal human viruses are only a step away.  The
prospect of
such dangerous organisms being produced relatively easily has left
bioterrorism experts fearful of killer global epidemics.  [These are
highly
emotive and alarmist statements. To put the matter in perspective, it
should have been made clear that Ectromelia virus (also called
mousepox
virus) is one of 9 distinct virus species (infecting different
mammalian
hosts) which make up the genus _Orthopoxvirus_ of the family
_Poxviridae_.  So far the experiments involve only laboratory mice. -
Mod.CP].

The Australian researchers, reported New Scientist magazine, made one
simple genetic change to a "mousepox" virus in an attempt to produce
an
effective contraceptive vaccine.  "Mousepox" normally causes only mild
illness, and when all the animals undergoing the experiment died
within
days, the scientist realized the potential of their discovery.  They
say a
similar [mutation] in human smallpox virus [theoretically] could
produce a
far more virulent strain which could even be resistant to vaccines.
[It
should be remembered that the human smallpox virus has been
eradicated from
nature, and survives only in 2 high security laboratories. - Mod.CP]

[The experiment referred to apparently involved the insertion of] a
gene
which produces a [cytokine] called interleukin-4 (Il-4) into the
mousepox
virus genome.  The idea was to stimulate an immune reaction against
mouse
eggs, [thereby producing] a contraceptive effect.  However, the
effect was
to completely suppress the part of the immune system normally
mobilized to
fight viral infection.  Dr. Ron Jackson, who led the research,
said: "It
would be safe to assume that if some idiot did put human IL-4 into
human
smallpox [virus] they'd increase the lethality quite dramatically."
In
addition, vaccination against mousepox appeared to have far less of a
protective effect for those infected with the new strain.  In fact,
only
half those mice vaccinated survived infection.

Professor John Bartlett, co-director of the Johns Hopkins Center for
Civil
Biodefense Studies in Baltimore, was quoted as saying that "I
wouldn't have
thought you would need anything more virulent than smallpox already
is to
cause a global epidemic.  There is a lot of concern about it -- the
entire
world is vulnerable because no one has immunity."  He added that "If
a new
vaccine needs to be developed from scratch, we are talking about
several
years minimum.  There are enough rogue nations and dissidents trying
to do
this."

A spokesman for Friends of the Earth called for much closer scrutiny
of
laboratory experiments.  Susan Meyer, of the pressure group Genewatch,
which is calling for more openness on the part of the biotechnology
industry, said that: "This discovery should really alert people to
the fact
that genetically altering organisms can have unexpected outcomes.

A spokesman for the UK Ministry of Defence's biological research
facility
at Porton Down said that "Making scientists aware of the full
potential of
their discoveries is important, but inevitably it carries the same
risk in
bringing possibilities to the attention of the unscrupulous.  We seek
to be
aware of what possibilities are open to aggressor countries or
terrorists.  By the nature of things, this is always a game of
catch-up.  And there are already so many possibilities that absolute
protection is not possible without the sort of constraints that are
not
acceptable in a free society."

--
Patricia A. Doyle, PhD
<dr_p_doyle@h...>

[Viruses that successfully replicate within the host have devised
strategies to subvert or evade the challenges posed by the innate and
adaptive immune responses.  Many investigators are beginning to
dissect the
diverse and complex interactions involving cytokines, chemokines,
chemokine
receptors and viral infection, and much attention has been focused on
the
role of secreted cytokine and chemokine inhibitors, and chemokines in
antiviral defense.  Ectromelia virus (EV) is a natural mouse pathogen
that
causes a generalized infection termed mousepox, which, in the
genetically-resistant C57BL/6 (B6) mouse, is an inapparent disease.
In
contrast, BALB/c and A strain mice are highly susceptible; one
infectious
virus particle can result in 100% mortality.  The contribution of
cytokines
in the induction of protective immune responses and recovery from
infection
with EV in B6, BALB/c and A strain mice is well known.  This type of
research will promote better understanding of protective immune
responses
and their experimental enhancement as much as their inhibition.  An
unfortunate by-product of this New Scientist article is that it has
provoked a negative response from Friends of the Earth to the effect
that:
"We simply don't know enough to allow these experiments at present." -
Mod.CP]

H. Lynn Knapp, M.A.
February  22, 2001
lynnknapp@...


      Welcome new members!

      Hopefully this support group will offer the opportunity for
those who have suffered from the Stealth Virus, to share journeys,
and treatment protocols that have been successful to some degree.

      I am looking forward to meeting you and welcome you to join.

      I have been ill for 22yrs, diagnosed by spinal tap for Lyme
Disease in 1990, and was treated aggressively for many years.
However, my disease progressed.  It was not until Feb. 1999 that I
tested positive for Stealth Virus by blood culture at the Center for
Complex Infectious Diseases, www.ccid.org.  Since initial diagnosis
and treatment, I am slowly regaining a great degree of good health,
though the progress has been slow but steady.

      I was in heart failure, in and out of hemolytic crisis, on 15
liters of O2 continuously via a non-rebreather O2 mask.  I slept and
lived in a hospital bed. My hemoglobin wavered at 5, with
transfusions no longer helping.  I suffered severe immune deficiency,
with hypogammagloblinemia.  I had atrial arrhythmia's, with Brady-
tachy Syndrome,(SSS), and a permanent Cardiac Pacemaker was
implanted.  I suffered from seizures, fevers and cold sweats.  I
developed Capillary Leak Syndrome, which caused acute pulmonary and
Systemic edema.  There was also severe peripheral, and autonomic
neuropathy. I had acute hypothyroidism, and adrenal insufficiency.  I
elicited hemosiderosis, with "0" stored iron in my bone marrow and
marked storage of iron in my liver, which left me severely cyanotic.
I even developed a pulmonary embolism.

      It was in this condition that I began I.V. Cytovene therapy in
March 1999.   It is now January 26, 2001 and I am pleased to report
the following:  I no longer have a permanent cardiac pacemaker.  It
was removed due to a Staff infection in my port-o-cath.  When
removed, we discovered I no longer needed it.  My hemoglobin is 10-
11.5, with my last transfusion dating March 1999.  I am no longer
confined to a hospital bed, nor am I confined to a non-rebreather O2
mask with 15 liters of O2.  I am on 2 liters continuously, and hope
in time to be O2 free.  My peripheral neuropathy is markedly
improved, and my orthostatic hypotension, secondary to autonomic
neuropathy, is almost completely gone.  My thyroid is finally
responding to thyroid replacement therapy, and I suspect my adrenals
are responding in turn due to an improved thyroid condition. Best of
all, is this, my recent bone marrow bx shows the markedly stored iron
to be gone, without any liver damage.  My bone marrow still tests
positive for Stealth Virus, and the recent bone marrow bx's still
show "0" iron storage and the result is continued cyanosis.  My
fevers are now low grade and transient; my cold sweats also less
severe and transient. I am no longer in heart failure, though I still
suffer from a much less severe state of pulmonary edema,  and my
Capillary Leak Syndrome is also under much better control. My
seizures are also under control with no phenabarbitol needed. My
immune system is also showing signs of life with lymphatic
involvement when the viral activity is active.

      I do not know how it is with others, but with me the Stealth
Virus has a dormant and active cycle.  Each week I have a few days
the virus is more virulent and my symptoms worsen; and then I have a
few days the virus is more dormant and I feel the closest to "normal"
than I have in years.  This cycle is reflected in my weekly blood
work.  When active my hemoglobin drops a little; my iron drops
considerably; my triglycerides shoot up and so does my potassium; my
bleeding factor shoots way out of range with very high INR levels;
and sometimes there are elevated liver functions.

      I have found that a very low carbohydrate diet greatly
decreases the virus's degree of activity.  Taking the prescription
drug glucophage, which lowers insulin, also helps greatly.  I
personally believe it is the hyperinsulinemia that stimulates the
virus and not the sugar.  The sugar just produces more insulin.  When
I began to take the glucophage, my cyclic seizures stopped.  I now
only have them if I go off the low carb diet.  Within a few hours of
ingesting concentrated sugar, I will experience severe seizures.  The
type of seizure I experience is called "tetany".  It is very violent.

      I have also discovered that the elevated triglycerides that
accompany my active cycle, are secondary to hyperinsulinemia.  When
the insulin factor is less, so are the level of triglycerides.  I
found 500mg of L-Carnitine, four times a day; along with 25mg of
vanadyl sulfate, help to lower triglycerides, which in turn help to
lower insulin.  Somehow the high triglycerides and hyperinsulinemia
are connected.

      The greatest thing Dr. Martin has recommended in his protocol,
is quercetin.  Dr. Martin suggests it may have powerful anti-reverse
transcriptase activity.  I am certain it does.  Prior to taking
quercetin, when I would go into my active cycle, I would have severe
lymphatic involvement, under my arms and the back of my neck.  I was
also developing a face lesion.  Within 24 hrs. of taking quercetin,
1,000mg 3 times daily, my enlarged lymph nodes completely
disappeared, and have not resurfaced during any subsequent active
cycles.  My face lesion stopped growing and has faded somewhat.  I
cancelled my appointment to have my lymph nodes and face lesion
biopsied.

      The other great help in suppressing the Stealth Virus has been
the different modalities Dr. Martin has suggested that may be
effective in suppressing cytokine/chemokine production. So far I am
having very good results with thyroxin, quercetin, and oral
vancomycin.(I can not take Biaxin due to severe hemolytic crisis
secondary to the administration of systemic antibiotics; cause not
clearly understood.) I will soon be trying other natural and
prescription modalities that Dr. Martin thinks may also have the
ability to suppress cytokine/chemokine production.

      I'd like to end with this:  I am no longer living in the
expectation of my next medical crisis, but rather in the expectation
of increasingly improved health.  I have gone from the land of the
dying to the land of the living!


       I'm looking forward to reading your "stealth journey" stories!


                                                   Sincerely yours,

                                                   H. Lynn Knapp, M.A.