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Camouflage Disease
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The Leprosy bacteria eats myelin off the nerves

Smallpox eradication impossible?

A Commentator wrote:

``Regarding Lyme disease, there are two camps in the medical community.
Camp A says that it is strictly a bacterial problem, and we don't want
to look at any autoimmune aspects. Camp B says that Lyme is easily
treatable and, after that, it is an autoimmune problem; but we don't
want to try anything to fix it.''

Another Commentator wrote:

``There is a basis for a third theory.

I still think that Lyme spirochetes cause some of our neurological
problems by eating the myelin off our nerve cells. But in January,
2002, I completed reading "Germs" by Judith Miller and others; and now
I think a major component of the attack may be similar to autoimmune
disease, but it should be called something like "camouflage" disease.

Among many horrible pieces of information, Miller describes the work of
the Russian germ warrior Sergei Popov who has defected to the U.S.
Popov's most ingenious trick was to snip out the gene for myelin from a
human (or other, e.g. mouse) chromosome, and insert it into a virus,
for example smallpox, which the Russians made by the ton after signing
the 1972 treaty outlawing germ warfare (hopefully without Popov's
insertion).

When exposed to Popov's chimera, the test animals (mice) would develop
the viral disease. Those that did not die then developed a one hundred
percent fatal multiple sclerosis. Popov also inserted the gene into
bacteria which gave the same sequence of events.

In a moment of inspiration, Popov discovered he could infect a bacteria
such as plague (the black death) with a virus such as smallpox that
contained the gene for making myelin. Now he had a 3-wave weapon: Some
of the people exposed to the plague bacteria would survive with
antibiotic treatment. On dying, the bacteria would release the virus
causing, for example, a second wave of smallpox. Those who survived the
smallpox would then die of MS.

How does it work? Apparently the body recognizes the microbe with the
myelin on its cell wall and produces antibodies for the myelin. These
antibodies then attack the myelin in our nerve cells. Because the
antibodes are diluted by attacking the host's nerve cells, the microbe
has improved its chance of survival.

Could some microbes have developed this talent for picking up host
"surface" genes naturally? It would be a most useful adaptation because
the host would be firing indiscriminately at the microbe and its own
tissues, reducing the probabilty that the microbe would be hit. The
microbe has camouflaged itself.

Of course, it would be of little use to a spirochete living in the
cartilage of a knee joint to absorb a gene for making myelin, but it
would be most useful for it to absorb a gene for making collagen. Such
a microbe would also be camouflaged, and the victim would develop
arthritis because of his body's indiscriminate attempt to kill the
microbe.''

Commentator 1 wrote:

`` "Blebbing" is fascinating, kind of like a jet dropping flares to
attract the incoming missles. The blebs are left wherever they were
dropped and should be able to continue an antigen response.

This is a play on what you're talking about: ''

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

ARTICLE from The Scientist, Vol:10, #14, pg.13, July 8, 1996, 1996, By
Karen Hopkin

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``Searching The Surface

.... Many researchers believe that the secret to B. burgdorferi's
infectivity and inflammatory capacity lies in the interaction of its
surface proteins with the host's immunological system.

Yale researcher Stephen Barthold, a veterinarian and professor of
comparative medicine who developed the first mouse model of Lyme
disease, studies the expression of B. burgdorferi surface proteins
throughout various stages of the spirochete's life cycle.

He finds that during the early stages of infection, B. burgdorferi
avoids immune detection by decreasing its expression of surface
proteins or cloaking its expressed surface proteins under a layer of
slime. "It's using some sort of stealth-bomber-type mechanism," he
says. Or, using another diversionary tactic called blebbing, the
spirochete can pinch off bits of its membrane in order to release its
surface proteins.

Explains Barbour: "It's like a bacterial Star Wars defense program," in
which released surface proteins might intercept incoming host
antibodies, keeping the spirochete safe from immunological attack ...''


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

ARTICLE from Infection 2001 Dec;29):315-9, By Brorson O, Brorson SH,
Henriksen TH, Skogen PR, Schoyen R., Dept. of Microbiology, Vestfold
Sentralsykehus, Tonsberg, Norway.

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``Association between multiple sclerosis and cystic structures in
cerebrospinal fluid.

BACKGROUND: The aim of the study was to search for infectious agents in
the cerebrospinal fluid of patients with multiple sclerosis (MS).

PATIENTS AND METHODS: cerebrospinal fluid from ten patients with the
diagnosis relapsing remitting MS and from five controls without MS were
examined by transmission electron microscopy, dark field microscopy,
interference contrast microscopy and UV-microscopic examination of
acridine orange staining (AO). All cerebrospinal fluid samples from
patients and controls were cultured.

RESULTS: Cystic structures were observed in cerebrospinal fluid of all
ten patients by AO and transmission electron microscopy. dark field
miscroscopy revealed eight cyst-positive patients out of nine. One of
five control persons had such structures in the cerebrospinal fluid;
this person had suffered from erythema migrans. Spirochete or rod-like
structures emerged after culturing two of the MS patient cerebrospinal
fluid samples and these structures could be propagated.

CONCLUSION: A significant association of cerebrospinal fluid cysts and
MS was identified in this small study among residents in a coastal area
of southern Norway. The cysts could be of spirochetal origin. Our study
may encourage other researchers to study larger patient groups.''

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

ARTICLE from APMIS 2001 May;109(5):383-8, Gruntar I, Malovrh T, Murgia
R, Cinco M., Institute of Microbiology and Parasitology, Veterinary
Faculty, Ljubljana, Slovenia. gruntaig@xxxxxxxxxxxxxxxxx

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``Conversion of Borrelia garinii cystic forms to motile spirochetes in
vivo.

Cystic forms (also called spheroplasts or starvation forms) and their
ability to reconvert into normal motile spirochetes have already been
demonstrated in the Borrelia burgdorferi sensu lato complex.

The aim of this study was to determine whether motile Borrelia garinii
could develop from cystic forms, not only in vitro but also in vivo, in
cyst-inoculated mice.

The cysts prepared in distilled water were able to reconvert into
normal motile spirochetes at any time during in vitro experiments,
lasting one month, even after freeze-thawing of the cysts. Motile
spirochetes were successfully isolated from 2 out of 15 mice inoculated
intraperitoneally with cystic forms, showing the infectivity of the
cysts.

The demonstrated capacity of the cysts to reconvert into motile
spirochetes in vivo and their surprising resistance to adverse
environmental conditions should lead to further studies on the role and
function of these forms in Lyme disease.''

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


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ARTICLE from Nature, 22 February 2001, By TOM CLARKE

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``Comparing the gene sequence of M. leprae with that of its close
relative M. tuberculosis which causes TB, [M. tuberculosis is an
aerobic, non-motile, rod-shaped bacterium], Stephen Cole of the Pasteur
Institute in Paris and colleagues found that over millennia the leprosy
bacterium has undergone major 'reductive evolution' -- losing genes and
therefore the ability to adapt ...

Leprosy has been largely absent from Europe since the fourteenth
century, but as many as 700,000 new cases of the disease still occur
each year, mostly in the developing world ...

Unlike most invaders, M. leprae can withstand the body's shock troops.
In the initial stages of infection, the bacteria are engulfed by white
blood cells but they are not destroyed. Instead, the blood cells
unwittingly carry the bacteria to their new home inside cells known as
macrophages, which are also part of the body's immune response. Here,
the bacteria invade certain types of nerve cell, eventually causing the
skin lesions and loss of sensation so characteristic of leprosy ...''

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

ARTICLE from Science, published by The American Association for the
Advancement of Science, By Peter J. Brophy

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Volume 296, Number 5569, Issue of 3 May 2002, pp. 862-863.

``MICROBIOLOGY: Subversion of Schwann Cells ...

The authors RULE OUT INVOLVEMENT OF THE IMMUNE SYSTEM IN THE NERVE
DEMYELINATION CHARACTERISTIC OF LEPROSY.

They infected the peripheral nerves of Rag1-deficient mice with M.
leprae. These mice lack both B cells and T cells of the immune system,
and so they cannot mount either a humoral or a cell-mediated immune
response to bacterial infection.

Demyelination induced by the bacillus was just as effective in these
immune-deficient mice as in animals with a normal immune system. The
authors reasonably conclude that binding of bacterial PGL-1 to
a-dystroglycan on the surface of myelinating Schwann cells is
sufficient ...

CHRONIC EXPOSURE of peripheral nerves to M. leprae could prevent
remyelination by stalling Schwann cell differentiation and increasing
the available pool of cells susceptible to colonization.

Both the loss of myelin and the block in remyelination would contribute
to the death of axons. It is now appreciated that the severe damage
observed in a variety of human demyelinating peripheral neuropathies is
the result of axonal damage attendant on the loss of the myelin sheath
....''

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

REPORT from THE ROCKEFELLER UNIVERSITY

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OFFICE OF PUBLIC AFFAIRS

1230 YORK AVENUE, NEW YORK, NY 10021-6399 N E W S

Issued: November 13, 2000

runews@xxxxxxxxxxxxxxxxxxxxxxx

``Researchers Find How Leprosy Bacterium Selects and Attacks Nerves

Mode of invasion may provide clues to the early events of other
neurological diseases

Researchers at Rockefeller University who study the bacterium that
causes leprosy say they have identified a component on the microbe's
surface that allows it to specifically select and attack the peripheral
nerves.

The finding clarifies how the bacterium, Mycobacterium leprae (M.
leprae) precisely seeks out peripheral nerves, and it sheds light on
the early stages of nerve damage in other neurodegenerative diseases
such as Guillain-Barre syndrome and MULTIPLE SCLEROSIS.

"If we can understand what neural cell molecules the bacteria use to
infect the nerves, we'll gain more insight into what kinds of signaling
pathways are involved in bacterial-induced nerve degeneration," says
Anura Rambukkana, Ph.D., principal investigator and research associate
in the Laboratory of Bacterial Pathogenesis.

In addition, learning what M. leprae does to perturb neural signaling
may help researchers understand how the pathway normally works, a
process that is still poorly understood. The research was reported in
the Oct. 27 issue of the journal Cell by Rambukkana together with
Vincent Ng, a graduate student at Rockefeller, and researchers at three
other institutions ...

The peripheral nervous system consists of all the nerves that fan out
from the brain and spinal cord and includes the muscles, skin and
internal organs.


During development, Schwann cells encase nerve fibers and wrap around
the axon to form the myelin sheath. This sheath greatly improves the
reliability and speed of the electric impulse, much like insulation on
electrical wires.

WHEN MYELIN IS DAMAGED, AS with M. leprae infection and IN PATIENTS
WITH Guillain-Barre syndrome and MULTIPLE SCLEROSIS, the nerve fibers
are no longer insulated and nerve impulses cannot be conducted
efficiently.

The Schwann cell-axon unit is surrounded by an outer layer called the
basal lamina, a matrix secreted by the Schwann cells. The components of
the basal lamina that are targeted by M. leprae play a vital role in
myelination.

Rambukkana and colleagues previously reported that a major component in
the Schwann cell basal lamina, called lamina-2, and its receptor,
called dystroglycan, are involved in M. leprae's interaction with
Schwann cells. This interplay allows the bacterium to infect the
peripheral nerves, which eventually causes nerve damage.

The new research focuses on the invader's side of the interaction,
specifically, on identifying the part of the microbe's cell wall that
allows the interaction to occur.

The cell wall of M. leprae is endowed with large quantities of a
glycolipid called phenolic glycolipid (PGL-1). PGL-1 contains a
trisaccharide unit that exists only in M. leprae. This uniqueness led
researchers to speculate that PGL-1 plays an essential role in
functions that are specific to the leprosy bacterium, such as infecting
peripheral nerve cells, but they had no proof ...

Now the researchers have demonstrated that PGL-1 binds specifically to
native laminin-2 but not to other proteins in the basal lamina of the
Schwann cell-axon unit. It turns out that invasion of the Schwann cell
is ultimately controlled by the neural target, not the invading
microbe.

The basal lamina is a dynamic action zone that functions to instruct
neural cell phenotypes and activation. Modulation of the basal lamina
has profound effects both on its function and the consequent behavior
of cells residing within it. Therefore, it is not surprising that the
basal lamina and Schwann cells respond to PGL-1 upon contact with the
bacterium by opening the pathway to allow the intruder to enter ...

"We think clarifying PGL-1's role in nerve infection will eventually
make it possible to develop strategies to block bacterial invasion of
the peripheral nerve cells at an early stage and thus prevent
neurological damage before the immune system gets involved," Rambukkana
says.

Leprosy is a chronic bacterial infection that damages nerves, mainly in
the limbs and facial area, and also leads to skin lesions.

M. leprae is the only known human bacterial pathogen that attacks the
Schwann cell of the peripheral nervous system, and the nerve damage it
induces is by far one of the leading cause of peripheral nerve disease
in the world. [Has any research been done to determine if the Lyme
spirochete attacks the Schwann cell?]

The disease can be treated ith multidrug therapy that kills most of the
M. leprae in a few weeks. However, nerve function loss caused by M.
leprae invasion of Schwann cells is irreversible.

Rambukkana and his colleagues are now focusing on how neurotropic
pathogens, both M. leprae and viruses, attack the peripheral nervous
system, and they hope to use these pathogens and their products as
tools to identify early molecular events of neurodegenerative diseases.


The researchers will focus especially on DEMYELINATING DISEASES, both
those of infectious origin, known to be caused either by bacteria or
viruses, AND THOSE WITH UNKNOWN CAUSES, SUCH AS Guillain-Barre syndrome
and MULTIPLE SCLEROSIS ...''


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ARTICLE from Science News, Week of July 13, 2002; Vol. 162, No. 2, By
John Travis

``Do-It-Yourself: Virus recreated from synthetic DNA

In an experiment with implications for bioterrorism and the worldwide
campaign to eradicate polio, scientists have used poliovirus' widely
known genetic sequence to synthesize that virus from the building
blocks of DNA and a broth of other chemicals.

"It's the first time someone has started with a sequence on paper and
put together the necessary ingredients chemically to create the virus
specified," says Eckard Wimmer of the State University of New York at
Stony Brook, who led the work. "We don't need any nature-formed
template anymore. We just need the Internet to tell us the sequence of
a virus. You can make pretty much any virus this way."

"Scientifically, the results are not surprising or astounding in any
way," says virologist Vincent Racaniello of Columbia University. "The
point here, of course, is that the DNA can be synthesized from the
[genetic] sequence, and this could be done by any third-rate
terrorist." ...

Wimmer and his colleagues used common laboratory machines to synthesize
DNA strands harboring the same protein-encoding instructions that a
typical poliovirus carries ...

Wimmer, Racaniello, and other scientists suggest that the new findings
could make it pointless to destroy the last few stockpiles of viruses
such as smallpox. "The sequence [of the smallpox virus has been
published and is available. It's a difficult virus to recreate, but it
will be possible," says Wimmer ...

"In the posteradication era, we must always have plans for what to do
in the event that the virus reappears, whether by accident or by evil
intent," Racaniello says. "Unfortunately, and frighteningly, there are
no such plans at hand."''

References:

Cello, J., A.V. Paul, and E. Wimmer. In press. Chemical synthesis of
poliovirus cDNA: Generation of infections virus in the absence of
natural template. Science. Abstract available at
http://www.sciencemag.org/cgi/content/abstract/1072266v1

Further Readings:

Nomoto, A., and I. Arita. 2002. Eradication of poliomyelitis. Nature
Immunology 3(March):205.

Racaniello, V.R. 2000. It is too early to stop polio vaccination.
Bulletin of the World Health Organization 78(March):359-360. See
http://www.who.int/bulletin/pdf/2000/issue3/round.pdf.

Sources:

Vincent R. Racaniello

Department of Microbiology

Columbia University College of Physicians and Surgeons

701 West 168th Street

New York, NY 10032

Eckard Wimmer

Department of Molecular Genetics and Microbiology

School of Medicine

State University of New York at Stony Brook

Stony Brook, NY 11794

>>From Science News, Vol. 162, No. 2, July 13, 2002, p. 22.


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