MS/HERPESVIRUS

[Bb]

Lähettäjä: Soijuv Lähetetty: 8.10.2005 17:38

Uuden tutkimuksen mukaan herpesviruksen (HHV 6)
ja MS-taudin välillä on todettu olevan tekemistä keskenään.
Herpesviruksethan ovat borrelioosia sairastavienkin riesana
useimmiten.


http://www.primezone.com/newsroom/news.html?d=87395

Source: HHV-6 Foundation

Multiple Sclerosis Linked to HHV-6A Virus

Evidence Presented at American Neurology Association Annual Meeting

SAN DIEGO, Oct. 5, 2005 (PRIMEZONE) -- Dr. Claude Genain of the University
of California San Francisco Medical Center presented evidence at the
American Neurology Association Annual Meeting this week that shows a direct
link between human herpes virus 6 variant A (HHV-6A) and a multiple
sclerosis-like illness.

Dr. Genain injected common marmoset monkeys with HHV-6 variants A & B. Most
notably, only infection with HHV-6 variant A resulted in illness. The
monkeys developed lab evidence and signs of chronic autoimmune demyelination
of the central nervous system, the hallmark of multiple sclerosis. This is
the first time that any animal infected with HHV-6A has developed clinical
pathology of the central nervous system, and the most direct evidence to
date of a possible causal connection between HHV-6A and multiple sclerosis.

Dr. Genain's marmoset developed weight loss and paralysis with sensory
deficits after exposure to HHV-6A. Inflammatory lesions of the central
nervous system and evidence of demyelination were seen on MRI and microscope
slides of the brain tissue. However, the important finding of the study was
direct evidence of the presence of HHV-6 viral antigen within the nerve
cells of the brain stained with an HHV-6-specific antibody.

HHV-6 variant B (HHV-6B) causes roseola, a self-limited fever and rash, in
over 95% of young children by age 2. After the initial illness, HHV-6
persists indefinitely in its quiescent, latent form in the cells of the
central nervous system, bone marrow and immune system. However, HHV-6 can
reemerge and actively replicate later in life, producing new virus particles
that can cause illness. HHV-6 can reactivate in immunosuppressed patients
and cause life threatening complications, such as opportunistic infections
and encephalitis, in post-transplant patients.

The quest for a theory of viruses as a causative agent for multiple
sclerosis and other diseases has long eluded scientists. A direct link
between infection with HHV-6A and multiple sclerosis has been lacking until
now.

According to Dr. Genain, "For the first time, scientists will be able to
look into the biological process leading to multiple sclerosis at its very
beginning, when no one suspects the disease and people have not yet
experienced its symptoms." In recent years there has been a considerable
degree of interest in the relationship between HHV-6A and multiple
sclerosis, because HHV-6A DNA has repeatedly been found in brain tissue and
the cerebrospinal fluid of affected patients, and increased levels of
antibodies to viral antigens in their blood only present during replication
of HHV-6A are frequently detected.

A comprehensive analysis presented by Dr. Dharam Ablashi, co-discoverer of
HHV-6 and Scientific Director of the HHV-6 Foundation, at the International
Fatigue Conference on Fatigue Science held during February 2005 in Osaka,
Japan, discussed all clinical studies published in the medical literature on
the association between HHV-6A and multiple sclerosis.

His summary of the existing literature demonstrates that when lab methods
detecting the presence of active HHV-6A infection are used, an exceptionally
strong, statistically significant association between HHV-6A and both
multiple sclerosis and chronic fatigue syndrome (CFS) is consistently seen.
Lab methods that detect latent HHV-6A virus are not able to consistently
identify either MS or CFS patients.

Having an experimental animal model linking HHV-6A infection to central
nervous system pathology will open the door to new types of research
investigations. The common marmoset has a well-known propensity to develop
experimental autoimmune encephalitis, a chemically-induced animal model of
multiple sclerosis that is commonly used when investigating the efficacy of
new MS drugs. The inflammatory demyelination of nerve cells in a live
primate model after exposure to the HHV-6A virus has now been demonstrated
for the first time. This marmoset model will add a new dimension to the drug
discovery and development process for multiple sclerosis.

Dr. Ablashi, who has published numerous medical studies demonstrating the
causative role of human and primate herpes viruses in various types of
lymphomas and leukemia, commented, "Nonhuman primates are genetically
closest to man. Dr. Genain's pathogenic model of HHV-6A infection in the
common marmoset will enhance our understanding of the role that the HHV-6A
virus plays in the induction of typical MS lesions. This model will be very
important in the study of the disease process, and evaluation of new
molecules that can prevent active HHV-6A viral infection and the development
of multiple sclerosis."

Dr. Genain's work was supported by grants from the HHV-6 Foundation,
Multiple Sclerosis Society, Cure MS Now, DANA Foundation and Lunardi
Foundation.

The HHV-6 Foundation logo can be found at:
http://www.primezone.com/newsroom/prs/?pkgid=1968


CONTACT: HHV-6 Foundation
Kristin Loomis, Executive Director
(805) 969-1174
kristin_loomis@hhv-6foundation.org
http://www.hhv-6foundation.org

Dr. Claude Genain
claudeg@itsa.ucsf.edu