Multiple Sclerosis & CFS Linked to HHV-6A Virus - - American Neurology Associati

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Multiple Sclerosis & CFS 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.