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.
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