Human Herpes Virus 6 variant A (HHV-6A) directly linked to multiple sclerosis-like illness.

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.