Infection with the most common member of the herpes virus family, called HHV-6, may pass unnoticed and without symptoms, but the very act of being infected significantly accelerated the development and progression of a multiple sclerosis-like disease in nonhuman primates, a study reports.
Its findings support the role of viral infection in triggering “inflammatory-mediated neurologic conditions” like MS, it concluded.
The study, “Herpesvirus trigger accelerates neuroinflammation in a nonhuman primate model of multiple sclerosis,” was published in the journal Proceedings of the National Academy of Sciences of the United States of America (PNAS).
Several herpes viruses — including HHV-6, one of the most common and estimated to infect 80 percent of people during childhood — are linked with MS.
Specifically, a previous study reported that HHV-6 is found at increased frequency in MS lesions and outside the brain (for example, in circulating blood) in periods of MS clinical exacerbation. Another study suggested that dormant HHV-6 can hinder the repair mechanisms of the myelin sheath (the protective coat surrounding neurons), and the loss of myelin is the underlying cause of MS.
Since HHV-6 is almost always acquired in early childhood, it is difficult to assess its role in MS, a disease that usually manifests in early adulthood.
Mice and other rodents are not susceptible to HHV-6 infection. So to study how HHV-6 infection affects MS onset, researchers at the National Institute of Neurological Disorders and Stroke (NINDS) used a monkey species, called marmosets, as animal models.
“Marmosets are excellent models of experimental autoimmune encephalomyelitis (EAE),” the researchers wrote, noting they better captures features of human MS than do rodents.
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