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Herpes virus variant suggested as trigger for multiple sclerosis

Herpes virus variant suggested as trigger for multiple sclerosis
Antibodies against a specific herpes variant, known as HHV-6A, were found at significantly higher levels in the blood of subjects with MS
Antibodies against a specific herpes variant, known as HHV-6A, were found at significantly higher levels in the blood of subjects with MS
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Antibodies against a specific herpes variant, known as HHV-6A, were found at significantly higher levels in the blood of subjects with MS
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Antibodies against a specific herpes variant, known as HHV-6A, were found at significantly higher levels in the blood of subjects with MS

A study, led by scientists at Sweden’s Karolinska Institutet, has demonstrated a new method that can distinguish between two different, but closely related, strains of the herpes virus. The novel screening system was subsequently tested on a large cohort with multiple sclerosis to offer new evidence that a specific herpes strain might play a role in the onset of the autoimmune disease.

In the 1990s, a scientist named Peter Challoner discovered an unusually high expression of viral DNA in certain brain cells from patients with MS. The virus was identified as human herpesvirus 6 (HHV-6) and since then it has been the focus of much research, with some scientists hypothesizing the virus may be a trigger for the neuroinflammatory flare-ups seen in MS.

Scientists have known for several decades that HHV-6 seemed to express two relatively distinct subtypes, known as HHV-6A and HHV-6B. However, it is only recently that research begun to reveal how different the two subtypes were, and in 2012 the International Committee on Taxonomy of Viruses ultimately classified the viruses as entirely distinct and separate strains.

A body of research has accumulated over the past 10 to 20 years suggesting a strong link between HHV-6 and MS. In blood and brain tissue studies a distinct correlation has been identified associating HHV-6 viral loads with exacerbations in MS disease activity. But, until now there frustratingly has not been an easy way to distinguish between the two different HHV-6 species.

The new study demonstrates the efficacy of a novel screening system that can identify the differences between HHV-6A and HHV-6B antibodies. Over 8,000 blood samples from MS patients were tested, against a healthy control cohort of more than 7,000 subjects. The results revealed HHV-6A antibodies were significantly more prominent in the blood of MS patients. This positive correlation was not seen with HHV-6B antibodies, verifying prior research suggesting HHV-6A is the more neurovirulant strain of the virus.

"This is a big breakthrough for both the MS and herpes virus research," explains one of the senior authors on the new study, Anna Fogdell-Hahn. "For one, it supports the theory that HHV-6A could be a contributing factor to the development of MS. On top of that, we are now able, with this new method, to find out how common these two different types of HHV-6 are, something we haven't been able to do previously."

The researchers are clear in noting their study does not at all imply HHV-6A is an explicit causal factor for MS. The disease is most likely the result of a number of different environmental and genetic factors, however, this research does offer intriguing evidence pointing to some kind of viral influence in triggering acute flare-ups.

This is not the first neurological disorder that has been linked with the herpes virus. An increasingly popular hypothesis has linked HHV-6A and Alzheimer’s disease, with studies finding abundant volumes of the virus in the brains of those suffering from the neurodegenerative disease. As with this new MS research, any causal mechanism linking the virus with dementia is still yet to be discovered but there are many scientists hypothesizing ways the virus could trigger these diseases.

"Both HHV-6A and 6B can infect our braincells, but they do it in slightly different ways,” Fogdell-Hahn says. “Therefore, it is now interesting to go forward and attempt to map out exactly how the viruses could affect the onset of MS.”

The new research was published in the journal Frontiers in Immunology.

Source: Karolinska Institutet

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