New research distinguishes between two similar variants of the human herpesvirus 6 and finds that one variant significantly increases the risk of developing multiple sclerosis (MS).

illustration of epstein barr virusShare on Pinterest
Scientists have linked the Epstein-Barr virus (depicted here) with MS.

MS is an autoimmune condition that affects around 400,000 people in the United States and 2.5 million people worldwide.

The condition affects the central nervous system, “tricking” the immune system into attacking the protective myelin sheath that surrounds the nerve cells.

The medical community has not yet identified the cause of MS. Many health professionals believe that genetic predisposition plays a role, with environmental factors such as smoking and viral infections potentially triggering MS risk genes.

Of all the viruses that may play a role in the development of MS, the Epstein-Barr virus (EBV) — which causes mononucleosis — has received the most attention from researchers.

EBV, also known as human herpesvirus 4, is part of the herpesvirus family. A significant number of epidemiological studies have pointed to EBV infection, as well as a number of other environmental factors, as potential causes of MS.

In addition, recent research has suggested that EBV can activate risk genes for other autoimmune conditions, such as lupus.

Scientists have also associated human herpesvirus 6 (HHV-6) with MS. However, previous studies linking HHV-6 and MS were not able to differentiate between herpesvirus 6A (HHV-6A) and herpesvirus 6B (HHV-6B).

So, new research — which appears in the journal Frontiers in Immunology — aimed to make this distinction and examine the associations with MS.

Anna Fogdell-Hahn — an associate professor in the Department of Clinical Neuroscience at the Karolinska Institutet in Solna, Sweden — is one of the senior investigators and the corresponding author of the new study.

Fogdell-Hahn and team examined the antibodies in the blood of 8,742 people with MS and 7,215 matched controls. They then did the same in a pre-MS cohort of 478 people and 476 matched controls.

In the MS cohort, the participants were matched for age at diagnosis, sex, and residency, while in the pre-MS cohort, they were matched for “biobank, sex, date of blood sampling, and date of birth.”

The researchers examined the antibodies against two proteins that differ the most between HHV-6A and HHV-6B, thus distinguishing between the two forms of the virus.

The research concluded that participants with MS were 55% more likely to have antibodies against the HHV-6A protein than the controls.

In the pre-MS group, people with a 6A viral infection were more than twice as likely to go on to develop MS than the controls. By contrast, HHV-6B was not associated with MS.

Also, the earlier in life the discovery of the virus, the higher the person’s likelihood of developing MS.

The scientists also found that people who had EBV in addition to HHV-6A had an even higher risk of developing MS.

“This is a big breakthrough for both the MS and herpesvirus research,” says 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.”

Anna Fogdell-Hahn

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