A herpes virus strain that infects nearly all of us at an early age may be the hidden agent behind multiple sclerosis and other tough neurological diseases, according to a new study in the journal Scientific Reports.

The herpesvirus 6 (HHV-6A) could be the culprit impeding the brain’s ability to repair nerve damage, leading to the diseases, according to the team from the University of Rochester.

HHV-6 never really leaves the human body – instead enmeshing itself in DNA, only to potentially reemerge without warning later in life. 

“These findings show that, while in the process of hiding from the immune system, the virus produces a protein that has the potential to impair the normal ability of cells in the brain to repair damaged myelin,” said Margot Mayer-Proschel, Rochester associate professor, and co-author of the study.

The HHV-6A connection to the loss of myelin was first noted by one of the current Rochester co-authors, David Mock, in 2003.

Fourteen years ago, they discovered the trail: the HHV6 genetic code was wound through the brain cells of people with severe multiple sclerosis. 

The latest theory by the Rochester team proposed that the virus shuts down the oligodendrocyte progenitor cells, OPCs, used to repair myelin damage. The virus, they hypothesized, accomplished this through producing a protein called U94A that helps it hide from the immune system.

OPCs taken from human fetal tissue were exposed to the U94A in an in vitro experiment.

The in-vivo model includes immunocompromised mice being infused with U94A over a matter of weeks, after which they were killed and their brains were harvested.

In both models, the OPCs were significantly impaired, preventing the appropriate nerve repair, they report.

“Our data raise the possibility that CNS viral latency is not a benign state, but can contribute to defective myelin repair through impaired recruitment of myelinating OPCs after injury,” they conclude. “These data suggest, for the first time, a potential contribution of latent HHV-6A infection in the progression of demyelinating diseases.”

The demyelinating diseases include MS, but also leukodystrophies, and the vanishing white matter disease, according to the scientists.

Some 80 percent of all people get HHV-6A in early childhood. About one percent are born with it, passed on from mother or father.

But whether the rarer congenital forms of the virus, or a certain viral threshold, produces the tipping point leading to disease pathology, remains to be determined, they add.

“It is clear that HHV-6A, while not necessarily the cause of demyelinating disease, is limiting the ability of the brain to repair damage to myelin thereby potentially accelerating the progression of these diseases,” said Mayer-Proschel.