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Dormant Herpes Virus Can Impede Repair of Myelin Sheath Whose Deterioration Causes MS

July 25, 2017

A new study has found that a herpes virus, HHV-6, lies dormant in many people can hinder the repair of the neuron-protecting myelin sheath whose deterioration causes multiple sclerosis (MS). The article appeared in journal Scientific Reports under the title “Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration.” HHV-6 is one of the most common human herpes viruses, infecting an estimated 80% of people during childhood. Some people will show symptoms, but in many cases, the virus will go unnoticed because it produces a protein known as U94 that prevents the immune system from detecting it.

Dr. Margot Mayer-Proschel, an associate professor at the University of Rochester Medical Center Department of Biomedical Genetics, and her team decided to see if HHV-6 could affect brain cells called oligodendrocyte progenitor cells that play a key role in providing myelin to neurons.  When the disease occurs, an injury or age causes myelin loss, the progenitor cells, also known as OPCs, migrate to the place that needs repair. There, they mature into myelin-producing cells called oligodendrocytes to fix the damage. The researchers discovered that OPCs containing the U94 viral protein were unable to migrate to the places that needed myelin restored.  

“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,” Mayer-Proschel said. Although the research suggested that HHV-6 might contribute to myelin loss, it did not make clear whether the virus can influence the severity of myelin-loss diseases, including MS. It also did not specify whether those with congenital HHV-6 may be at risk of developing such a disease.