In a new study, a research team has shed light on a novel axon damage mechanism which could be highly relevant for progressive multiple sclerosis patients.

According to researchers in Heinrich-Heine University’s Department of Neurology in Duesseldorf, Germany, the envelope protein of the pathogenic human endogenous retrovirus type W was found to be a major contributor to nerve damage in MS. In collaboration with research teams in Cleveland and Montreal, the authors demonstrated that the envelope protein drives central nervous system resident microglial cells to contact and damage myelinated axons.

Alongside the scientific research into determining how the damage mechanism works, clinical developments aiming at neutralizing the harmful envelope protein in MS patients have also progressed. Two clinical studies have already successfully tested the envelope-neutralising antibody temelimab. MRI scans of the participants treated in the study showed reduced damage to the nerve tissue.

The researchers can therefore explain why neurodegeneration is decreased in patients treated with temelimab. This antibody specifically binds to the envelope protein of the retrovirus and blocks its activity in the central nervous system. The study’s authors said future clinical studies in progressive MS patients will now have to demonstrate whether temelimab treatment can also improve clinical symptoms resulting from neurodegeneration.

The findings were published in the journal PNAS.