Mechanism Behind Retrovirus HERV-W 2

Mechanism Behind Retrovirus HERV-W

Retroviruses are viruses that thousands of years can integrate into their host DNA. If they are able to build in the line cells, they will continue to inherit and become "endogenous". Human retroviruses are therefore termed "HERV" for human endogenous retro viruses.

In February 2019, amsel.de reported that "a positive result for a potential neuroprotector" was already reported by amsel.de in the fact that the remedy for MS called telemimab was effective in inactive cases and could reduce axon loss. Now researchers in Düsseldorf and their colleagues across the Atlantic have been able to prove that HERV-W is associated with multiple sclerosis (previously only suspected) and that Temelimab is right here.

Active substance in Progressive Multiple Sclerosis?

Research team led by prof. Dr. Honey. Patrick Küry (Dusseldorf) recently, along with colleagues from Canada and the US, showed that axons were damaged by HERV-W coatings. Especially for people with progressive multiple sclerosis this may be important.

Scientists have shown that the protein coat (ENV) of pathogenic human endogenous retrovirus type W (pHERV-W) specifically destroys nerve tissue in multiple sclerosis. This causes microglial cells in the central nervous system to destroy myelinated axons. This clarifies the mechanism of damage in multiple sclerosis.

Hans-Peter Hartung, head of the Department of Neurology at the University Hospital in Düsseldorf (UKD), also managed to demonstrate in two studies that antibodies to temelimab can successfully neutralize harmful ENV protein. MRI surveys from research participants showed that nerve tissue was less damaged.

Less neurodegeneration, even in the active phase?

Researchers from Düsseldorf and their colleagues could therefore explain why patients treated with temelimab have less neurodegeneration. Temelimab specifically binds to the ENV protein of the retrovirus and thus blocks its activity in the central nervous system.

Whether this can improve clinical symptoms, future research must show. Also, for which target group the drug is questioned: only patients with progressive MS or possibly with other immunomodulators, also in patients with relapsing-remitting MS. Temelimab will probably take several years.

Sources: Proceedings of the National Academy of Sciences of the United States, 18.06.2019; Announcement of the University Hospital Düsseldorf, 27.06.2019.