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Scientists have identified a new mechanism used by the varicella-zoster virus (VZV), which causes chickenpox and shingles, to evade the immune system and potentially affect distant tissues.
The study, conducted by the University of Colorado-Anschutz Medical Campus in the US, focuses on a viral protein called IE62, which is transported throughout the body in small extracellular vesicles (sEVs).
Researchers found that IE62 within these sEVs can travel from the initial infection site, infiltrate cells, and suppress their antiviral responses, facilitating further viral spread. The findings were published in the Journal of Virology.
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Calling it a “clear mechanism”, Dr Christy Niemeyer, Assistant professor of neurology at the varsity stated that it “shuts down the immune response”.
Dr Andrew Bubak, the study’s senior author and assistant professor of neurology at CU School of Medicine, noted that IE62 protein acts much earlier in the infection process than previously known.
Bubak explained that the IE62 gets into the sEVs and then travels “down the neurons that go to your skin, making the cells under the skin vulnerable to the whole infection”.
While a shingles vaccine exists, there are no drugs targeting this specific viral mechanism. Niemeyer highlighted the potential for new therapeutics: “This study is the first to identify a different antiviral target that perhaps we can develop therapeutics for.”
The researchers suggest that this mechanism might explain the frequent co-infections and immunosuppressive events in VZV patients.
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