Childhood herpes simplex encephalitis (HSE) is a rare but serious complication of HSV-1. Genetic deficiencies in an anti-viral pathway, TLR3-IFN mean that patients are unable to produce anti-viral factors. However, these cases only account for around 10 % of encephalitis cases. The HSEPID project has looked at other genes responsible for protection in such HSE patients. Furthermore, the scientists explored another anti-viral strategy, autophagy, normally reserved for clearing old cell components. Researchers identified a new gene in an HSE patient previously not known to be involved in the HSE-causing TLR3 pathway. Knock-down of the gene in control cells caused impaired production of protective antiviral interferons following stimulation of the TLR3 pathway. Autophagy is also linked with elimination of materials after viral infections. The scientists proposed that the process prevents brain damage caused by HSV-1 infection. Using skin cells, they studied autophagy after viral infections and they intend to culture the skin cells into brain cells to study viral infection impact non-invasively. Not only will the research aid understanding of herpes infection per se, new targeted therapies for HSV-1 and brain or nerve damage caused by the virus could follow. The research will continue on this high impact project as a result of continued funding.
Cold sore, virus, HSV-1, HSE, encephalitis, autophagy, interferons, therapies