The discovery has important implications for the treatment of herpes simplex virus, as well as many other viruses that replicate in the cell nucleus, such as HIV and hepatitis. Scientists can now develop more effective drugs because they better understand the mechanism of the virus’s attack on cells and the immune system’s work against the pathogen.
After entering the body, the herpes simplex virus (HSV) causes an infection that can be periodically activated, but most of the time remains in a latent state. According to WHO estimates, about 67% of people under the age of 50 are infected with HSV. In a new study reported by Science Daily, scientists sought to understand the reasons why herpes provokes severe infections in some people, while in others it regularly triggers the reactivation of the virus.
It turned out that the battle of HSV at the cellular level affects the signaling proteins interferons, which use other molecules to protect against the virus. Interferon distress signals activate genes in cells to produce protective proteins, the authors explain.
For example, to combat HSV, the protein IFI16 is used, which creates a kind of shell around the viral DNA genome, thus blocking the spread of the virus. HSV, for its part, produces molecules called VP16 and ICP0, which can remove the protective membrane, but IFI16 is able to neutralize them.
It is noteworthy that at the “background” level of IFI16, the protein is not enough to fight the virus, but when interferon signals attract more IFI16, the immune system wins. Interestingly, previous studies have shown an association of elevated IFI16 levels with better control of type 2 HBV.
So far, the researchers are only at the beginning of their journey. They expect to be able to apply their findings not only to herpes, but also to other viruses that replicate in the cell nucleus, such as human papillomavirus, hepatitis, smallpox, and others.
