Interferon non-dependent STING signaling pathways promote resistance to HSV-1 in the body.

Recently, scientists from the University of California, Berkeley and other units in the Department of Molecular and Cell Biology, Russell EVance led a new study that found that although the statin 365 mutation in STING caused mice to lack sting-induced IfN response, it was surprising that these mutant mice were still resistant to herpes simplex virus (Herpes Simplex Virus, HSVV)-1, published recently in the Journal of NatureThe researchers found that mice without STING CTT's resistance to HSV-1 disappeared compared to mice with S365A mutations, suggesting that STING CTT initiated a protective response to HSV-1, which occurred independently of type I IFNInterestingly, the researchers found that STING-induced autophagy was a process that relied on CTT and TBK1 but did not rely on IRF3, a process that was conservative in STING S365A miceOverall, this study suggests that, at least in mice, stinging, which does not rely on interferon, mediates an antiviral response that relies on STING, providing new ideas for revealing the process and mechanism of antiviral responseReferences: Yamashiro, L.H., Wilson, S.C., Morrison, H.Met alInterferon-independent STING signal sing promotes to HSV-1 in vivoNat Commun 11, 3382 (2020)https://doi.org/10.1038/s41467-020-17156-x.