Abstract
Abstract In this study, we identify GBP4 as a virus-induced protein interacting with IRF7, which is the master regulator in virus triggered induction of type I IFNs. Overexpression of GBP4 inhibits virus triggered activation of IRF7 dependent signaling, but has no effect on NF-kB signaling, whereas the knockdown of GBP4 has opposite effects. Consistently, the supernatant from sendai virus (SeV) infected cells in which GBP4 has been silenced inhibits the replication of vesicular stomatitis virus (VSV) more efficiently. Competitive coimmunoprecipitation experiments indicate that GBP4 disrupts the interactions between TRAF6 and IRF7, resulting in the impaired virus induced IRF7 phosphorylation. Collectively, our results suggest that GBP4 is a negative regulator of virus triggered type I interferon production, and it is identified as a novel protein targeting IRF7 and inhibiting its function.
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