Host protein, HSP90β, antagonizes IFN-β signaling pathway and facilitates the proliferation of encephalomyocarditis virus in vitro.

Encephalomyocarditis virus (EMCV) is a small, non-enveloped, single stranded RNA virus which infects a wide variety of mammalian species, and has zoonotic importance. Many host proteins are known to regulate EMCV proliferation by interacting with its structural or nonstructural proteins, but the regulatory role and mechanism of heat shock protein 90β (HSP90β), in EMCV infection has not been reported yet. Here, we report that overexpression of HSP90β significantly promotes the growth and proliferation of EMCV in vitro. On the contrary, down-regulation of HSP90β by RNAi or geldanamycin inhibits EMCV replication. HSP90β suppresses IFN-β responses in the RLRs pathway by targeting the expression of the key adaptor molecules MAVS, TBK1, and IRF3, but not MDA5. This study demonstrates the firsthand information that HSP90β plays a positive role in viral proliferation by inhibiting EMCV induced IFN-β production. Collectively, the results reveal new insights into HSP90β-assisted progression of EMCV infection.