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.

脑心肌炎病毒 (EMCV) 是一种小型、无包膜、单链 RNA 病毒，可感染多种哺乳动物，具有人畜共患病的重要性。已知许多宿主蛋白通过与其结构或非结构蛋白相互作用来调节 EMCV 增殖，但热休克蛋白 90β (HSP90β) 在 EMCV 感染中的调节作用和机制尚未见报道。在这里，我们报道了 HSP90β 的过表达显着促进了体外EMCV 的生长和增殖. 相反，RNAi 或格尔德霉素对 HSP90β 的下调会抑制 EMCV 复制。HSP90β 通过靶向关键接头分子 MAVS、TBK1 和 IRF3（而不是 MDA5）的表达来抑制 RLRs 通路中的 IFN-β 反应。这项研究证明了HSP90β通过抑制EMCV诱导的IFN-β产生在病毒增殖中起积极作用的第一手信息。总的来说，这些结果揭示了对 HSP90β 辅助的 EMCV 感染进展的新见解。