Infectious bursal disease virus VP5 triggers host shutoff in a transcription-dependent manner.

ABSTRACT: Viruses have evolved intricate mechanisms to evade host antiviral responses and exploit cellular resources by manipulating the expression profile of host genes. During infection, viruses encode proteins with shutoff activity to globally inhibit host protein synthesis, which is an effective strategy for immune evasion. In this study, compelling evidence shows that infectious bursal disease virus (IBDV) infection triggers the suppression of host protein synthesis. Furthermore, using both in vitro and in vivo viral infection models, we have identified that IBDV specifically impedes the transcription of host genes via the shutoff activity of viral VP5, simultaneously conferring advantages to IBDV infection in these circumstances. The proposed mechanism suggests that VP5 competiti

SUBMITTER: Niu X 

PROVIDER: S-EPMC10936426 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature