SARS-CoV-2 Nsp1 regulates translation start site fidelity to promote infection.

ABSTRACT: A better mechanistic understanding of virus-host interactions can help reveal vulnerabilities and identify opportunities for therapeutic interventions. Of particular interest are essential interactions that enable production of viral proteins, as those could target an early step in the virus lifecycle. Here, we use subcellular proteomics, ribosome profiling analyses and reporter assays to detect changes in polysome composition and protein synthesis during SARS-CoV-2 (CoV2) infection. We identify specific translation factors and molecular chaperones whose inhibition impairs infectious particle production without major toxicity to the host. We find that CoV2 non-structural protein Nsp1 selectively enhances virus translation through functional interactions with initiation factor EIF1A. When E

SUBMITTER: Aviner R 

PROVIDER: S-EPMC10350044 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature