4.3 Review

Viral and cellular translation during SARS-CoV-2 infection

Journal

FEBS OPEN BIO
Volume 12, Issue 9, Pages 1584-1601

Publisher

WILEY
DOI: 10.1002/2211-5463.13413

Keywords

immune response; interferon; NSP1-SL1; ribosome; SARS-CoV-2; translation

Funding

  1. Agence Nationale pour la Recherche [ANR-17-CE12-0025-01, ANR-17-CE11-0024, ANR-20-COVI-0078]
  2. Fondation pour la Recherche Medicale (project CoronaIRES)
  3. Fondation Bettencourt Schueller
  4. University of Strasbourg
  5. Centre National de la Recherche Scientifique
  6. Agence Nationale de la Recherche (ANR) [ANR-17-CE12-0025, ANR-17-CE11-0024, ANR-20-COVI-0078] Funding Source: Agence Nationale de la Recherche (ANR)

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This review summarizes the current knowledge on the molecular mechanisms of SARS-CoV-2 viral and cellular RNA translation. The virus produces non-structural and structural proteins through different transcription processes, with non-structural protein 1 (NSP1) playing a key role in viral and cellular translation, as well as interfering with the host's antiviral responses.
SARS-CoV-2 is a betacoronavirus that emerged in China in December 2019 and which is the causative agent of the Covid-19 pandemic. This enveloped virus contains a large positive-sense single-stranded RNA genome. In this review, we summarize the current knowledge on the molecular mechanisms for the translation of both viral transcripts and cellular messenger RNAs. Non-structural proteins are encoded by the genomic RNA and are produced in the early steps of infection. In contrast, the structural proteins are produced from subgenomic RNAs that are translated in the late phase of the infectious program. Non-structural protein 1 (NSP1) is a key molecule that regulates both viral and cellular translation. In addition, NSP1 interferes with multiple steps of the interferon I pathway and thereby blocks host antiviral responses. Therefore, NSP1 is a drug target of choice for the development of antiviral therapies.

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