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Published on: June 6, 2025
681
Viral and cellular translation during SARS-CoV-2 infection
Gilbert Eriani1, Franck Martin1
1Architecture et Réactivité de l'ARN, CNRS UPR9002, Institut de Biologie Moléculaire et Cellulaire, Université de Strasbourg, France.
FEBS Open Bio
|April 16, 2022
Summary
The SARS-CoV-2 virus uses Non-structural protein 1 (NSP1) to control viral and host cell translation and block antiviral defenses. Targeting NSP1 offers a promising strategy for developing new COVID-19 antiviral therapies.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) causes the COVID-19 pandemic.
- The virus is an enveloped, positive-sense single-stranded RNA virus.
- Understanding viral and cellular translation is crucial for combating SARS-CoV-2.
Purpose of the Study:
- To review the molecular mechanisms of viral and cellular mRNA translation during SARS-CoV-2 infection.
- To highlight the role of Non-structural protein 1 (NSP1) in regulating translation.
- To explore NSP1 as a potential drug target for antiviral therapies.
Main Methods:
- Literature review of current knowledge on SARS-CoV-2 translation.
- Analysis of the function of viral non-structural and structural proteins.
- Investigation of NSP1's impact on host antiviral responses.
Main Results:
- Viral non-structural proteins are produced early; structural proteins are produced late from subgenomic RNAs.
- NSP1 is a critical regulator of both viral and cellular translation.
- NSP1 inhibits the interferon I pathway, suppressing host antiviral immunity.
Conclusions:
- NSP1 plays a central role in SARS-CoV-2 replication by manipulating host and viral translation.
- NSP1's interference with host antiviral responses makes it a key target for therapeutic intervention.
- Targeting NSP1 presents a viable strategy for developing novel antiviral drugs against SARS-CoV-2.
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