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SARS-CoV-2 hijacks p38β/MAPK11 to promote virus replication
Christina A Higgins1,2,3,4, Benjamin E Nilsson-Payant1, Boris Bonaventure1,2
1Department of Microbiology, Icahn School of Medicine at Mount Sinai , New York, New York, USA.
Mbio
|June 22, 2023
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijacks the p38 mitogen-activated protein kinase (MAPK) pathway, specifically p38β, for replication. Inhibiting p38β may offer new COVID-19 therapeutic strategies.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, characterized by inflammatory cytokine production.
- The host p38 mitogen-activated protein kinase (MAPK) pathway is activated during SARS-CoV-2 infection and linked to severe disease.
- Previous work showed p38/MAPK inhibition reduces cytokine production and viral replication.
Purpose of the Study:
- To elucidate the mechanisms by which SARS-CoV-2 depends on the p38 pathway.
- To identify specific p38 isoforms and substrates critical for viral replication.
- To explore p38 pathway modulation as a therapeutic strategy for COVID-19.
Main Methods:
- Quantitative genetic screening
- Genomics
- Proteomics
- Phosphoproteomics
- Systems biology approaches
Main Results:
- p38β was identified as a critical host factor for SARS-CoV-2 replication post-viral mRNA expression.
- Putative host and viral p38β substrates were identified during infection.
- Many identified host substrates possess intrinsic antiviral activities.
Conclusions:
- SARS-CoV-2 utilizes a proviral function of p38β for replication.
- Targeting p38β presents a potential therapeutic avenue for developing new COVID-19 treatments.
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