Journal
BIOMOLECULES & THERAPEUTICS
Volume 29, Issue 3, Pages 273-281Publisher
KOREAN SOC APPLIED PHARMACOLOGY
DOI: 10.4062/biomolther.2020.226
Keywords
Apoptosis; COVID-19; SARS-CoV-2; STAT1; STAT3; STAT3 phosphorylation
Funding
- National Research Foundation [NRF-2016M3A9B6916708, NRF-2020R1A2B5B02001806, NRF-2020M3A9I2107294]
- Ministry of Science and ICT in the Republic of Korea
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The study reveals that different cell lines, Vero and Calu-3, exhibit varying cellular responses to SARS-CoV-2 infection, resulting in different virus production and apoptosis rates. In Calu-3 cells, inhibitors targeting STAT3 phosphorylation and dimerization have a certain effect on reducing virus production. Therefore, evaluating cellular responses to SARS-CoV-2 infection in different cell lines is crucial for studying virus treatments.
Severe acute respiratory syndrome CoV-2 (SARS-CoV-2) is responsible for the current coronavirus disease 2019 (COVID-19) pandemic. Signaling pathways that are essential for virus production have potential as therapeutic targets against COVID-19. In this study, we investigated cellular responses in two cell lines, Vero and Calu-3, upon SARS-CoV-2 infection and evaluated the effects of pathway-specific inhibitors on virus production. SARS-CoV-2 infection induced dephosphorylation of STAT1 and STAT3, high virus production, and apoptosis in Vero cells. However, in Calu-3 cells, SARS-CoV-2 infection induced long-lasting phosphorylation of STAT1 and STAT3, low virus production, and no prominent apoptosis. Inhibitors that target STAT3 phosphorylation and dimerization reduced SARS-CoV-2 production in Calu-3 cells, but not in Vero cells. These results suggest a necessity to evaluate cellular consequences upon SARS-CoV-2 infection using various model cell lines to find out more appropriate cells recapitulating relevant responses to SARS-CoV-2 infection in vitro.
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