tetano
Editor, Senior Moderator
iScience
. 2021 Nov 18;103469.
doi: 10.1016/j.isci.2021.103469. Online ahead of print.
Fluvastatin mitigates SARS-CoV-2 infection in human lung cells
Francisco J Zapatero-Belinchón[SUP] 1 2 3 4 [/SUP], Rebecca Moeller[SUP] 1 4 [/SUP], Lisa Lasswitz[SUP] 1 4 [/SUP], Marco van Ham[SUP] 5 [/SUP], Miriam Becker[SUP] 1 2 3 [/SUP], Graham Brogden[SUP] 1 4 [/SUP], Ebba Rosendal[SUP] 2 6 [/SUP], Wenjie Bi[SUP] 5 [/SUP], Belén Carriquí-Madroñal[SUP] 1 4 [/SUP], Koushikul Islam[SUP] 2 3 [/SUP], Annasara Lenman[SUP] 2 3 [/SUP], Antonia P Gunesch[SUP] 1 7 8 [/SUP], Jared Kirui[SUP] 1 4 [/SUP], Thomas Pietschmann[SUP] 1 8 [/SUP], Anna K Överby[SUP] 2 6 [/SUP], Lothar Jänsch[SUP] 5 [/SUP], Gisa Gerold[SUP] 1 2 3 4 [/SUP]
Affiliations
Abstract
Clinical data of patients suffering from COVID-19 indicates that statin therapy, used to treat hypercholesterolemia, is associated with a better disease outcome. Whether statins directly affect virus replication or influence the clinical outcome through modulation of immune responses is unknown. We therefore investigated the effect of statins on SARS-CoV-2 infection in human lung cells and found that only fluvastatin inhibited low and high pathogenic coronaviruses in vitro and ex vivo in a dose-dependent manner. Quantitative proteomics revealed that fluvastatin and other tested statins modulated the cholesterol synthesis pathway without altering innate antiviral immune responses in infected lung epithelial cells. However, fluvastatin treatment specifically downregulated proteins that modulate protein translation and viral replication. Collectively, these results support the notion that statin therapy poses no additional risk to individuals exposed to SARS-CoV-2 and that fluvastatin has a moderate beneficial effect on SARS-CoV-2 infection of human lung cells.
. 2021 Nov 18;103469.
doi: 10.1016/j.isci.2021.103469. Online ahead of print.
Fluvastatin mitigates SARS-CoV-2 infection in human lung cells
Francisco J Zapatero-Belinchón[SUP] 1 2 3 4 [/SUP], Rebecca Moeller[SUP] 1 4 [/SUP], Lisa Lasswitz[SUP] 1 4 [/SUP], Marco van Ham[SUP] 5 [/SUP], Miriam Becker[SUP] 1 2 3 [/SUP], Graham Brogden[SUP] 1 4 [/SUP], Ebba Rosendal[SUP] 2 6 [/SUP], Wenjie Bi[SUP] 5 [/SUP], Belén Carriquí-Madroñal[SUP] 1 4 [/SUP], Koushikul Islam[SUP] 2 3 [/SUP], Annasara Lenman[SUP] 2 3 [/SUP], Antonia P Gunesch[SUP] 1 7 8 [/SUP], Jared Kirui[SUP] 1 4 [/SUP], Thomas Pietschmann[SUP] 1 8 [/SUP], Anna K Överby[SUP] 2 6 [/SUP], Lothar Jänsch[SUP] 5 [/SUP], Gisa Gerold[SUP] 1 2 3 4 [/SUP]
Affiliations
- PMID: 34812415
- PMCID: PMC8599137
- DOI: 10.1016/j.isci.2021.103469
Abstract
Clinical data of patients suffering from COVID-19 indicates that statin therapy, used to treat hypercholesterolemia, is associated with a better disease outcome. Whether statins directly affect virus replication or influence the clinical outcome through modulation of immune responses is unknown. We therefore investigated the effect of statins on SARS-CoV-2 infection in human lung cells and found that only fluvastatin inhibited low and high pathogenic coronaviruses in vitro and ex vivo in a dose-dependent manner. Quantitative proteomics revealed that fluvastatin and other tested statins modulated the cholesterol synthesis pathway without altering innate antiviral immune responses in infected lung epithelial cells. However, fluvastatin treatment specifically downregulated proteins that modulate protein translation and viral replication. Collectively, these results support the notion that statin therapy poses no additional risk to individuals exposed to SARS-CoV-2 and that fluvastatin has a moderate beneficial effect on SARS-CoV-2 infection of human lung cells.