摘要:SummaryClinical 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 coronavirusesin vitroandex vivoin 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.Graphical abstractDisplay OmittedHighlights•Fluvastatin inhibits low (HCoV-229E) and high (SARS-CoV-2) pathogenic coronaviruses•SARS-CoV-2 infection does not affect statin-induced cholesterol biosynthesis arrest•Statin treatment does not alter SARS-CoV-2 innate immune responsesin vitro•Fluvastatin downregulates protein translation and viral replication pathwaysDrugs; Virology