Journal article

Publication year: 2020

Pages: 13958-13964

Journal: Journal of Biological Chemistry

Volume number: 295

Issue number: 41

eISSN: 1083-351X

Open access status: Green

DOI Link: https://doi.org/10.1074/jbc.AC120.013788

Publisher: Elsevier

Abstract: 

The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-alpha) and type III (IFN-lambda) against SARS-CoV-2 and compared them with those against SARS-CoV-1, which emerged in 2003. Using two mammalian epithelial cell lines (human Calu-3 and simian Vero E6), we found that both IFNs dose-dependently inhibit SARS-CoV-2. In contrast, SARS-CoV-1 was restricted only by IFN-alpha in these cell lines. SARS-CoV-2 generally exhibited a broader IFN sensitivity than SARS-CoV-1. Moreover, ruxolitinib, an inhibitor of IFN-triggered Janus kinase/signal transducer and activator of transcription signaling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells. We conclude that SARS-CoV-2 is sensitive to exogenously added IFNs. This finding suggests that type I and especially the less adverse effect-prone type III IFN are good candidates for the management of COVID-19.

Harvard Citation style: Felgenhauer, U., Schoen, A., Gad, H., Hartmann, R., Schaubmar, A., Failing, K., et al. (2020) Inhibition of SARS-CoV-2 by type I and type III interferons, Journal of Biological Chemistry, 295(41), pp. 13958-13964. https://doi.org/10.1074/jbc.AC120.013788

APA Citation style: Felgenhauer, U., Schoen, A., Gad, H., Hartmann, R., Schaubmar, A., Failing, K., Drosten, C., & Weber, F. (2020). Inhibition of SARS-CoV-2 by type I and type III interferons. Journal of Biological Chemistry. 295(41), 13958-13964. https://doi.org/10.1074/jbc.AC120.013788