tetano
Editor, Senior Moderator
J Biol Chem
. 2020 Jun 25;jbc.AC120.013788.
doi: 10.1074/jbc.AC120.013788. Online ahead of print.
Inhibition of SARS-CoV-2 by Type I and Type III Interferons
Ulrike Felgenhauer[SUP] 1 [/SUP], Andreas Schoen[SUP] 1 [/SUP], Hans Henrik Gad[SUP] 2 [/SUP], Rune Hartmann[SUP] 2 [/SUP], Andreas R Schaubmar[SUP] 1 [/SUP], Klaus Failing[SUP] 1 [/SUP], Christian Drosten[SUP] 3 [/SUP], Friedemann Weber[SUP] 1 [/SUP]
Affiliations
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 (JAK)/signal transducer and activator of transcription (STAT) 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.
Keywords: COVID-19; Ruxolitinib; SARS-CoV-2; antiviral agent; cytokine action; infection; innate immunity; interferon; interferon-alpha/beta; interferon-lambda; virology; virus.
. 2020 Jun 25;jbc.AC120.013788.
doi: 10.1074/jbc.AC120.013788. Online ahead of print.
Inhibition of SARS-CoV-2 by Type I and Type III Interferons
Ulrike Felgenhauer[SUP] 1 [/SUP], Andreas Schoen[SUP] 1 [/SUP], Hans Henrik Gad[SUP] 2 [/SUP], Rune Hartmann[SUP] 2 [/SUP], Andreas R Schaubmar[SUP] 1 [/SUP], Klaus Failing[SUP] 1 [/SUP], Christian Drosten[SUP] 3 [/SUP], Friedemann Weber[SUP] 1 [/SUP]
Affiliations
- PMID: 32587093
- DOI: 10.1074/jbc.AC120.013788
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 (JAK)/signal transducer and activator of transcription (STAT) 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.
Keywords: COVID-19; Ruxolitinib; SARS-CoV-2; antiviral agent; cytokine action; infection; innate immunity; interferon; interferon-alpha/beta; interferon-lambda; virology; virus.