期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 295, 期 41, 页码 13958-13964出版社
ELSEVIER
DOI: 10.1074/jbc.AC120.013788
关键词
virology; infection; innate immunity; interferon; virus; antiviral agent; cytokine action; COVID-19; interferon-alpha; beta; interferon-lambda; ruxolitinib; SARS-CoV-2
资金
- Deutsche Forschungsgemeinschaft [SFB 1021, 197785619, We 2616/7-2, DR 772/10-2]
- RAPID (Risk assessment in pre-pandemic respiratory infectious diseases) Consortium of the Bundesministerium fur Bildung und Forschung [01KI1723E, 01KI1723A]
- European Union's Horizon 2020 Research and Innovation Program [101003666]
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.
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