Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Mar;60(3):290-299.
doi: 10.1007/s12275-022-1525-1. Epub 2022 Feb 5.

SARS-CoV-2-mediated evasion strategies for antiviral interferon pathways

Soo-Jin Oh  1 , Ok Sarah Shin  2
Affiliations
Review

SARS-CoV-2-mediated evasion strategies for antiviral interferon pathways

Soo-Jin Oh et al. J Microbiol. 2022 Mar.

Abstract

With global expansion of the COVID-19 pandemic and the emergence of new variants, extensive efforts have been made to develop highly effective antiviral drugs and vaccines against SARS-CoV-2. The interactions of coronaviruses with host antiviral interferon pathways ultimately determine successful viral replication and SARS-CoV-2-induced pathogenesis. Innate immune receptors play an essential role in host defense against SARS-CoV-2 via the induction of IFN production and signaling. Here, we summarize the recent advances in innate immune sensing mechanisms of SARS-CoV-2 and various strategies by which SARS-CoV-2 antagonizes antiviral innate immune signaling pathways, with a particular focus on mechanisms utilized by multiple SARS-CoV-2 proteins to evade interferon induction and signaling in host cell. Understanding the underlying immune evasion mechanisms of SARS-CoV-2 is essential for the improvement of vaccines and therapeutic strategies.

Keywords: COVID-19; SARS-CoV-2; immunity; interferon.

PubMed Disclaimer

References

    1. Acharya D, Liu G, Gack MU. Dysregulation of type I interferon responses in COVID-19. Nat. Rev. Immunol. 2020;20:397–398. doi: 10.1038/s41577-020-0346-x. - DOI - PMC - PubMed
    1. Addetia A, Lieberman NAP, Phung Q, Hsiang TY, Xie H, Roychoudhury P, Shrestha L, Loprieno MA, Huang ML, Gale M, Jr., et al. SARS-CoV-2 ORF6 disrupts bidirectional nucleocytoplasmic transport through interactions with Rae1 and Nup98. mBio. 2021;12:e00065–21. doi: 10.1128/mBio.00065-21. - DOI - PMC - PubMed
    1. Banerjee AK, Blanco MR, Bruce EA, Honson DD, Chen LM, Chow A, Bhat P, Ollikainen N, Quinodoz SA, Loney C, et al. SARS-CoV-2 disrupts splicing, translation, and protein trafficking to suppress host defenses. Cell. 2020;183:1325–1339. doi: 10.1016/j.cell.2020.10.004. - DOI - PMC - PubMed
    1. Bastard P, Rosen LB, Zhang Q, Michailidis E, Hoffmann HH, Zhang Y, Dorgham K, Philippot Q, Rosain J, Béziat V, et al. Autoantibodies against type I IFNs in patients with life-threatening COVID-19. Science. 2020;370:eabd4585. doi: 10.1126/science.abd4585. - DOI - PMC - PubMed
    1. Blanco-Melo D, Nilsson-Payant BE, Liu WC, Uhl S, Hoagland D, Møller R, Jordan TX, Oishi K, Panis M, Sachs D, et al. Imbalanced host response to SARS-CoV-2 drives development of COVID-19. Cell. 2020;181:1036–1045. doi: 10.1016/j.cell.2020.04.026. - DOI - PMC - PubMed