Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation

Cecile King; Jonathan Sprent

doi:10.1016/j.it.2021.02.003

Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation

Trends Immunol. 2021 Apr;42(4):312-322. doi: 10.1016/j.it.2021.02.003. Epub 2021 Feb 12.

Authors

Cecile King¹, Jonathan Sprent²

Affiliations

¹ Department of Immunology, The Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010, Australia; St Vincent's Clinical School, Department of Medicine, UNSW, Sydney, NSW 2010, Australia. Electronic address: c.king@garvan.org.au.
² Department of Immunology, The Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010, Australia; St Vincent's Clinical School, Department of Medicine, UNSW, Sydney, NSW 2010, Australia.

Abstract

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The ability of our cells to secrete type I interferons (IFN-Is) is essential for the control of virus replication and for effective antiviral immune responses; for this reason, viruses have evolved the means to antagonize IFN-I. Inhibition of IFN-I production is pronounced in SARS-CoV-2 infection, which can impair the adaptive immune response and exacerbate inflammatory disease at late stages of infection. However, therapeutic boosting of IFN-I offers a narrow time window for efficacy and safety. Here, we discuss how limits placed on IFN-I by SARS-CoV-2 shape the immune response and whether this might be countered with therapeutic approaches and vaccine design.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

COVID-19 / complications
COVID-19 / immunology*
Humans
Inflammation / immunology*
Inflammation / virology
Interferon Type I / immunology*
Virus Replication

Substances

Interferon Type I