Trends in Immunology
Volume 42, Issue 4, April 2021, Pages 312-322
Journal home page for Trends in Immunology

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

https://doi.org/10.1016/j.it.2021.02.003Get rights and content

Highlights

  • Evidence suggests that defects in responsiveness to type I interferons (IFN-I) s is of prime importance in determining the severity of coronavirus disease 2019 (COVID-19).

  • Genetic polymorphisms that decrease IFN-I production and the development of anti-IFN-I autoantibodies have been associated with more severe cases of COVID-19.

  • IFN-I is important to control virus infection, acting on both innate and adaptive arms of the immune response. Yet, it can also exacerbate inflammatory disease at late stages of respiratory virus infection.

  • Recent findings suggest conspicuous T cell and germinal center dysfunction in severe COVID-19.

  • A predominance of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-specific CD8+ T cells is associated with mild COVID-19.

  • T cells play an important role in regulating the intensity of the proinflammatory response of the innate immune system.

  • The positive effects of IFN-I on the immune response may apply only during the initial stage of the immune response; once respiratory virus infection has been established, it may be too late for safe and effective IFN-I therapy, but prophylactic use of IFN-1 (or IFN-III) might have considerable potential, pending further investigations.

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.

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