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Interferon deficiency can lead to severe COVID

Understanding what contributes to the development of severe COVID-19 would be of great clinical benefit. Analysis of people in whom this occurred pinpoints a key role for the signalling pathway mediated by type I interferon proteins.
  1. Eric Meffre

    1. Eric Meffre is in the Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.

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  2. Akiko Iwasaki

    1. Akiko Iwasaki is in the Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA, and at the Howard Hughes Medical Institute, Chevy Chase, Maryland.

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Infection with the SARS-CoV-2 coronavirus results in diverse outcomes for COVID-19, with the disease tending to be more severe and lethal for older males1,2. Yet some young people can also have severe COVID-19. What determines susceptibility to this disease? Writing in Science, Zhang et al.3 and Bastard et al.4 shed light on a key factor that affects whether life-threatening COVID-19 develops. The studies implicate deficiencies in interferon proteins, specifically, type I interferons (IFN-I). Such deficiencies might arise, as Zhang and colleagues report, through inherited mutations in genes encoding key antiviral signalling molecules, or, as Bastard and colleagues describe, by the development of antibodies that bind to and ‘neutralize’ IFN-I. Among people who developed severe COVID-19, such neutralizing antibodies were mostly in older males.

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Nature 587, 374-376 (2020)

doi: https://doi.org/10.1038/d41586-020-03070-1

Updates & Corrections

  • Correction 12 November 2020: The protein UNC93B was spelt incorrectly in Figure 1.

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Competing Interests

E.M. is an adviser for and receives funding from AbbVie.

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