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Comment
. 2020 Dec 7;217(12):e20201748.
doi: 10.1084/jem.20201748.

An ace model for SARS-CoV-2 infection

Jack Major  1 , Andreas Wack  1
Affiliations
Comment

An ace model for SARS-CoV-2 infection

Jack Major et al. J Exp Med. .

Abstract

Developing effective in vivo models for SARS-CoV-2 infection is crucial for mechanistic studies of COVID-19 disease progression. In this issue of JEM, Israelow et al. (https://doi.org/10.1084/jem.20201241) generate a model that supports SARS-CoV-2 infection in mice, which they use to characterize type I IFN-driven pulmonary inflammation.

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Figures

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Insights from Jack Major and Andreas Wack.
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IFN-independent viral control in hACE2-transduced mice. Viral titers peak on day 2 after SARS-CoV-2 infection in hACE2-expressing wild type mice, triggering IFNAR1-dependent expression of ISGs and pulmonary inflammation characterized by immune cell recruitment and activation. Mice deficient for IFN signaling (either by IRF3 and IRF7 deficiency, or a potential IFN-priming defect in IFNAR1 KO mice), therefore lacking ISG induction, have reduced inflammation, and surprisingly, a comparable viral burden compared to wild type mice. This may occur for a number of reasons, including a possible type I and III IFN–independent mechanism of viral control or efficient viral mechanisms of IFN antagonism. Created with BioRender.com.
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