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Innate immune and inflammatory responses to SARS-CoV-2: implications for COVID-19
Journal article   Open access   Peer reviewed

Innate immune and inflammatory responses to SARS-CoV-2: implications for COVID-19

Shea A Lowery, Alan Sariol and Stanley Perlman
Cell host & microbe, Vol.29(7), pp.1052-1062
07/14/2021
DOI: 10.1016/j.chom.2021.05.004
PMCID: PMC8126603
PMID: 34022154
url
https://doi.org/10.1016/j.chom.2021.05.004View
Published (Version of record) Open Access

Abstract

COVID-19 can result in severe disease characterized by significant immunopathology that is spurred by an exuberant, yet dysregulated, innate immune response with a poor adaptive response. A limited and delayed interferon I (IFN-I) and IFN-III response results in exacerbated proinflammatory cytokine production and in extensive cellular infiltrates in the respiratory tract, resulting in lung pathology. The development of effective therapeutics for patients with severe COVID-19 depends on our understanding the pathological elements of this unbalanced innate immune response. Here, we review the mechanisms by which SARS-CoV-2 both activates and antagonizes the IFN and inflammatory response following infection, how a dysregulated cytokine and cellular response contributes to immune-mediated pathology in COVID-19, and therapeutic strategies that target elements of the innate response.\nLowery et al. review the mechanisms by which SARS-CoV-2 activates and antagonizes the interferon and inflammatory response following infection, how a dysregulated cytokine and cellular response contributes to immune-mediated pathology in COVID-19, and therapeutic strategies that target elements of the innate response.
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