Interferon at the crossroads of SARS-CoV-2 infection and COVID-19 disease

被引：26

作者：

Samuel, Charles E. ^{[1
]}

机构：

[1] Univ Calif Santa Barbara, Dept Mol Cellular & Dev Biol, Santa Barbara, CA 93106 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2023年 / 299卷 / 08期

基金：

美国国家卫生研究院;

关键词：

ADENOSINE-DEAMINASE; I INTERFERON; VIRUS-REPLICATION; NUCLEAR IMPORT; MEASLES-VIRUS; RNASE-L; PROTEIN; ADAR1; ANTAGONIZES; ACTIVATION;

D O I：

10.1016/j.jbc.2023.104960

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

A novel coronavirus now known as SARS-CoV-2 emerged in late 2019, possibly following a zoonotic crossover from a coronavirus present in bats. This virus was identified as the pathogen responsible for the severe respiratory disease, coronavirus disease-19 (COVID-19), which as of May 2023, has killed an estimated 6.9 million people globally according to the World Health Organization. The interferon (IFN) response, a cornerstone of antiviral innate immunity, plays a key role in determining the outcome of infection by SARS-CoV-2. This review considers evidence that SARS-CoV-2 infection leads to IFN production; that virus replication is sensitive to IFN antiviral action; molecular mechanisms by which the SARS-CoV-2 virus antagonizes IFN action; and how genetic variability of SARS-CoV-2 and the human host affects the IFN response at the level of IFN production or action or both. Taken together, the current understanding suggests that deficiency of an effective IFN response is an important determinant underlying some cases of critical COVID-19 disease and that IFN lambda and IFN alpha/beta have potential as therapeutics for the treatment of SARS-CoV-2 infection.

引用

页数：15

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