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Review
. 2023 Jun;1869(5):166671.
doi: 10.1016/j.bbadis.2023.166671. Epub 2023 Feb 27.

Insight into the mechanisms of coronaviruses evading host innate immunity

Tengteng Yao  1 , Chingchoon Foo  2 , Guopei Zheng  3 , Rui Huang  3 , Qian Li  3 , Jianfeng Shen  4 , Zhaoyang Wang  5
Affiliations
Review

Insight into the mechanisms of coronaviruses evading host innate immunity

Tengteng Yao et al. Biochim Biophys Acta Mol Basis Dis. 2023 Jun.

Abstract

The severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) induced coronavirus disease 2019 (COVID-19) has recently caused a pandemic. Patients with COVID-19 presented with a wide spectrum of symptoms for the disease, from entirely asymptomatic disease to full-blown pneumonia and multiorgan failures. More evidence emerged, showing the production of interferons (IFNs) in the severe cases were significantly lower than their milder counterparts, suggesting linkage of COVID-19 to impaired innate immunity. This review presents a brief overview of how coronaviruses evade innate immunity, according to the current studies about SARS-CoV and middle-east respiratory syndrome-coronavirus (MERS-CoV). The coronaviruses manage to block, escape, or dampen the innate immune response by antagonizing double-stranded RNA (dsRNA) sensor, mitochondrial antiviral-signaling protein (MAVS) and stimulator of IFN genes (STING) pathways, epigenetic modification, posttranslational modifications, and host mRNA translation. We provide novel insights into a comprehensive therapy to combat SARS-CoV-2 infection.

Keywords: COVID-19; Coronavirus; Epigenetics; Immune evasion; Innate immunity.

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Conflict of interest statement

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
Schematic diagram of mechanisms by which coronavirus evade or inactivate the host innate immune response. Sequestering of viral RNA in double membrane vesicles (DMVs) prevents dsRNA from being recognized by retinoic acid-inducible gene-I (RIG-I)-like-receptors (RLRs). The the 3′ → 5′ exonuclease (ExoN) in RNA-PAMPs degradation acts as an interferon (IFN) antagonist. Endonuclease, Poly(U) Specific (EndoU) targets dsRNA sensor to cleave polyU sequences. Both protein M and N inhibit the PAMP and MDA5 to recognize the virus. Papain-like protease (PLpro) impedes STING dimerization, IRF3 phosphorylation, and deubiquitinate RIG-I. Protein N and ORF block IFN promotor region. ORF promotes proteolytic degradation of interferon alpha and beta receptor subunit (IFNAR). Non-structural protein 1 (NSP1) promotes host mRNA degradation.
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