An Update on Innate Immune Responses during SARS-CoV-2 Infection.

Yu Zhang,Guangcai Duan,Weiguo Zhang,Wangquan Ji,Yuefei Jin,Shuaiyin Chen

doi:10.3390/v13102060

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a member of the Coronaviridae family, which is responsible for the COVID-19 pandemic followed by unprecedented global societal and economic disruptive impact. The innate immune system is the body’s first line of defense against invading pathogens and is induced by a variety of cellular receptors that sense viral components. However, various strategies are exploited by SARS-CoV-2 to disrupt the antiviral innate immune responses. Innate immune dysfunction is characterized by the weak generation of type I interferons (IFNs) and the hypersecretion of pro-inflammatory cytokines, leading to mortality and organ injury in patients with COVID-19. This review summarizes the existing understanding of the mutual effects between SARS-CoV-2 and the type I IFN (IFN-α/β) responses, emphasizing the relationship between host innate immune signaling and viral proteases with an insight on tackling potential therapeutic targets.

Highlights

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a member of the Coronaviridae family, which is responsible for the COVID-19 pandemic followed by unprecedented global societal and economic disruptive impact
The clinical manifestations of patients included fever, cough, pyrexia, acute respiratory distress, lymphopenia, and so on [2]. This emerging infectious disease was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [3], and the World Health Organization (WHO) subsequently announced the name “Coronavirus
COVID-19 has the characteristics of high infectivity, fast transmission, long incubation period, and high concealment [5], which has made it rapidly spread all over the world [6]

Summary

Introduction

At the end of 2019, a pneumonia outbreak associated with a novel coronavirus (CoV). was reported [1]. Our review mainly focused on the existing understanding of the mutual effects between SARS-CoV-2 and the type I IFN response, emphasizing the relationship between host innate immune signaling and viral proteases with an insight on tackling potential therapeutic targets. The 50 -end ORF1a/b accounts for approximately two-thirds of the genome of SARS-CoV-2 and are translated to the large replicase polyprotein 1a (pp1a) and pp1ab [16]. RNA into the cytoplasm, the genomic RNA uses Hel and RdRp to start replicating and translating into structural proteins to assemble mature virions for release, leading to an immune response to SARS-CoV-2 infection [26] (see Figure 1). 2; ORF1ab: open reading frame 1ab; ER: endoplasmic reticulum; ERGIC: ER-Golgi intermediate intermediate compartment

Innate Immune Responses to SARS-CoV-2 Infection

IFNs signaling pathwa

Conclusions and Perspectives