tetano
Editor, Senior Moderator
Viruses
. 2021 Oct 14;13(10):2060.
doi: 10.3390/v13102060.
An Update on Innate Immune Responses during SARS-CoV-2 Infection
Yu Zhang[SUP] 1 [/SUP], Shuaiyin Chen[SUP] 1 [/SUP], Yuefei Jin[SUP] 1 [/SUP], Wangquan Ji[SUP] 1 [/SUP], Weiguo Zhang[SUP] 1 2 [/SUP], Guangcai Duan[SUP] 1 [/SUP]
Affiliations
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.
Keywords: SARS-CoV-2; innate immune response; type I interferons.
. 2021 Oct 14;13(10):2060.
doi: 10.3390/v13102060.
An Update on Innate Immune Responses during SARS-CoV-2 Infection
Yu Zhang[SUP] 1 [/SUP], Shuaiyin Chen[SUP] 1 [/SUP], Yuefei Jin[SUP] 1 [/SUP], Wangquan Ji[SUP] 1 [/SUP], Weiguo Zhang[SUP] 1 2 [/SUP], Guangcai Duan[SUP] 1 [/SUP]
Affiliations
- PMID: 34696490
- 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.
Keywords: SARS-CoV-2; innate immune response; type I interferons.