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.
【저자키워드】 SARS-CoV-2, innate immune response, type I interferons, 【초록키워드】 coronavirus, Cytokines, Mortality, Antiviral, COVID-19 pandemic, interferons, protease, severe acute respiratory syndrome Coronavirus, type I interferon, innate immune system, Viral, immune responses, type I interferons, Pathogens, pro-inflammatory cytokines, respiratory, IFNs, Signaling, innate immune, Innate, immune dysfunction, Type I IFN, followed by, acute respiratory syndrome, acute respiratory syndrome coronavirus, acute respiratory syndrome coronavirus 2, components, organ injury, Coronaviridae family, invading pathogens, member, potential therapeutic targets, innate immune responses, Defense, cellular receptors, cellular receptor, hypersecretion, IFN-α/β, Host, Effect, responses, responsible, characterized, variety, the Coronaviridae, disrupt, invading pathogen, patients with COVID-19, 【제목키워드】 response, Innate,