Abstract
The global expansion of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged as one of the greatest public health challenges and imposes a great threat to human health. Innate immunity plays vital roles in eliminating viruses through initiating type I interferons (IFNs)-dependent antiviral responses and inducing inflammation. Therefore, optimal activation of innate immunity and balanced type I IFN responses and inflammation are beneficial for efficient elimination of invading viruses. However, SARS-CoV-2 manipulates the host’s innate immune system by multiple mechanisms, leading to aberrant type I IFN responses and excessive inflammation. In this review, we will emphasize the recent advances in the understanding of the crosstalk between host innate immunity and SARS-CoV-2 to explain the imbalance between inflammation and type I IFN responses caused by viral infection, and explore potential therapeutic targets for COVID-19.
Highlights
The global expansion of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged as one of the greatest public health challenges and imposes a considerable threat to human health
SARS-CoV-2 releases viral RNA and proteins into cells, which are recognized by the host immune system as pathogen associated molecular patterns (PAMPs), initiating the secretion of IFNs and antiviral innate immune responses [25]
Existed studies demonstrated that the administration of resveratrol could inhibit SARS-CoV-2 infection in vitro and ameliorate the pulmonary inflammation and lung injury induced by respiratory viruses in vivo [86, 87]
Summary
The global expansion of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged as one of the greatest public health challenges and imposes a considerable threat to human health. We will emphasize recent advances in understanding the crosstalk between host innate immunity and SARS-CoV-2, and explain the imbalance between inflammation and IFN I responses to explore potential therapeutic targets for COVID-19. To effectively defend against viruses, host cells initiate antiviral innate immune responses by producing a number of IFNs and other proinflammatory cytokines.
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