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Virus Caused Imbalance of Type I IFN Responses and Inflammation in COVID-19.
Zhang, Jintao; Zhao, Chunyuan; Zhao, Wei.
  • Zhang J; Department of Immunology, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, China.
  • Zhao C; State Key Laboratory of Microbial Technology, Shandong University, Jinan, China.
  • Zhao W; Department of Immunology, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, China.
Front Immunol ; 12: 633769, 2021.
Article in English | MEDLINE | ID: covidwho-1207696
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.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Interferon Type I / SARS-CoV-2 / COVID-19 Limits: Humans Language: English Journal: Front Immunol Year: 2021 Document Type: Article Affiliation country: Fimmu.2021.633769

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Interferon Type I / SARS-CoV-2 / COVID-19 Limits: Humans Language: English Journal: Front Immunol Year: 2021 Document Type: Article Affiliation country: Fimmu.2021.633769