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Innate immunity in COVID-19: Drivers of pathogenesis and potential therapeutic targets
Author(s) -
Vichaya Ruenjaiman,
Nattiya Hirankarn,
Tanapat Palaga
Publication year - 2021
Publication title -
asian pacific journal of allergy and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.405
H-Index - 33
ISSN - 0125-877X
DOI - 10.12932/ap-130121-1037
Subject(s) - innate immune system , covid-19 , immunity , pathogenesis , immunology , virology , medicine , immune system , disease , outbreak , infectious disease (medical specialty)
A novel severe acute respiratory syndrome COVID-19 caused by coronavirus SARS-CoV-2 has been confirmed to infect more than 100 million people globally, with mortality reaching nearly 3 million as of March 2021. The symptoms vary widely, from the absence of any symptoms to death. The severity of COVID-19 relates to hyperinflammatory conditions with acute respiratory distress syndrome (ARDS), which leads to multiple-organ failure and death. Innate immunity plays an important role in the early response to SARS-CoV-2 infection and regulates the pathogenesis and its clinical outcomes. The most severe cases of COVID-19 present with increased innate immune cell infiltration in the lung, and elevated pro-inflammatory cytokines in the blood serum that are associated with disease severity. Here we review the innate immune response to SARS-CoV-2 infection based on the recent reports and discuss the potential roles of innate immune cells and their mediators in pathogenesis that dictate the outcome of the disease. Understanding the roles of innate immune responses at the initial stages of infection may provide early windows into treatment and clues for vaccine development.

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