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SARS‐CoV ‐2 multifaceted interaction with the human host. Part II : Innate immunity response, immunopathology, and epigenetics
Author(s) -
Beacon Tasnim H.,
Su RueyChyi,
Lakowski Ted M.,
Delcuve Geneviève P.,
Davie James R.
Publication year - 2020
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.2379
Subject(s) - innate immune system , immune system , cytokine storm , immunology , chemokine , biology , epigenetics , acquired immune system , inflammation , immunity , medicine , disease , gene , covid-19 , genetics , pathology , infectious disease (medical specialty)
The SARS‐CoV‐2 makes its way into the cell via the ACE2 receptor and the proteolytic action of TMPRSS2. In response to the SARS‐CoV‐2 infection, the innate immune response is the first line of defense, triggering multiple signaling pathways to produce interferons, pro‐inflammatory cytokines and chemokines, and initiating the adaptive immune response against the virus. Unsurprisingly, the virus has developed strategies to evade detection, which can result in delayed, excessive activation of the innate immune system. The response elicited by the host depends on multiple factors, including health status, age, and sex. An overactive innate immune response can lead to a cytokine storm, inflammation, and vascular disruption, leading to the vast array of symptoms exhibited by COVID‐19 patients. What is known about the expression and epigenetic regulation of the ACE2 gene and the various players in the host response are explored in this review.