SARS-CoV-2 multifaceted interaction with the human host. PartII: Innate immunity response, immunopathology, and epigenetics

被引:26
|
作者
Beacon, Tasnim H. [1 ]
Su, Ruey-Chyi [2 ]
Lakowski, Ted M. [3 ]
Delcuve, Genevieve P. [1 ]
Davie, James R. [1 ]
机构
[1] Univ Manitoba, Dept Biochem & Med Genet, 745 Bannatyne Ave,Room 333A, Winnipeg, MB, Canada
[2] JC Wilt Infect Dis Res Ctr, Natl HIV & Retrovirol Lab, Winnipeg, MB, Canada
[3] Univ Manitoba, Coll Pharm, Pharmaceut Anal Lab, Winnipeg, MB, Canada
基金
加拿大自然科学与工程研究理事会; 加拿大健康研究院;
关键词
ACE2; COVID-19; epigenetics; innate immune response; SARS-CoV-2; RESPIRATORY SYNDROME-CORONAVIRUS; NF-KAPPA-B; CONVERTING ENZYME 2; RENIN-ANGIOTENSIN SYSTEM; SARS CORONAVIRUS; DENDRITIC CELLS; CYTOKINE STORM; RIG-I; INTERFERON INDUCTION; PATHOGEN RECOGNITION;
D O I
10.1002/iub.2379
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 theACE2gene and the various players in the host response are explored in this review.
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页码:2331 / 2354
页数:24
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