The roles of lipids in SARS-CoV-2 viral replication and the host immune response

被引:45
|
作者
Theken, Katherine N. [1 ,2 ,3 ]
Tang, Soon Yew [1 ,2 ]
Sengupta, Shaon [2 ,4 ]
FitzGerald, Garret A. [1 ,2 ,5 ]
机构
[1] Univ Penn, Dept Syst Pharmacol & Translat Therapeut, Perelman Sch Med, Philadelphia, PA 19104 USA
[2] Univ Penn, Inst Translat Med & Therapeut, Perelman Sch Med, Philadelphia, PA 19104 USA
[3] Univ Penn, Sch Dent Med, Dept Oral Surg & Pharmacol, Philadelphia, PA 19104 USA
[4] Univ Penn, Dept Pediat, Perelman Sch Med, Philadelphia, PA 19104 USA
[5] Univ Penn, Dept Med, Perelman Sch Med, Philadelphia, PA 19104 USA
基金
美国国家卫生研究院;
关键词
  lipidomics; lipid metabolism; cholesterol; eicosanoids; phospholipids; sphingolipids; viral infection; COVID-19; coronavirus; SARS-CoV-2; CELL-CELL FUSION; CYTOKINE STORM; VIRUS ENTRY; INFECTION; RAFTS; ACTIVATION; INHIBITION; PALMITOYLATION; IDENTIFICATION; DYSREGULATION;
D O I
10.1016/j.jlr.2021.100129
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 significant morbidity and mortality associated with severe acute respiratory syndrome coronavirus 2 infection has underscored the need for novel antiviral strategies. Lipids play essential roles in the viral life cycle. The lipid composition of cell membranes can influence viral entry by mediating fusion or affecting receptor conformation. Upon infection, viruses can reprogram cellular metabolism to remodel lipid membranes and fuel the production of new virions. Furthermore, several classes of lipid mediators, including eicosanoids and sphingolipids, can regulate the host immune response to viral infection. Here, we summarize the existing literature on the mechanisms through which these lipid mediators may regulate viral burden in COVID-19. Furthermore, we define the gaps in knowledge and identify the core areas in which lipids offer therapeutic promise for severe acute respiratory syndrome coronavirus 2.
引用
收藏
页数:11
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