Role of ARP2/3 Complex-Driven Actin Polymerization in RSV Infection

被引:13
|
作者
Paluck, Autumn [1 ]
Osan, Jaspreet [1 ,2 ]
Hollingsworth, Lauren [1 ]
Talukdar, Sattya Narayan [1 ]
Saegh, Ali Al [1 ]
Mehedi, Masfique [1 ]
机构
[1] Univ North Dakota, Sch Med & Hlth Sci, Grand Forks, ND 58202 USA
[2] Weill Cornell Med, Dept Radiat Oncol, New York, NY 10065 USA
来源
PATHOGENS | 2022年 / 11卷 / 01期
关键词
cytoskeleton dynamics; filopodia; ARP2; 3; complex; actin polymerization; cell-to-cell spread; RSV; bronchiolitis; therapeutics; RESPIRATORY SYNCYTIAL VIRUS; NF-KAPPA-B; FILOPODIA FORMATION; COXIELLA-BURNETII; CELLULAR ACTIN; PROTEINS ARP2; RHO GTPASES; CYTOSKELETON; DYNAMICS; MECHANISM;
D O I
10.3390/pathogens11010026
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Respiratory syncytial virus (RSV) is the leading viral agent causing bronchiolitis and pneumonia in children under five years old worldwide. The RSV infection cycle starts with macropinocytosis-based entry into the host airway epithelial cell membrane, followed by virus transcription, replication, assembly, budding, and spread. It is not surprising that the host actin cytoskeleton contributes to different stages of the RSV replication cycle. RSV modulates actin-related protein 2/3 (ARP2/3) complex-driven actin polymerization for a robust filopodia induction on the infected lung epithelial A549 cells, which contributes to the virus's budding, and cell-to-cell spread. Thus, a comprehensive understanding of RSV-induced cytoskeletal modulation and its role in lung pathobiology may identify novel intervention strategies. This review will focus on the role of the ARP2/3 complex in RSV's pathogenesis and possible therapeutic targets to the ARP2/3 complex for RSV.
引用
收藏
页数:12
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