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

Pathogens

Sattya Narayan Talukdar¹  Lauren Hollingsworth¹  Masfique Mehedi¹  Jaspreet Osan¹  Autumn Paluck¹  Ali Al Saegh¹ 

[1] School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58202, USA;

关键词: cytoskeleton dynamics;    filopodia;    ARP2/3 complex;    actin polymerization;    cell-to-cell spread;    RSV;   

DOI  :  10.3390/pathogens11010026

来源: DOAJ

【 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.

【 授权许可】

Unknown