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

Autumn Paluck1, Jaspreet Osan1,2, Lauren Hollingsworth1

  • 1School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58202, USA.

Pathogens (Basel, Switzerland)
|January 21, 2022
PubMed

Insights

Respiratory syncytial virus (RSV) utilizes the host actin cytoskeleton, specifically the ARP2/3 complex, to facilitate its replication and spread in lung cells. Targeting this complex may offer new therapeutic strategies against RSV infection.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Respiratory syncytial virus (RSV) is a major cause of severe respiratory infections in young children globally.
  • The RSV infection cycle involves host cell machinery, including the actin cytoskeleton, for entry, replication, and spread.

Purpose of the Study:

  • To review the critical role of the actin-related protein 2/3 (ARP2/3) complex in RSV pathogenesis.
  • To explore potential therapeutic targets within the ARP2/3 complex for combating RSV.

Main Methods:

  • This review synthesizes existing research on RSV's interaction with the host cytoskeleton.
  • Focuses on the mechanisms of ARP2/3 complex involvement in RSV replication and cell-to-cell transmission.

Main Results:

  • RSV infection hijacks the ARP2/3 complex to drive actin polymerization and filopodia formation in infected lung epithelial cells.
  • This cytoskeletal modulation is essential for efficient viral budding and intercellular spread of RSV.

Conclusions:

  • The ARP2/3 complex is a key player in RSV pathogenesis, influencing viral spread and disease development.
  • Targeting the ARP2/3 complex presents a promising avenue for developing novel antiviral therapies against RSV.
Keywords:
ARP2/3 complexRSVactin polymerizationbronchiolitiscell-to-cell spreadcytoskeleton dynamicsfilopodiatherapeutics

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