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An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
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A novel host factor for human respiratory syncytial virus
Masfique Mehedi1, Peter L Collins1, Ursula J Buchholz1
1RNA Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Communicative & Integrative Biology
|July 14, 2017
Summary
Human respiratory syncytial virus (RSV) uses actin-related protein 2 (ARP2) to spread between cells. This viral fusion protein and ARP2-mediated actin nucleation promote cell motility and filopodia formation, aiding RSV pathogenesis.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Human respiratory syncytial virus (RSV) is a major cause of severe lower respiratory disease in children.
- Host factors are crucial for viral replication and spread.
Purpose of the Study:
- To investigate the role of actin-related protein 2 (ARP2) in the human respiratory syncytial virus (RSV) replication cycle.
- To elucidate the mechanisms of RSV cell-to-cell spread.
Main Methods:
- Genome-wide siRNA screen to identify host factors.
- Infection of human lung epithelial A549 cells with RSV.
- Analysis of filopodia formation, cell motility, and viral spread.
- Depletion of ARP2 to assess its impact on RSV infection.
Main Results:
- Actin-related protein 2 (ARP2) was identified as a host factor essential for RSV replication.
- RSV infection induced filopodia formation and increased cell motility, partly mediated by the RSV fusion (F) protein.
- ARP2 depletion reduced virus production, filopodia formation, cell motility, and viral spread, but not early entry or gene expression.
- RSV cell-to-cell spread involves ARP2-mediated actin nucleation, filopodia, and cell motility.
Conclusions:
- The RSV fusion (F) protein and ARP2-mediated actin nucleation contribute to novel mechanisms of RSV cell-to-cell spread.
- These mechanisms, involving filopodia formation and enhanced cell motility, may promote RSV pathogenesis.
- Targeting these pathways could offer new therapeutic strategies against RSV.
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