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Masfique Mehedi, Ph.D.

Masfique Mehedi, Ph.D.

Host Factors for Human Respiratory Synctial Virus Cell-to-Cell Spread


August 23, 2017, 10:30 a.m. to 11:30 a.m.


Masfique Mehedi, Ph.D.

Research Fellow, Laboratory of Infectious Diseases National Institute of Allergy and Infectious Diseases National Institutes of Health Bethesda, Maryland


Fralin Biomedical Research Institute, 3012
2 Riverside Circle, Roanoke, VA 24016

Human respiratory syncytial virus (RSV) is the most common viral cause of serious lower respiratory disease in infants and young children worldwide, with an estimated 3.4 million RSV-associated hospitalizations annually among children younger than 5 years of age. There is currently no licensed RSV vaccine or suitable antiviral drug available. Dr. Mehedi and his team studied host-pathogen interactions to identify possible host or viral targets for therapeutic interventions. In a high-throughput human genome-wide siRNA screening on human lung epithelial A549 cells infected with RSV-GFP, approximately 21,500 genes were screened to identify genes with a role in the RSV replicative cycle. The researchers identified actin-related protein 2 (ARP2) as one of the host factors involved in the RSV life cycle. ARP2 is part of the ARP2/3 complex, which regulates actin polymerization and affects cellular shape, structure, and motility. ARP2 knockdown in A549 cells did not reduce RSV entry or gene expression at early time points after infection; however, virus budding, the release of infectious virions, and syncytia formation were reduced at late time points. This suggested that ARP2 plays a role in viral spread. Staining of A549 cells for filamentous actin, microtubulin, and RSV fusion (F) protein revealed that infection induced the extensive formation of finger-like actin protrusions that were mostly microtubulin-deficient, identifying them as filopodia. Using stimulated emission depletion (STED) microscopy, we found that the filopodia appeared to shuttle RSV particles to nearby uninfected cells. ARP2-knockdown reduced RSV-induced filopodia formation and infected-cell motility. Thus, RSV uses two previously unrecognized ARP2-dependent features to facilitate viral spread, namely filopodia formation and cell motility. This provides a new target for the development of RSV antivirals.

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