A leading cause of respiratory diseases, respiratory syncytial virus (RSV) is often responsible for cases of pneumonia and bronchitis in children. Recent research suggests that this virus manipulates host cells to increase its spread within a patient. The virus’ F-protein acts to increase the movement of infected cells and promote the growth of filopodia, thin cellular protrusions which contact neighbouring cells, allowing the virus to move between them. Pictured, virus particles (in green) travel along filopodia (visible in red) from an infected cell, on the left, to the surface of another. This process also depends on a host protein, ARP2, which associates with actin, a key component of the cytoskeleton, determining the shape and growth of cellular extensions. Eliminating ARP2 reduces the movement of infected cells, the development of filopodia and the spread of RSV, making the interaction between RSV and ARP2 a potential target for future treatments.
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