A sustained antiviral host response in respiratory syncytial virus infected human nasal epithelium does not prevent progeny virus production.

Respiratory syncytial virus infection was examined using a human nasal epithelial cell model. Maximum levels of shed-virus were produced at between 3 and 5 days post-infection (dpi), and the infectivity of the shed-virus was stable up to 10 dpi. The highest levels of interferon signalling were recorded at 2dpi, and infection induced a widespread antivirus response in the nasal epithelium, involving both infected cells and non-infected cells. Although these cellular responses were associated with reduced levels of progeny virus production and restricted virus spread, they did not inhibit the infectivity virus that is shed early in infection. In the clinical context these data suggest that although the host cell response in the nasal epithelium may restrict the levels of progeny virus particles produced, the stability of the shed-virus in the nasal mucosa may be an important factor in both disease progression and virus transmission.