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

• Published in: Virology (New York, N.Y.) N.Y.), 2018-08, Vol.521, p.20-32
• Main Authors: Huong, Tra Nguyen, Yan, Yan, Jumat, Muhammad Raihan, Lui, Jing, Tan, Boon Huan, Wang, De Yun, Sugrue, Richard J.
• Format: Article
• Language: English
• Subjects: Cells, Cultured; disease progression; epithelial cells; Host response; Humans; Interferon signalling; Interferon-beta - immunology; Interferons; Interleukins - immunology; Nasal epithelium; nasal mucosa; Nasal Mucosa - immunology; Nasal Mucosa - virology; Oxidoreductases Acting on CH-CH Group Donors; pathogenicity; Polymerase Chain Reaction; progeny; Proteins - metabolism; Respiratory syncytial virus; Respiratory Syncytial Virus, Human - genetics; Respiratory Syncytial Virus, Human - physiology; Signal Transduction; Viperin; virion; Virus Replication; Virus Shedding; virus transmission; viruses
• ISSN: 0042-6822; 1096-0341
• DOI: 10.1016/j.virol.2018.05.012

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. •In RSV-infected nasal epithelium virus production occurs early in infection.•RSV infection induces sustained β-interferon and IL29 gene expression.•A general antiviral response is subsequently induced in non-infected cells.•The sustained antivirus responses correlate with reduced rates of virus production.•These antiviral responses do not inhibit the infectivity of the progeny virus.