Investigating Viral Interference Between Influenza A Virus and Human Respiratory Syncytial Virus in a Ferret Model of Infection. (8th May 2018)

• Record Type: Journal Article
• Authors: Chan, Kok Fei; Carolan, Louise A; Korenkov, Daniil; Druce, Julian; McCaw, James; Reading, Patrick C; Barr, Ian G; Laurie, Karen L
• Is Part Of: Journal of infectious diseases. Volume 218:Number 3(2018)
• Page Start: 406
• Page End: 417
• Publication Date: 2018-05-08
• Subjects: Influenza -- RSV -- viral interference -- ferret; Communicable diseases -- Periodicals; Diseases -- Causes and theories of causation -- Periodicals; Medicine -- Periodicals; Communicable Diseases -- Periodicals; Electronic journals; 616.9
• DOI: 10.1093/infdis/jiy184
• Languages: English
• ISSNs: 0022-1899

Abstract

Abstract : Using ferret models of influenza virus and human respiratory syncytial virus (hRSV), we demonstrate that infection with influenza virus can prevent or limit infection with hRSV, whereas infection with hRSV reduces morbidity attributed to influenza virus infection. Abstract: Epidemiological studies have observed that the seasonal peak incidence of influenza virus infection is sometimes separate from the peak incidence of human respiratory syncytial virus (hRSV) infection, with the peak incidence of hRSV infection delayed. This is proposed to be due to viral interference, whereby infection with one virus prevents or delays infection with a different virus. We investigated viral interference between hRSV and 2009 pandemic influenza A(H1N1) virus (A[H1N1]pdm09) in the ferret model. Infection with A(H1N1)pdm09 prevented subsequent infection with hRSV. Infection with hRSV reduced morbidity attributed to infection with A(H1N1)pdm09 but not infection, even when an increased inoculum dose of hRSV was used. Notably, infection with A(H1N1)pdm09 induced higher levels of proinflammatory cytokines, chemokines, and immune mediators in the ferret than hRSV. Minimal cross-reactive serological responses or interferon γ–expressing cells were induced by either virus ≥14 days after infection. These data indicate that antigen-independent mechanisms may drive viral interference between unrelated respiratory viruses that can limit subsequent infection or disease.