Karen L Laurie1,2,3, William Horman2, Louise A Carolan1, Kok Fei Chan1, Daniel Layton4, Andrew Bean4, Dhanasekaran Vijaykrishna5,6, Patrick C Reading1,2, James M McCaw7,8, Ian G Barr1,3. 1. WHO Collaborating Centre for Reference and Research on Influenza, Victorian Infectious Diseases Reference Laboratory, Melbourne, Australia. 2. Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne and Royal Melbourne Hospital, Melbourne, Australia. 3. School of Applied and Biomedical Sciences, Federation University, Churchill, Australia. 4. Australian Animal Health Laboratory, Health and Biosecurity Unit, Commonwealth Scientific and Industrial Research Organisation, Geelong, Australia. 5. Department of Microbiology, School of Biomedical Sciences, Monash University, Clayton, Australia. 6. Infection and Immunity Program, Biomedicine Discovery Institute, Faculty of Medicine, Nursing, and Health Sciences, Monash University, Clayton, Australia. 7. Centre for Epidemiology and Biostatistics, School of Mathematics and Statistics and Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Australia. 8. Modelling and Simulation Unit, Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, Australia.
Abstract
Background: Two influenza B virus lineages, B/Victoria and B/Yamagata, cocirculate in the human population. While the lineages are serologically distinct, cross-reactive responses to both lineages have been detected. Viral interference describes the situation whereby infection with one virus limits infection and replication of a second virus. We investigated the potential for viral interference between the influenza B virus lineages. Methods: Ferrets were infected and then challenged 3, 10, or 28 days later with pairs of influenza B/Victoria and B/Yamagata viruses. Results: Viral interference occurred at challenge intervals of 3 and 10 days and occasionally at 28 days. At the longer interval, shedding of challenge virus was reduced, and this correlated with cross-reactive interferon γ responses from lymph nodes from virus-infected animals. Viruses from both lineages could prevent or significantly limit subsequent infection with a virus from the other lineage. Coinfections were rare, indicating the potential for reassortment between lineages is limited. Conclusions: These data suggest that innate and cross-reactive immunity mediate viral interference and that this may contribute to the dominance of a specific influenza B virus lineage in any given influenza season. Furthermore, infection with one influenza B virus lineage may be beneficial in protecting against subsequent infection with either influenza B virus lineage.
Background: Two influenza B virus lineages, B/Victoria and B/Yamagata, cocirculate in the human population. While the lineages are serologically distinct, cross-reactive responses to both lineages have been detected. Viral interference describes the situation whereby infection with one virus limits infection and replication of a second virus. We investigated the potential for viral interference between the influenza B virus lineages. Methods:Ferrets were infected and then challenged 3, 10, or 28 days later with pairs of influenza B/Victoria and B/Yamagata viruses. Results: Viral interference occurred at challenge intervals of 3 and 10 days and occasionally at 28 days. At the longer interval, shedding of challenge virus was reduced, and this correlated with cross-reactive interferon γ responses from lymph nodes from virus-infected animals. Viruses from both lineages could prevent or significantly limit subsequent infection with a virus from the other lineage. Coinfections were rare, indicating the potential for reassortment between lineages is limited. Conclusions: These data suggest that innate and cross-reactive immunity mediate viral interference and that this may contribute to the dominance of a specific influenza B virus lineage in any given influenza season. Furthermore, infection with one influenza B virus lineage may be beneficial in protecting against subsequent infection with either influenza B virus lineage.
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