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Influenza Virus

tetano

Editor, Senior Moderator
Trends Microbiol. 2018 Jun 13. pii: S0966-842X(18)30131-8. doi: 10.1016/j.tim.2018.05.013. [Epub ahead of print]
[h=1]Influenza Virus.[/h] Hutchinson EC[SUP]1[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] This infographic briefly summarises the natural history, replication cycle, and pathogenesis of influenza viruses, the cause of seasonal influenza and of influenza pandemics. Influenza viruses infect many vertebrates, with Influenza A, B and C viruses (IAV, IBV, and ICV) infecting humans. High mutation rates allow the evasion of immunity. IAV from different host species can 'reassort' their segmented genomes, producing pandemic strains that are antigenically novel but otherwise well adapted to humans. The 'Great Influenza' pandemic of 1918 remains the worst outbreak of infectious disease in history. There is concern that highly pathogenic avian influenza viruses of the H5 and H7 subtypes may evolve to cause similar pandemics. In humans, influenza viruses infect the respiratory epithelium. The haemagglutinin (HA) proteins of IAV and IBV, or the haemagglutinin-esterase-fusion (HEF) proteins of ICV, bind sialic acid, causing endocytosis. Unusually among RNA viruses, the viral genome replicates in the nucleus. New viruses assemble at the cell surface and are released by the receptor-cleaving neuraminidase (NA) proteins of IAV and IBV or the ICV HEF protein.


PMID: 29909041 DOI: 10.1016/j.tim.2018.05.013
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