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Virol J. 2017 Aug 22;14(1):162. doi: 10.1186/s12985-017-0827-0.

Rapid evolution of the PB1-F2 virulence protein expressed by human seasonal H3N2 influenza viruses reduces inflammatory responses to infection.

Author information

1
Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, 792 Elizabeth St, Melbourne, VIC, 3000, Australia. jmcauley@unimelb.edu.au.
2
WHO Collaborating Centre for Reference and Research on Influenza (WHO-CCRRI) at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia.
3
Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, 792 Elizabeth St, Melbourne, VIC, 3000, Australia.

Abstract

Influenza A virus (IAV) PB1-F2 protein has been linked to viral virulence. Strains of the H3N2 subtype historically express full-length PB1-F2 proteins but during the 2010-2011 influenza seasons, nearly half of the circulating H3N2 IAVs encoded truncated PB1-F2 protein. Using a panel of reverse engineered H3N2 IAVs differing only in the origin of the PB1 gene segment, we found that only the virus encoding the avian-derived 1968 PB1 gene matching the human pandemic strain enhanced cellular infiltrate into the alveolar spaces of infected mice. We linked this phenomenon to expression of full-length PB1-F2 protein encompassing critical "inflammatory" residues.

KEYWORDS:

Inflammation; Influenza A virus; PB1-F2; Pandemic; Pathogenicity; Respiratory disease; Seasonal; Virulence

PMID:
28830486
PMCID:
PMC5568198
DOI:
10.1186/s12985-017-0827-0
[Indexed for MEDLINE]
Free PMC Article

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