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.
Highlights
The 1968 influenza pandemic, caused by the newly emerged H3N2 virus, was associated with 3 million deaths
Our analysis of H3N2 PB1 sequences deposited in the GISAID database between 1968 and 2013 revealed that the 90 amino acids (AA) PB1-F2 is the dominant form of this predicted protein in circulation (80%) (Table 1)
We provide evidence that the PB1 gene and the encoded avian PB1-F2 protein constitute virulence factors that enhance the mammalian cellular responses to infection in what would be an otherwise mildly-inflammatory virus
Summary
The 1968 influenza pandemic, caused by the newly emerged H3N2 virus, was associated with 3 million deaths. Illness caused by the recent 2009 H1N1 pandemic was, for most infected individuals, no worse than a seasonal influenza infection and the resulting death toll was estimated at
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