H7N9 Carries Genes from Rare H9N2, H7N3, H4N9, H11N9 Bird Flu Viruses

According to recent studies of H7N9 collected from live poultry markets, these viruses are reassortants in which the six internal genes were derived from avian H9N2 viruses. However, the origins of their hemagglutinin (HA) and neuraminidase (NA) genes have been unclear.

The team collected 970 samples (drinking water, feces, contaminated soil, and cloacal and tracheal swabs) from live poultry markets and poultry farms located in China. 20 samples were positive for the presence of H7N9 influenza viruses. All of the positive samples originated from live poultry markets in Shanghai. Ten of them were isolated from chickens, three from pigeons, and seven were from environmental samples.

The scientists sequenced the complete genome of three H7N9 isolates – from a chicken, pigeon, and environmental sample. Genetic analysis of these isolates revealed high homology across all eight gene segments. Phylogenetic analysis of these novel H7N9 influenza virus isolates showed that that the six internal genes were derived from avian H9N2 viruses.

According to the GenBank database, the HA genes of the novel isolated viruses were most similar to those from duck H7N3 influenza viruses, sharing 95.2-95.8 per cent homology at the nucleotide level. The NA gene of the virus isolates shared highest homology (97.3-97.9 per cent) with NA genes from H4N9, H11N9 influenza viruses isolated from ducks, and environmental samples from duck farms.

“It is clear that the novel H7N9 viruses are the product of gene reassortment, with the internal genes from one donor, and HA and NA genes from one or several other donors.”

HA receptor-binding specificity is a major molecular determinant for the host range of influenza viruses. Amino acids at positions 226 and 228 of HA are critical for specificity of receptor-binding in influenza viruses. Within the HA protein of novel H7N9 viruses, there was a leucine residue at position 226, which is characteristic of the HA gene in human influenza viruses.

“This finding implies that H7N9 viruses have partially acquired human receptor-binding specificity. All of the H7N9 human isolates examined contained a lysine residue at position 627 in the PB2 protein. It is well known that this lysine residue contributes to the replication and transmission of avian influenza viruses in mammalian hosts. It is likely that the acquisition of this lysine in H7N9 viruses during their replication in human hosts has significantly contributed to their virulence and lethality in humans.”
Read more: http://link.springer.com/article/10.1007/s11434-013-5873-4