Epidemiology, evolution, and biological characteristics of avian influenza A (H11) viruses from wild birds

TL;DR

This paper studies H11 avian influenza viruses in wild birds, showing they can evolve to bind human cells and cause disease in mice, posing a public health risk.

Contribution

The study reveals new mutations in H11 viruses that enhance human receptor binding and mammalian virulence, highlighting their pandemic potential.

Findings

H11 viruses from wild birds have acquired mutations linked to human receptor binding and increased mammalian virulence.

Seven genotypes of H11 viruses were identified through genomic recombination with other avian influenza subtypes.

Some H11 isolates can infect mice directly and exhibit dual receptor binding specificity.

Abstract

H11 subtype avian influenza viruses (AIVs) have been identified in both wild and domestic birds. H11N9 viruses from wild birds provided the NA gene to human H7N9 virus in 2013 in China, which caused five waves of human infections. During active surveillance in wild birds in China, 17 H11 viruses were isolated between December 2022 and January 2024, including six H11N1, one H11N2, one H11N3, and nine H11N9. The epidemiology of H11 subtype viruses in public databases revealed that they distributed across seven continents, and more than 54.9% of H11 viruses originated from wild Anseriformes. Phylogenetic analysis of the HA genes indicated that H11 viruses were classified into Eurasian and North American lineages, and our isolates belonged to the Eurasian lineage. Bayesian phylogeographic analysis suggested that Bangladesh served as a crucial geographical transmission center for H11 viruses in Eurasian lineage. Reassortment indicated that the H11 isolates in the study underwent complex genomic recombination with various subtype AIVs circulating in wild and domestic birds, including the clade 2.3.4.4b H5N1 highly pathogenic viruses, and formed seven genotypes. Notably, 17 H11 isolates acquired several mutations associated with enhanced human-type receptor binding in HA (S137A) and increased mammalian virulence in PB1 (D3V, D622G), PB1-F2 (N66S), M1 (N30D, I43M, T215A), and NS1 (P42S, I106M). Seven representative viruses exhibited dual receptor binding specificity and could infect mice directly without prior adaptation. These findings highlight the potential public health risks posed by H11 viruses from wild birds and emphasize the necessity of enhancing routine surveillance.

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