Abstract
ABSTRACT The H3N2 influenza viruses became widespread in humans during the 1968 H3N2 pandemic and have been a major cause of influenza epidemics ever since. Different lineages of H3N2 influenza viruses are also commonly found in animals. If a different lineage of H3N2 virus jumps to humans, a human influenza pandemic could occur with devastating consequences. Here, we studied the genetics, receptor-binding properties, and replication and transmission in mammals of 15 H3N2 avian influenza viruses detected in live poultry markets in China. We found that the H3N2 avian influenza viruses are complicated reassortants with distinct replication phenotypes in mice. Five viruses replicated efficiently in mice and bound to both human-type and avian-type receptors. These viruses transmitted efficiently to direct-contact guinea pigs, and three of them also transmitted among guinea pigs and ferrets via respiratory droplets. Moreover, ferret antiserum induced by human H3N2 viruses did not react with any of the H3N2 avian influenza viruses. Our study demonstrates that the H3N2 avian influenza viruses pose a clear threat to human health and emphasizes the need for continued surveillance and evaluation of the H3N2 influenza viruses circulating in nature.
Highlights
Influenza A viruses continue to challenge human health
The HA genes of the 15 viruses shared 87.4%– 99.7% identity at the nucleotide level and formed 11 different groups in the phylogenetic tree (95% sequence identity cutoffs were used to categorize each gene group in all of the phylogenetic trees); they were closely related to the HA genes of the H3N2, H3N8, and H3N9 viruses that were previously detected in wild birds from different countries (Figure 1(a))
We extensively characterized 15 H3N2 avian viruses that were isolated from live poultry markets in China, and found that H3N2 viruses circulating in avian species in nature have undergone frequent reassortment and formed complicated genotypes
Summary
Influenza A viruses continue to challenge human health. The viruses are divided into different subtypes on the basis of the antigenicity of their two surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA). The highly pathogenic H5 and H7 viruses often cause severe disease outbreaks in domestic poultry and wild birds. The H7N9 viruses that emerged in China in 2013 were low pathogenic for animals but caused severe disease in humans [1]. These viruses mutated to a highly pathogenic form in 2017 and caused influenza outbreaks in chickens in several provinces in China [2,3]. Active control strategies implemented in poultry have since essentially eliminated human infections with the H7N9 avian influenza viruses [4,5,6]
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