Avian influenza viruses are ribonucleic acid viruses of the family Orthomyxoviridae and possess 8 negative-sense RNA segments encoding 11 known proteins [30]. Of these, the two major surface antigens, hemagglutinin (HA) and neuraminidase (NA), form the basis of multiple serologically distinct virus subtypes. With 18 hemagglutinin (H1– H18) and 11 (N1–N11) neuraminidase subtypes, there is considerable antigenic differences among influenza viruses [15, 25]. Currently, 16 HA and 9 NA subtypes combinations exist in harmony with wild waterfowl, the major natural reservoir for all influenza A viruses, cause no overt disease, and emerge to infect domestic poultry and occasionally mammals [3, 15].
Influenza A viruses can be divided into two distinct groups of high or low pathogenicity on the basis of their pathogenicity in chickens. All highly pathogenic avian influenza viruses known to date that mutate from LPAIV have been restricted to subtypes H5 and H7 [1, 23]. Highly pathogenic avian influenza A virus infections caused by H5 and H7 subtypes in humans have been placed on the top priority list among other zoonotic AIVs and have raised concerns that a new influenza pandemic will occur in the future [11, 22]. H7N9 infections caused significant negative impacts on public health, the economy, and national and even global security that had resulted in 1,567 human cases with 615 deaths. Human H7N9 has almost disappeared in 2018 because the effective response including management of LPMs and the vaccination strategy [4, 26]. However, H7N9 AIVs isolated in 2019 were antigenically distinct from the vaccine strain, so that the H7N9 AIV has not been eradicated from poultry in China [34].
The NA gene of human influenza A(H7N9) virus might have originated from influenza A (H2N9, H4N9, H11N9) viruses that circulated in eastern China [17, 27, 28]. Most H11N9 strains usually were found in wild birds. Some studies have described that H11N9 isolated in China can replicate in mammalian cells in vitro [18], and even in mice in vivo without prior adaption [32, 33].Although no H11N9 virus was isolated from human till now, serologic evidence of human past infection with influenza A/H11N9 suggested a potent risk of direct transmission of AIV to humans [7, 16, 31].
Considering that H11N9 viruses might contributed to H7N9 ressortment and have the threat to public health, active surveillance on influenza was required urgently. Recently, H11N9 viruses were detected in China (Feb 2016) [33] and South Korea (2016–2018)[16, 31]. However, the prevalence of them afterward in China was unclear. Thus, this study focused on the surveillance of H11N9 viruses during 2016–2020 to analyze their evolution and epidemic risk. As a result, we isolated one strain of the H11N9 influenza virus in Shanghai in November 2016, and analyzed the genetic origin of it, indicating that it was a local inter-subtype reassortant present in China and might be transmitted to Japan and South Korea, which prompted us to conduct further influenza surveillance in wild birds in the future.