Abstract
H9N2 avian influenza virus is one of the most widely circulating viruses in poultry and poses a huge potential threat to human health due to its frequent gene reassortment with other influenza viruses. In this study, we generated a series of H9N2-H7N9 reassortant viruses and examined their pathogenicity in a mouse model. We found that HA or combined HA and NA replacement on the H9N2 background led to no substantial change in the virus-induced pathogenicity, whereas H9N2 virus containing H7N9 internal genes had significantly higher virulence in comparison to the parental H9N2 virus. This increased pathogenicity is associated with enhanced viral replication both in mice and in MDCK cells. We further demonstrated that the viral ribonucleoprotein complex from H7N9 virus possessed higher activity than that from its H9N2 counterpart. Collectively, our data demonstrated that genetic compatibility between H9N2 and H7N9 viruses facilitated the reassortment between H7N9 and H9N2 viruses co-circulated in poultry and that internal gene replacement would convert H9N2 virus into a novel threat to human health.
Highlights
H9N2 avian influenza virus (AIV) is the most widely circulating AIV in poultry populations globally
We selected two viruses identified in China, namely, H9N2 avian strain CK/F98 and H7N9 SH/4664 strain, to study the effect of genetic reassortment with human H7N9 on the replication and pathogenicity of avian H9N2 using a mouse infection model (Figure 1)
In this study, utilizing recombinant virus generated by reverse genetics, we discovered that the capability of an avian H9N2 virus to infect and replicate in mice could be remarkably enhanced by obtaining an internal gene constellation from an H7N9 virus that has been transmitted to human since 2013 and has caused hundreds of human deaths to date
Summary
H9N2 avian influenza virus (AIV) is the most widely circulating AIV in poultry populations globally. In the early 1990s, H9N2 virus became endemic in poultry across most of Asia, the Middle East, and North and West Africa (Guan et al, 1999). An early H9N2 human infection cases in China could be traced back to two cases of child infection reported in Hong Kong in 1998 and 1999, respectively (Guo et al, 1999; Peiris et al, 1999). Subsequent human infections were confirmed in several countries, including Egypt, Pakistan, Bangladesh, and Oman (Ali et al, 2019; Peacock et al, 2019). The reported incidence of H9N2 infection has significantly increased in China, most likely owing to the ongoing screening for zoonotic H7N9 infections (Peacock et al, 2019). Approximately 60 human H9N2 infections have been confirmed in the laboratory, and most of those cases had a history of
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