ABSTRACT
To investigate the susceptibility of Chukars to duck avian influenza virus H9N2 and explore their role in interspecies transmission of influenza viruses. Chukars were inoculated with duck avian influenza viruses H9N2. The present study demonstrated that inflammatory lesions and virus antigen were present in the trachea, bronchus, and parabronchus, and the viruses could be isolated from throat swabs and lung tissue homogenate supernatants. At 14 d post virus inoculation, anti-H9 influenza virus antibody in the serum was detected. The results indicated that Chukars are susceptible to duck avian influenza virus and serve as an intermediate host, thereby facilitating viral gene evolution and supporting the need for continued surveillance of epidemiology and evolution of the influenza virus in Chukars.
Subject(s)
Animals , Galliformes , Influenza A Virus, H9N2 Subtype , Virulence , Physiology , Influenza in Birds , Virology , Respiratory System , Pathology , Virology , Virus Replication , PhysiologyABSTRACT
Avian influenza virus subtype H9N2 has been circulating in multiple terrestrial birds and repeatedly infecting mammals, including swines and humans to pose a significant threat to public health. The cross-species infection of human, replication activity and tissue tropism of avian influenza virus H9N2 was evaluated in this study. The results showed that surgically removed human lung tissue samples were infected ex vivo by avian influenza virus subtype H9N2 (Ck/GX/1875/04, Ck/GX/187/05) and seasonal human influenza virus H3N2 (A/ST/602/05). Examination of nucleoprotein expression replication in the infected human lung tissue samples showed that the replication of avian influenza virus H9N2 and seasonal human influenza virus H3N2 were mainly prevalent in alveolar epithelial cells, respiratory bronchiole epithelial cells and bronchial epithelial cells. Double-immunostaining for viral antigens and cellular markers indicated that avian influenza virus subtype H9N2 replicated in type 2 alveolar epithelial cells. These findings suggest that the H9N2 virus may be better adapted to the human host and replicates efficiently in human lung epithelial cells. Moreover, H9N2 avian influenza virus repeatedly infecting human, may favor gene evolution and the potential emergence of pandemic influenza virus.