Abstract
To better understand the influence of different NA genes on pathogenicity of H9 viruses, three reassortant H9 viruses (rH9N1, H9N2 and rH9N3) were generated and characterized. All three viruses replicated efficiently in eggs and MDCK cells, whereas the rH9N1 and rH9N3 replicated more efficiently than H9N2 in A549 cells. The rH9N3 replicated more efficiently than rH9N1 and H9N2 viruses in mice, however, rH9N3 replicated and shed less efficiently than the H9N2 virus in chickens. Further studies indicate that N3 had higher NA activity and released virus from erythrocytes faster, which may improve the adaptation of H9 influenza virus to mammals.
Highlights
To better understand the influence of different NA genes on pathogenicity of H9 viruses, three reassortant H9 viruses were generated and characterized
To check the virus replication in vitro, monolayers of MDCK cells and A549 cells were cultured in six-well plates and infected with the different viruses propagated in embryonated chicken eggs (ECE) at a multiplicity of infection (MOI) of 0.01
The presented data indicate that the rH9N3 with high NA activity replicated more efficiently in mice and in A549 cells compared with rH9N1 and H9N2, suggesting that NA activity is critical for the adaptation of avian influenza viruses (AIV) in mammalian hosts, which was in agreement with the previous studies [20, 23, 24]
Summary
To better understand the influence of different NA genes on pathogenicity of H9 viruses, three reassortant H9 viruses (rH9N1, H9N2 and rH9N3) were generated and characterized. Since H9N2 virus is widespread in chickens, co-circulation with other subtype influenza viruses may result in novel H9 reassortants with different NA genes. In A549 cells, the reassortant rH9N3 and rH9N1 viruses grew to significantly higher titers than wild-type H9N2 (Figure 1), which suggests that the N1 and N3 genes enhance the replication of H9 viruses in human cells compared to the wild type H9N2.
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