【Objective】 To understand the potentially molecular mechanism about pathogenicity of the avian influenza A H7N9 virus

to provide the scientific foundation for the prevention and treatment of avian influenza A H7N9. 【Methods】 All the gene and protein sequences of avian influenza A H7N9 virus isolated in China in 2013 were downloaded from GISAID. The sequences using for the homologous analysis were downloaded from NCBI. Then the origins and the sites related to the receptor binding property

host specificity

droplet transmissibility

virulence and drug resistance of the avian influenza A H7N9 virus were analyzed by a variety of bioinformatics software. 【Results】 The avian influenza A H7N9 virus epidemic in China in 2013 was evolved from four origins

all genes were of avian origin and none was of human origin. Mutations G186V and Q226L at the receptor binding sites in the HA were found in almost all isolates; Two mutation sites (T160A\Q226L) were identified at the sites associated with droplet transmission;eight virulence enhanced sites were found; mutation S31N was found in the M2 in all isolates; mutation R294K was only found in NA of A/Shanghai/1/2013; All potential glycosylation motifs were relatively conservative. 【Conclusions】 The avian influenza A H7N9 virus was a novel avian influenza virus with four origins. The virus had the molecular basis of binding the human receptor SAa-2

6 Gal on the epithelial cells in the upper respiratory tract

but was not rendered the sufficient conditions to confer droplet transmission between mammals

so was less likely to be transmitted human-to-human. The Low pathogenic property of the virus could be attributed to the weak pathogenicity to avian. The high pathogenicity to human might have a relationship with the property of virulence sites. All isolates showed ion channel inhibitors(amantadine) resistance and individual isolate showed resistance mutations with neuraminidase inhibitors (oseltamivir).