Influenza A virus is subtyped by its two major surface proteins,the hemagglutinin (H1 to H18) that attaches the virus to host sialic acid receptor and the neuraminidase (N1 to N11,N10 lacks enzymatic function) that releases the progeny virus from infected cells by hydrolyzing the sialic acid receptor.Historically,seasonal and pandemic influenza due to human-to-human transmission are caused by subtypes of combinations of H1,H2 and H3 with N1 and N2.Since 1997,outbreaks or sporadic human infections due to avian-to-human transmission of avian influenza A virus subtypes H5N1,H9N2,H7N7,H7N2,H7N3,H10N7 and H6N 1 have been reported.Except for the H5N1 virus that killed nearly 60% of all reported cases,most of these human cases were self-limiting mild acute upper respiratory tract infections and conjunctivitis.However,in 2013,the H7N9 virus emerged in China,which has affected 135 patients with 45 deaths.This number of HTN9 patients is over three times the total number of H5N1 patients in China within the last ten years [1].Phylogenetic analysis of the human and avian virus isolates from epidemiologically-linked live poultry market suggested that patients acquired the H7N9 virus from contacts with live poultry [2].Furthermore,genetic analysis of these viral isolates showed evidence of mammalian adaptation.Two important questions have to be answered urgently.How does this novel virus jump from poultry to human and what drug treatment can be used to treat this disease with such a high mortality of 33%.