The outbreak of avian influenza A virus subtype H7N9 in humans in China has aroused our attention to low pathogenic avian influenza(LPAI) viruses recently.Although the transmission of avian influenza from birds to humans has proved to be sporadic,the mortality of infected humans is very high.No specific vaccine has been produced to prevent avian influenza which means that we still have a long way to cure and/or eliminate the disease.We review the pathogenicity of H7 and H7N9 subtype viruses,the mechanisms of how H7N9 subtype virus infect humans and its molecular pathogenesis of transformation from low pathogenic avian influenza viruses to highly pathogenic avian influenza viruses,in order to understand the pathogenesis of H7N9 avian influenza viruses.

Objective To explore the role of 4-hydroxynonenal(HNE)in alleviating acute lung injury(ALI)induced by neonatal sepsis by inhibiting the focal death of endothelial cells(ECs).Methods Newborn mice were randomly divided into five groups:(1)Sham operation group(Sham group),(2)sham operation mice receiving HNE treatment group(Sham + HNE group),(3)cecal serosity(CS group),and(4)CS-treated GS-DMD-/-mice group(CS + GSDMD-/-group).The degree of lung injury was evaluated by lung histopathology and lung wet/dry weight ratio.The ECs of mice were isolated and divided into the Ctrl group,LPS + ATP group,LPS + ATP + HNE-L group and LPS + ATP + HNE-H group.Western blot was used to evaluate the expression of HNE and caspase-1 pathway.Results Compared with CS group,the lung tissue scores of CS + HNE group and CS + GSDMD-/-group were significantly decreased(P<0.05),and the ratio of wet to dry weight of lung tissues was significantly decreased(P<0.05).Compared with the CS group,the 72-hour survival rates of mice in the CS + HNE group and CS + GSDMD-/-group were significantly improved(P<0.05).The expressions of GSDMD-N,C-caspase-1,NLRP3,IL-18 and IL-1β in lung ECs of the CS + HNE group and CS + GSDMD-/-group were signifi-cantly lower than those of the CS group(P<005).Compared with the Ctrl cells,LPS + ATP significantly decreased the cell viability(P<0.05)and increased the protein expressions of GSDMD,C-caspase-1,NLRP3,IL-18 and IL-1β(P<0.05),and these effects were also inhibited by HNE.Conclusion HNE can inhibit the focal death of lung ECs cells by inhibiting NLRP3/caspase-1 signal transduction,and improve ALI in septic mice.