Of the few avian influenza viruses that have crossed the species barrier to infect humans, the highly pathogenic influenza A （H5NI） strain has claimed the lives of more than half of the infected patients. With large...Of the few avian influenza viruses that have crossed the species barrier to infect humans, the highly pathogenic influenza A （H5NI） strain has claimed the lives of more than half of the infected patients. With largely unknown mechanism of lung injury by H5N1 infection, acute respiratory distress syndrome （ARDS） is the major cause of death among the victims. Here we present the fact that HSN 1 caused autophagic cell death through suppression of mTOR signaling. Inhibition of autophagy, either by depletion of autophagy gene Beclinl or by autophagy inhibitor 3-methyladenine （3-MA）, significantly reduced H5N1 mediated cell death. We suggest that autophagic cell death may contribute to the development of ARDS in H5N1 influenza patients and inhibition of autophagy could therefore become a novel strategy for the treatment of H5N1 infection.展开更多
基金supported by the National Natural Science Foundation of China(No.30788004)the National Basic Research Program of China(973 Program)(No. 2009CB522106)Ministry of Education of China(111 Project)(No.B08007)
文摘Of the few avian influenza viruses that have crossed the species barrier to infect humans, the highly pathogenic influenza A （H5NI） strain has claimed the lives of more than half of the infected patients. With largely unknown mechanism of lung injury by H5N1 infection, acute respiratory distress syndrome （ARDS） is the major cause of death among the victims. Here we present the fact that HSN 1 caused autophagic cell death through suppression of mTOR signaling. Inhibition of autophagy, either by depletion of autophagy gene Beclinl or by autophagy inhibitor 3-methyladenine （3-MA）, significantly reduced H5N1 mediated cell death. We suggest that autophagic cell death may contribute to the development of ARDS in H5N1 influenza patients and inhibition of autophagy could therefore become a novel strategy for the treatment of H5N1 infection.
