Dear Editor,Since the first recognized case of human infection with avian influenza H5N1 virus in 1997,the worldwide spread and re-emergence of this highly pathogenic influenza virus have led to 694 human infection ca...Dear Editor,Since the first recognized case of human infection with avian influenza H5N1 virus in 1997,the worldwide spread and re-emergence of this highly pathogenic influenza virus have led to 694 human infection cases.Of these cases,402died from 2003 to 2015（http://www.who.int/influenza/humananimalinterface/ENGIP20150106CumulativeNumber H5N1cases.pdf?ua=1）,with a morbidity rate展开更多
Ebola virus(EBOV)causes a highly lethal hemorrhagic fever syndrome in humans and has been associated with mortality rates of up to 91%in Zaire,the most lethal strain.Though the viral envelope glycoprotein(GP)mediates ...Ebola virus(EBOV)causes a highly lethal hemorrhagic fever syndrome in humans and has been associated with mortality rates of up to 91%in Zaire,the most lethal strain.Though the viral envelope glycoprotein(GP)mediates widespread inflammation and cellular damage,these changes have mainly focused on alterations at the protein level,the role of microRNAs(miRNAs)in the molecular pathogenesis underlying this lethal disease is not fully understood.Here,we report that the miRNAs hsa-miR-1246,hsa-miR-320a and hsa-miR-196b-5p were induced in human umbilical vein endothelial cells(HUVECs)following expression of EBOV GP.Among the proteins encoded by predicted targets of these miRNAs,the adhesion-related molecules tissue factor pathway inhibitor(TFPI),dystroglycan1(DAG1)and the caspase 8 and FADD-like apoptosis regulator(CFLAR)were significantly downregulated in EBOV GP-expressing HUVECs.Moreover,inhibition of hsa-miR-1246,hsa-miR-320a and hsa-miR-196b-5p,or overexpression of TFPI,DAG1 and CFLAR rescued the cell viability that was induced by EBOV GP.Our results provide a novel molecular basis for EBOV pathogenesis and may contribute to the development of strategies to protect against future EBOV pandemics.展开更多
基金supported by the Ministry of Science and Technology of China(2015CB553400/6)National Natural Science Foundation of China(81230002 and 81490531)
文摘Dear Editor,Since the first recognized case of human infection with avian influenza H5N1 virus in 1997,the worldwide spread and re-emergence of this highly pathogenic influenza virus have led to 694 human infection cases.Of these cases,402died from 2003 to 2015（http://www.who.int/influenza/humananimalinterface/ENGIP20150106CumulativeNumber H5N1cases.pdf?ua=1）,with a morbidity rate
基金supported by the National Natural Science Foundation of China(81230002,81300057,91019016,31361163004)National Basic Research Program of China(2012CB316503)+3 种基金Ministry of Health(201302017)Ministry of Science and Technology of China(2006AA02Z152)Program of Introducing Talents of Discipline to Universities(B08007)the support of the Science and Technology Commission of Shanghai Municipality(07pj14096)
文摘Ebola virus(EBOV)causes a highly lethal hemorrhagic fever syndrome in humans and has been associated with mortality rates of up to 91%in Zaire,the most lethal strain.Though the viral envelope glycoprotein(GP)mediates widespread inflammation and cellular damage,these changes have mainly focused on alterations at the protein level,the role of microRNAs(miRNAs)in the molecular pathogenesis underlying this lethal disease is not fully understood.Here,we report that the miRNAs hsa-miR-1246,hsa-miR-320a and hsa-miR-196b-5p were induced in human umbilical vein endothelial cells(HUVECs)following expression of EBOV GP.Among the proteins encoded by predicted targets of these miRNAs,the adhesion-related molecules tissue factor pathway inhibitor(TFPI),dystroglycan1(DAG1)and the caspase 8 and FADD-like apoptosis regulator(CFLAR)were significantly downregulated in EBOV GP-expressing HUVECs.Moreover,inhibition of hsa-miR-1246,hsa-miR-320a and hsa-miR-196b-5p,or overexpression of TFPI,DAG1 and CFLAR rescued the cell viability that was induced by EBOV GP.Our results provide a novel molecular basis for EBOV pathogenesis and may contribute to the development of strategies to protect against future EBOV pandemics.
