Distinct and Overlapping Roles of Nipah Virus P Gene Products in Modulating the Human Endothelial Cell Antiviral Response 英文参考文献.docVIP

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Distinct and Overlapping Roles of Nipah Virus P Gene Products in Modulating the Human Endothelial Cell Antiviral Response 英文参考文献.doc

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Distinct and Overlapping Roles of Nipah Virus P Gene Products in Modulating the Human Endothelial Cell Antiviral Response 英文参考文献

DistinctandOverlappingRolesofNipahVirusPGene ProductsinModulatingtheHumanEndothelialCell AntiviralResponse MichaelK.Lo1,2*,MarkE.Peeples3,4,WilliamJ.Bellini2,StuartT.Nichol1,PaulA.Rota2, ChristinaF.Spiropoulou1 1Centers for Disease Control Prevention,Viral Special PathogensBranch, Atlanta, Georgia, United States of America, 2Centers for Disease Control and Prevention, Measles,Mumps,Rubella,andHerpesVirusBranch,Atlanta,Georgia,UnitedStatesofAmerica,3TheResearchInstituteattheNationwideChildren’sHospital,Columbus, Ohio,UnitedStatesofAmerica,4TheOhioStateUniversity,DepartmentofPediatrics,Columbus,Ohio,UnitedStatesofAmerica Abstract Nipah virus (NiV) is a highly pathogenic zoonotic paramyxovirus that causes fatal encephalitis in up to 75% of infected humans. Like other paramyxoviruses, NiV employs co-transcriptional mRNA editing during transcription of the phosphoprotein (P) gene to generate additional mRNAs encoding the V and W proteins. The C protein is translated fromthePmRNA,butinanalternativereadingframe.Thereisevidencefrombothinvitroandinvivostudiestoshowthat thePgeneproductsplayaroleinNiVpathogenesis.Wehavedevelopedareversegeneticsystemtodissecttheindividual rolesoftheNiVPgeneproductsinlimitingtheantiviralresponseinprimaryhumanmicrovascularlungendothelialcells, whichrepresentimportanttargetsinhumanNiVinfection.Bycharacterizinggrowthcurvesandearlyantiviralresponses against a number of recombinant NiVs with genetic modifications altering expression of the proteins encoded by the P gene,weobservedthatmultipleelementsencodedbythePgenehavebothdistinctandoverlappingrolesinmodulating virus replication as well as in limiting expression of antiviral mediators such as IFN-b, CXCL10, and CCL5. Our findings corroborateobservationsfrominvivohamsterinfectionstudies,andprovidemolecularinsightsintotheattenuationand thehistopathologyobservedinhamstersinfectedwithC,V,andW-deficientNiVs.Theresultsofthisstudyalsoprovidean opportunitytoverifytheresultsofearlierartificialplasmidex