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1、JOURNALOFVIROLOGY,Feb.2005,p.20792086Vol.79,No.40022-538X/05/$08.000doi:10.1128/JVI.79.4.20792086.2005Copyright©2005,AmericanSocietyforMicrobiology.AllRightsReserved.InhibitionofBetaInterferonInductionbySevereAcuteRespiratorySyndromeCoronavirusSuggestsaTwo-StepModelforActivationofInterferonRegulato
2、ryFactor31122MartinSpiegel,AndreasPichlmair,LuisMartı´nez-Sobrido,JeromeCros,211AdolfoGarcı´a-Sastre,OttoHaller,andFriedemannWeber*1AbteilungVirologie,Institutfu¨rMedizinischeMikrobiologieundHygiene,Universita¨tFreiburg,Freiburg,Germany,2andDepartmentofMicrobiology,MountSinaiSchoolofMedicine,NewYork
3、,NewYorkReceived7June2004/Accepted20September2004Severeacuterespiratorysyndrome(SARS)iscausedbyanovelcoronavirustermedSARS-CoV.WeandothershavepreviouslyshownthatthereplicationofSARS-CoVcanbesuppressedbyexogenouslyaddedinterferon(IFN),acytokinewhichisnormallysynthesizedbycellsasareactiontovirusinfect
4、ion.Here,wedemonstratethatSARS-CoVescapesIFN-mediatedgrowthinhibitionbypreventingtheinductionofIFN-.InSARS-CoV-infectedcells,noendogenousIFN-transcriptsandnoIFN-promoteractivityweredetected.Nevertheless,thetranscriptionfactorinterferonregulatoryfactor3(IRF-3),whichisessentialforIFN-promoteractiv
5、ity,wastransportedfromthecytoplasmtothenucleusearlyafterinfectionwithSARS-CoV.However,atalatertimepointininfection,IRF-3wasagainlocalizedinthecytoplasm.Bycontrast,IRF-3remainedinthenucleusofcellsinfectedwiththeIFN-inducingcontrolvirusBunyamweradelNSs.OthersignsofIRF-3activationsuchashyperphosphoryla
6、tion,homodimerformation,andrecruitmentofthecoactivatorCREB-bindingprotein(CBP)werefoundlateafterinfectionwiththecontrolvirusbutnotwithSARS-CoV.OurdatasuggestthatnucleartransportofIRF-3isanimmediate-earlyreactiontovirusinfectionandmayprecedeitshyperphosphorylation,homodimerformation,andbindingtoCBP.I
7、nordertoescapeactivationoftheIFNsystem,SARS-CoVappearstoblockastepaftertheearlynucleartransportofIRF-3.Severeacuterespiratorysyndrome(SARS)isalife-threat-Viruseshaveevolvedeffectivestrategiestoevadeth
