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1、JournalofGeneralVirology(2009),90,2686–2694DOI10.1099/vir.0.013599-0InterferonprimingenablescellstopartiallyoverturntheSARScoronavirus-inducedblockininnateimmuneactivation121ThomasKuri,XiaonanZhang,MatthiasHabjan,342LuisMart?′nez-Sobrido,AdolfoGarc?′a-Sastre,ZhenghongYuan1andFriedemannWeb
2、erCorrespondence1AbteilungVirologie,Institutfu¨rMedizinischeMikrobiologieundHygiene,Universita¨tFreiburg,FriedemannWeberD-79008Freiburg,Germanyfriedemann.weber@2ResearchUnit,ShanghaiPublicHealthClinicalCenter,andKeyLaboratoryofMedicalMolecularuniklinik-freiburg.deVirology,FudanUniversity,
3、Shanghai,PRChina3SchoolofMedicineandDentistry,UniversityofRochester,Rochester,NY14642,USA4DepartmentofMicrobiology,DepartmentofMedicine(DivisionofInfectiousDiseases)andGlobalHealthandEmergingPathogensInstitute,MountSinaiSchoolofMedicine,NewYork,NY10029,USASARScoronavirus(SARS-CoV)isknownt
4、oefficientlysuppresstheinductionofantiviraltypeIinterferons(IFN-a/b)innon-lymphaticcellsthroughinhibitionofthetranscriptionfactorIRF-3.Plasmacytoiddendriticcells,incontrast,respondtoinfectionwithproductionofhighlevelsofIFNs.Here,weshowthatpretreatmentofnon-lymphaticcellswithsmallamountsof
5、IFN-a(IFNpriming)partiallyoverturnstheblockinIFNinductionimposedbySARS-CoV.IFNprimingcombinedwithSARS-CoVinfectionsubstantiallyinducedgenesforIFNinduction,IFNsignalling,antiviraleffectorproteins,ubiquitinationandISGylation,antigenpresentationandothercytokinesandchemokines,whereaseachindiv
6、idualtreatmenthadnomajoreffect.Curiously,however,despitethistypicalIFNresponse,neitherIRF-3norIRF-7wastransportedtothenucleusasasignofactivation.Takentogether,ourresultssuggestthat(i)IFN,asitisproducedbyplasmacytoiddendriticcells,couldenabletissuecellstolaunchahostresponsetoSARS-Received2
7、2May2009CoV,(ii)IRF-3andIRF-7maybeactiveatsubdetectablelevels,and(iii)SARS-CoVdoesnotAccepted18July2009activateIRF-7.INTRODUCTIONal.,2004).IFNsaresynthesizedandsecretedbyinfectedcellsandstimulateexpressionofpotentantiviralproteinsSARScoronavirus(SARS-CoV)isthecausat
