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1、ImmunityArticleInterferon-InducibleCholesterol-25-HydroxylaseBroadlyInhibitsViralEntrybyProductionof25-HydroxycholesterolSu-YangLiu,1,7RoghiyhAliyari,1,7KelechiChikere,1GuangmingLi,5MatthewD.Marsden,2,4JenniferK.Smith,6OlivierPernet,1HaitaoGuo,5RebeccaNusbaum,6JeromeA.Zack,1,2,4Alexande
2、rN.Freiberg,6LishanSu,5BenhurLee,1,2,3andGenhongCheng1,*1DepartmentofMicrobiology,Immunology,andMolecularGenetics2UCLAAIDSInstitute3DepartmentofPathologyandLaboratoryMedicine4DepartmentofMedicineUniversityofCalifornia,LosAngeles,LosAngeles,CA90095,USA5LinebergerComprehensiveCancerCenter
3、,SchoolofMedicine,UniversityofNorthCarolinaatChapelHill,ChapelHill,NC27599,USA6DepartmentofPathology,InstituteofHumanInfectionsandImmunity,UniversityofTexas,MedicalBranch,Galveston,TX77555,USA7Theseauthorscontributedequallytothiswork*Correspondence:gcheng@mednet.ucla.eduhttp://dx.doi.or
4、g/10.1016/j.immuni.2012.11.005SUMMARYproteinsmaybesufficienttoinitiateearlylifecycleprocesses,butfullreplication,transcription,andtranslationrequireutili-Interferons(IFN)areessentialantiviralcytokinesthatzationofcellularfactors.Thenewlysynthesizedviralproteinsestablishthecellularantivira
5、lstatethroughupregu-andgenomearecoordinatelyassembledintovirions,whichlationofhundredsofinterferon-stimulatedgenesthenexitthecellbylysisorbudding.(ISGs),mostofwhichhaveuncharacterizedfunc-Whereasvirusesexploithostfactorstosuccessfullyreplicate,tionsandmechanisms.Weidentifiedcholesterol-t
6、heinnateimmunesysteminhibitsviralgrowthbyproductionofinterferons(IFN),whichareessentialantiviralcytokinesthat25-hydroxylase(CH25H)asabroadlyantiviralISG.induceawidearrayofantiviraleffectors.ManyIFN-stimulatedCH25Hconvertscholesteroltoasolubleantiviralgenes(ISGs)workbyinhibitingaspecificv
7、irallifecyclestage.factor,25-hydroxycholesterol(25HC).25HCtreat-Interferon-inducedtransmembraneprotein3(IFITM3)proteinsmentinculturedcellsbroadlyinhibitedgrowthofen-blockviralentry,andISG20,a30-50exonuclease,degradesvelopedvirusesincludingVSV,HSV,HIV,andMHV68single-strandedvira
