Reassessing the Role of APOBEC3G in Human Immunodeficiency Virus Type 1 Infection of Quiescent CD4+ T-Cells 英文参考文献.docVIP

ReassessingtheRoleofAPOBEC3GinHuman ImmunodeficiencyVirusType1InfectionofQuiescent CD4+T-Cells MasakazuKamata1,YoshikoNagaoka2,IrvinS.Y.Chen1* 1DepartmentofMicrobiology,ImmunologyandMolecularGenetics,DavidGeffenSchoolofMedicine,UniversityofCaliforniaLosAngeles,LosAngeles,California,United StatesofAmerica,2DepartmentofMolecularandMedicalPharmacology,DavidGeffenSchoolofMedicine,UniversityofCaliforniaLosAngeles,LosAngeles,California, UnitedStatesofAmerica Abstract HIV-1 is restricted for infection of primary quiescent T-cells. After viral entry, reverse transcription is initiated but is not completed.Varioushypotheseshavebeenproposedforthiscellularrestrictionincludinginsufficientnucleotidepoolsand cellular factors, but none have been confirmed as the primary mechanism for restriction. A recent study by Chiu et al. implicatesAPOBEC3G,ananti-retroviralcytidinedeaminase,asthecellularrestrictionfactor.Here,weattemptedtoconfirm thesefindingsusingthesamestrategyasreportedbyChiuetal.ofsiRNAtargetingknock-downofAPOBEC3Gexpression. Incontrasttothepublishedstudy,ourresultsdonotsupportaroleforAPOBEC3GinrestrictionofHIV-1inquiescentCD4+ T-cells. In our study, we tested the same siRNA as reported by Chiu et al. as well as two additional siRNAs targeting APOBEC3G, one of which showed 2-fold greater knock-down of APOBEC3G mRNA. However, none of the three siRNAs testedhadadiscernableeffectonenhancinginfectionbyHIV-1inquiescentCD4+T-cells.Therefore,weconcludethatthe primarymechanismofHIV-1restrictioninquiescentCD4+T-cellsremainstobeelucidated. Citation:KamataM,NagaokaY,ChenISY(2009)ReassessingtheRoleofAPOBEC3GinHumanImmunodeficiencyVirusType1InfectionofQuiescentCD4+T- Cells.PLoSPathog5(3):e1000342.doi:10.1371/journal.ppat.1000342 Editor:ThomasJ.Hope,NorthwesternUniversity,UnitedStatesofAmerica ReceivedDecember4,2008;AcceptedFebruary18,2009;PublishedMarch20,2009 Copyright: ? 2009 Kamata et al. This is an open-access article distributed under the terms of the Creative Commons Attributi