Evidence for Direct Involvement of the Capsid Protein in HIV Infection of Nondividing Cells 英文参考文献.docVIP

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Evidence for Direct Involvement of the Capsid Protein in HIV Infection of Nondividing Cells 英文参考文献.doc

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Evidence for Direct Involvement of the Capsid Protein in HIV Infection of Nondividing Cells 英文参考文献

EvidenceforDirectInvolvement oftheCapsidProteininHIVInfection ofNondividingCells Masahiro Yamashita1,Omar Perez2,Thomas J.Hope3,Michael Emerman1* 1DivisionofHumanBiology,FredHutchinsonCancerResearchCenter,Seattle,Washington,UnitedStatesofAmerica, 2DepartmentofMicrobiologyandImmunology, University of Illinois at Chicago, Chicago, Illinois, United States of America, 3 Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University,Chicago,Illinois,UnitedStatesofAmerica HIVandotherlentivirusescanproductivelyinfectnondividingcells,whereasmostotherretroviruses,suchasmurine leukemiavirus,requirecelldivisionforefficientinfection.However,thedeterminantsforthisphenotypehavebeen controversial.Here,weshowthatHIV-1capsid(CA)isinvolvedinfacilitatingHIVinfectionofnondividingcellsbecause aminoacidchangesonCAseverelydisruptthecell-cycleindependenceofHIV.OnemutantintheN-terminaldomainof CAinparticularhaslostthecell-cycleindependenceinallcellstested,includingprimarymacrophages.Thedefectin thismutantappearstobeatastagepastnuclearentry.Wealsofindthatthelossofcell-cycleindependencecanbe cell-typespecific,whichsuggeststhatacellularfactoraffectstheabilityofHIVtoinfectnondividingcells.Ourdata suggestthatCAisdirectlyinvolvedatsomestepinthevirallifecyclethatisimportantforinfectionofnondividing cells. Citation:YamashitaM,PerezO,HopeTJ,EmermanM(2007)EvidencefordirectinvolvementofthecapsidproteininHIVinfectionofnondividingcells.PLoSPathog3(10): e156.doi:10.1371/journal.ppat.0030156 incoming virions [10–17], whereas a large amount of CA remains bound to intracellular complexes of MLV after Introduction OneofthepropertiesthatsetHIV-1andotherlentiviruses apart from most of the other retroviruses is the ability to infect cells independent of the cell cycle [1,2]. This ability allowsHIV-1topropagateinnondividingcellsinvivosuchas resting CD4t T cells [3] and terminally differentiated macrophages[4].Ontheotherhand,otherretroviruses,such as murine leukemia vir