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1、JOURNALOFVIROLOGY,June2004,p.56585669Vol.78,No.110022-538X/04/$08.000DOI:10.1128/JVI.78.11.56585669.2004Copyright©2004,AmericanSocietyforMicrobiology.AllRightsReserved.MurineCoronavirusReplicationInducesCellCycleArrestinG0/G1PhaseChun-JenChenandShin
2、jiMakino*DepartmentofMicrobiologyandImmunology,TheUniversityofTexasMedicalBranchatGalveston,Galveston,Texas77555-1019Received6November2003/Accepted2February2004Mousehepatitisvirus(MHV)replicationinactivelygrowingDBTand17Cl-1cellsresultedintheinhibiti
3、onofhostcellularDNAsynthesisandtheaccumulationofinfectedcellsintheG0/G1phaseofthecellcycle.UV-irradiatedMHVfailedtoinhibithostcellularDNAsynthesis.MHVinfectioninquiescent17Cl-1cellsthathadbeensynchronizedintheG0phasebyserumdeprivationpreventedinfecte
4、dcellsfromenteringtheSphaseafterserumstimulation.MHVreplicationinhibitedhyperphosphorylationoftheretinoblastomaprotein(pRb),theeventthatisnecessaryforcellcycleprogressionthroughlateG1andintotheSphase.WhiletheCip1Kip1INK4aamountsofthecellularcyclin-de
5、pendentkinase(Cdk)inhibitorsp21,p27,andp16didnotchangeininfectedcells,MHVinfectioninasynchronousculturesinducedaclearreductionintheamountsofCdk4andG1cyclins(cyclinsD1,D2,D3,andE)inbothDBTand17Cl-1cellsandareductioninCdk6levelsin17Cl-1cells.Infectiona
6、lsoresultedinadecreaseinCdk2activityinbothcelllines.MHVinfectioninquiescent17Cl-1cellspreventednormalincreasesinCdk4,Cdk6,cyclinD1,andcyclinD3levelsafterserumstimulation.TheamountsofcyclinD2andcyclinEwerenotincreasedsignificantlyafterserumstimulationi
7、nmock-infectedcells,whereastheyweredecreasedinMHV-infectedcells,suggestingthepossibilitythatMHVinfectionmayinducecyclinD2andcyclinEdegradation.OurdatasuggestedthatareductionintheamountsofG1cyclin-CdkcomplexesinMHV-infectedcellsledtoareductioninCdkact
8、ivitiesandinsufficienthyperphosphorylationofpRb,resultingininhibitionofthecellcycleintheG0/G1phase.ManyDNAvirusesusurphostcellcycleregulationfortheirCyclinsandcyclin-dependentkinases(Cdks)formcom-ownreplicationadvantage(reviewedinreference56).Smallple
