简介：TostudythemechanismofinfectionofEpstein-Barrvirus(EBV)ingastriccarcinomacells,theAkataandP3HR-1strainsofEBVwereusedastheteststrainsofviruses,andthesignetringcelllineHSC-39ofgastriccarcinomacellswasusedasthetargetcellsofinfection.Thevirus-infectedcellcloneswereisolatedbylimiteddilutionmethod.ItwasfoundthattheEBV-encodedsmallRNA(EBER)couldbedetectedintheinfectedcells.TheAkataandP3HR-1EBVinfectedparentalcellsandmostofclonesexpressedEBNA1,butnotEBNA2.Latentmembraneprotein(LMP-1)andLMP-2,andtheQpromoter(p),butnottheCp/WpforEBNAgenetranscriptionwasactiveintheinfectedparentalcellsaswellasalltheclones.UninfectedHSC-39cellsdidnotexpressCD21,however,AkatabutnotP3HR-1EBV-infectedclonesex-pressedlowlevelofCD21mRNA.TheseresultsdemonstratethatHSC-39cellsaresusceptibletobothEBVstrainsandEBVinfectsHSC-39cellsthroughtheCD21-independentpathway.ThisstudydefinesasignetringtypeofgastriccarcinomacellslineasauniquetargetcellsforthestudyofEBVinfectionmechanism.

简介：TheproteomicsofthedifferentialproteinexpressionsinhumangliomacelllineU251cellsinfectedwithhumancytomegalovirus(HCMV)wasinvestigatedattheproteinlevelbyusingthesurfaceenhancedlaserdesorption/ionization(SELDI)proteinchipsysteminordertodevelopamethodofstudyforthepathogenesisofHCMVinfection.Inthisstudy,theculturedU251cellswereinfectedwithHC-MVingoodconditionandthesupernatantsoflysatesandtheextracellularfluidsofthecultivatedinfect-edcellswerequantitativelydefinedfortheexpressedproteins.TheproteomicsofthedifferentialproteinexpressionincellsbeforeandafterinfectionwasanalyzedbyWCX2arraysontheproteinchipreader.Itwasdemonstratedthatthecytopathiceffectsofinfectedcellsappearedonthe5thdayafterinfection,however,thedifferentialproteinexpressionwasevidentat6hafterinfectionasrevealedbyRT-PCRandmassspectrometry.Theproteinpeakscapturedfromdifferentbatchesofsamples,fromthesamesampledetectedwithdifferentarraysorforthedifferentlimeswereallequivalent.Withthemolecularweightrangefrom2000Dato3000Da,chipcaptured82peaksfromtheintracellularfluidsand11proteinpeakfromthecellularfluidinwhichcomparedwiththecontrolgroup,theproteinpeakswithmolecularweightof13536.3Da,10046.1Daand17106.2Dawereclosetothoseofβ-amyloidpro-tein,caspase-1precursorandLPS-inducedTNF-αfactorrespectively,whichshowedbriefup-regulation4hafterinfection,andcontinuedtoraise48hlater.Theseresultsinferthattheseproteinsmaybere-latedtotheapoptosisinducedbyHCMVinfection,thussuggestingthattheapeptosisinducedbyHC-MVinfectionmayplayaroleinthepathogenesisofHCMVinfection.