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简介：ToobservetheeffectofGardeniaextractZGontheadsorptionquantityofherpessimplexvirustype1(HSV-1)soastoexplorethemechanismofitsantiviralactivity,fluoresceinisothiocyanate(FITC)wasusedasthefluorescentprobetolabelvirusesandheparinsodiumwasusedascontrol.Meanwhile,theeffectofGardeniaextractZGontheadsorptionquantityonthesurfaceofHep-2cellswasdeterminedbyflowcytometry.ItwasdemonstratedthatadsorptionofHSV-1onthesurfaceofHep-2cellsexhibitedthecharacterofsaturationandspecificityandheparinsodiumcouldpreventattachmentofvirusesonthesecells.Theseresultsareinaccordwiththosereportedpreviously.Itwasalsoprovedthatthemannerofdrug-usepriortoadsorptionorsimultaneoususeofdrugandadsorptionwasbetterthanadsorptionpriortodrug-use,andtheinhibitionratesoftheformerandlattermannerwere84.76%and82.92%respectively.Threemannersofdrug-usewithGardeniaextractZGwerealleffectivetoreducetheadsorptionquantityofviruses,especiallythemannerofsimultaneoususeofdrugandadsorptionwithanadsorptioninhibitionrateof68.46%.Fromtheaboveobservation,itisapparentthatthemechanismofanti-viralactivityofGardeniaextractZGmaybeviaseveralstepsinvolvedintheHSV-1adsorption.

简介：WeareracingwithHIV-1,theetiologicagentforAIDSinhumanbeings[1,2],withtwopossibleendconsequences:ifwewin,HIV-1willbeunderourcontrolbyimmunologicortherapeuticmeasures;ifHIV-1wins,theSIVAfricanmonkeys'storywouldrepeatinhumans,i.e.,onlythefewindividualsthatarenotkilledbythevirus

简介：Wehavepreviouslydemonstratedtheabilityofmalariaparasitestointerferewithspecificimmuneresponses.CD4Tcellsspecifictoparasiteantigens,butnotCD4Tcellsspecifictoanirrelevantantigen,ovalbumin(OVA),aredeletedviaapoptosisduringmalariainfection.Itisofinterest,therefore,toinvestigatetheimmuneresponsesthatdevelopedfollowingvaccinationwiththe19kDacarboxylterminusofthemerozoitesurfaceprotein1(MSP119)inmicethathadpreviouslyexperiencedmalariainfection.Inthisstudy,pre-exposureofmicetoPlasmodiumyoeliielicitednativeanti-MSP119antibodyresponses,whichcouldbeboostedbyvaccinationwithrecombinantMSP119，Likewise,infectionofMSP119-primedmicewithPlasmodiumyoelii(P.yoelii)ledtoanincreaseofanti-MSP119antibodies.MSP119vaccinationofmalariapreexposedmiceorimmunizationbyinfection/cureofMSP119-primedmiceenabledthemicetosurvivechallengeinfection,withtheformergrouphavingslightlylowerparasitaemia.Thedatasuggestthatexposuretomalariainfectionprimesanaturalimmuneresponsewhichcanbeboostedbyvaccination.Thisinformationisrelevanttothedevelopmentofavaccineforuseinindividualslivinginmalaria-endemicareas.

简介：ToexplorethemechanismoftheinhibitionofHIV-1byMycoplasmafermerttans,culturesupernatantsandthallodicproteinsfromM.fermerttansPG18werepreparedandtheproteincomponentsofthesupernatantswerepurifiedwithhighperformanceliquidchromatography(HPLC).Theinhibitoryactivitiestoreversetranscriptase(RT)andthenucleaseactivitiesweredetected;theinfluenceofM.fermerttansonIL-10secretionbybothnormalandH1V-1infectedhumanPBMCweredetermined,andtheinhibitoryeffectofrhIL-10onH1V-1replicationwasdetectedwithEI,ISAmethod.Theresultsshowedthatthepurifiedproteinswithamolecularweightof67-100kDaor10-25kDashoweda36%or34%inhibitoryac-tivitytoRTandpartialnucleaseactivity.ThethallodicproteincouldinducebothnormalandH1V-1infectedPBMCtosecretIL-10remarkably,andtothelatter,thiseffectwasmoreapparent.WhilerhIL-10couldinhibitreplicationofH1V-1inPB-MCinvitroinadose-dependantmanner.ItconcludesthattheinhibitoryeffectoftheM.fermentansPG18culturesupernatantsonRTandthepromotingeffectofPG18thallodicproteinonIL-10secretioninPBMCexplainthemechanismsofinhibitiontoHIV-1byM.fermentansPG18.

简介：ToinvestigatethephenotypicknockoutofHIV-1chemokinecoreceptorCXCR4andCCR5byintrakinesanditsinhibitoryeffectonHIV-1infection.PrimaryhumanPBLsweretransducedwiththerecombinantvectorpLNCX-R-K-S-K(△NGFR),followedbyanti-NGFR/anti-IgG-magneticbeadmethodselectionandFCMdetection.ThetransducedPBLswereinfectedwithDP1HIV-1virusthereafterenvelope-mediatedsyncytiumformationandp24detectionwerecarriedouttostudytheblockageofHIV-1infectionbyco-inactivationofCCR5andCXCR4.pLNCX-R-K-S-K(△NGFR)-transducedPBILswereisolatedwithananti-NGFR/anti-IgG-magneticbeadmethod.Afterisolation,about70%ofthePBLswerepositivefortheNGFRmarker.WhenthetransducedPBLswereinfectedwithDP1HIV-1virus,envelop-mediatedsyncytiumformationwasalmostcompletelyinhibitedbypLNCX-R-K-S-K(△NGFR)transfection.Also,p24antigenwasverylowintheculturesofpLNCX-R-K-S-K(△NGFR)transducedPBLs.pLNCX-R-K-S-K(△NGFR)transductioninhibitedtheproductionofDP1p24antigenby15%,43%and19%ondays4,7and10respectively.ThelymphocyteswiththephenotypicknockoutofCCR5andCXCR4couldprotectprimaryhumanPBLsfromDP1HIV-1virusinfection.

简介：TodeterminewhetherthepossessionofcertainHLA-DQA1alleleswasassociatedwiththeriskofdevelopingidiopathicdilatedcardiomyopathy(IDC)andtosubstantiatetheroleofanautoimmunologicpathogenesisinIDC.TypetheallelesofHLA-DQA1bypolymerasechainreactionwithsequence-specificprimers(PCR-SSP)techniquein38patientsofidiopathicdilatedcardiomyopathy(7womenand31men),agedfrom17to56yearsoldwithdiagnosisbeingaccordingtoWorldHealthOrganizationcriteria(IDCgroup),in50patientsofend-stageheartfailureofknownetiology(18womenand32men),withagesrangingfrom34to72(HFgroup),andinthecontrolgroupconsistingofpresumably100healthysubjects(39womenand61men)fromthehealthsurvey,agedfrom30to59yearsold.ThefrequencyofHLA-DQA1*0501intheDCMpatientswassignificantlyelevatedthanthatintheHFandthecontrolgroup.MolecularanalysisoftheDQA1genepolymorphismperformedinthethreesubgroupsshowsanincreasedfrequencyofDQA1*0501amongpatientswithlessEF.TheHFgroupcarriesahighfrequencyofHLA-DQA1*0301.AnincreasedfrequencyofDQA1*0201andDQA1*0103wasfoundinthecontrolgroup.HLA-DQA1*0501isanassociatedgeneofidiopathicdilatedcardiomyopathyandthepossessionofDQA1*0301maybeindicativeoftheknownetiologicheartfailure,suggestingthatthemechanismsinvolvedinthepathogenesisofIDCandotherwiseheartfailurearedifferent.ImmunologicabnormalitiesmaybeamajorcontributortothesusceptibilityofdevelopingofIDC.

简介：TofindouttheprotectivepolypeptideepitopesofHCVHVR1,theantigenieityofthesyntheticpepfidewaspredictedbycomputermodelingandverifiedbyELISAandlymphocytetransformationtest.Itwasfoundthattheoutcomeofthecomputermodelingwasinaccordwiththeexperimentalresults.Themethodbyusingcomputermodelingwouldbeaeconomicapproachbywhichtheprotectivepeptidescouldbeidentifiedquickly.

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简介：Inthepresentstudy,theeffectofblockageofthecostimulatorysignalCD86attimeofimplantationontheexpressionsofTGF-β1,MMP-9,TIMP-3andPAI-1proteinsatthematernal-fetalinterfaceandtheoutcomeofpregnancyinmurineabortion-pronemodelwasinvestigated,inwhichtheCBA/JxDBA/2matingswereusedastheabortion-pronemodelandtheCBA/J×BALB/cmatingsusedasthenormalpregnantmodel.Thestudywasperformedinfollowingthreegroups:2groupsoftheabortion-pronemodel,whichwereexperimentalgroupandcontrolexperimentalgroup,and1groupofnormalpregnantmodel,andeachgrouphad10pregnantCBA/Jmiceexclusively.FemalepregnantCBA/Jmiceintheexperimentalgroupreceivedanintraperitoneal(i.p.)injectionof100μgofantimouseCD86mAbin200μlofPBSatday4.5ofgestation,andtheirrelevant-isotopematchedratIgG2bwasadministratedinthecontrolexperimentalgroupwiththesamedosageandatsametime.Forthenormalpregnantgroup,notreatmentwasgiven.ThepregnantCBA/Jmicewerekilledonday13.5ofgestation.Then,theembryoresorptionratewascalculatedandtheexpressionsofTGF-β1,MMP-9,TIMP3andPAI-1weredetectedbyusingimmunohistochemicalmethods.Itwasdemonstratedthattheembryoresorptionrateintheexperimentalgroupwassignificantlyreducedincomparisonwiththatinthecontrolexperimentalgroup(x2=7.441,P=0.006),buttherewasnosignificantdifferencewiththatinnormalpregnantgroup(x2=0.016,P=0.898).TheexpressionsofTGF-β1andPAI-1intheexperimentalgroupweresignificantlyincreasedincomparisonwiththatinthecontrolexperimentalgroup(P=0.010,P=0.003,respectively),withnosignificantdifferencefromthatinthenormalpregnantgroup(P=0.500).However,theexpressionofMMP-9intheexperimentalgroupwassignificantlyreducedincomparisonwiththatinthecontrolexperimentalgroup(P=0.012)withnosignificantdifferencefromthatinthenormalpregnantgroup(P=0.500).Theexpression

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简介：Inthepastdecade,usesofantisepticsanddisinfectantsinhospitalsandotherhealthcarecentersarerathercommon,butthechancetodevelopresistancetoantisepticsanddisinfectantsisalsoincreased.Acinetobacterbaumanniiisoneoftheopportunisticbacteriainvolvinginthenosocomialinfection.Inthepresentstudy,thecorrelationoftheantisepticresistanceinA.baumanniiandtheantisepticresistancegeneqacEΔ1wasinvestigatedbymeansofdeterminationofMICs.Meanwhile,theMICsofglutaraldehyde,chlorhexidine,benzalkoniumbromide,iodophorandtrichloroisocyanurateto80clinicalisolatesofA.baumanniiweredetectedbytubedilutionassayandtheresistancegenesintI1andqacEΔ1intheseisolateswereamplifiedbyPCRandverifiedbyDNAsequencer.ItwasfoundthattheMIC50forthese5antisepticstestedwere32,8,8,4and1μg/mlrespectively,andthedetectionratesofintI1andqacEΔ1genewere60.0%and77.6%respectively.Inaddition,55%ofthe80isolatessimultaneouslypossessedbothintllandqacEΔ1gene,andthepercentageofantisepticresistanceofA.baumanniicarringbothgenestobenzalkoniumbromidewerehigherthanthatwithoutthesetwogenes,however,therewasnosignificantdifferencebetweenintllandqacEΔ1gene.Theresultinbactericidalefficiencyassayindicatedthatchlorhexidinecouldstillproducerapidandstrongbactericidaleffectatconcentrationof1MICafter10minexposure.TheseresultssuggestthattheantisepticresistanceofA.baumanniitovariousantisepticsiscorrelatedwiththepresenceoftheantisepticresistancegenesqacEΔ1inbacteria,thuswarningthattheincreaseoftheantisepticresistanceshouldnotbeignoredandtherelativehighconcentrationorprolongedapplicationtimeisrequiredtoachieveasufficientbactericidaleffect.

简介：Wereportedanovelmammalianreovirus,designedBYD1,isolatedfromthroatswabsofpatientswithsevereacuterespiratorysyndrome(SARS),in2003.Inthepresentstudy,wefirstlycomparedthegenomeelectrophoreticmigrationpatternsofreovirusBYD1with3prototypereovirusstrainsbypolyacrylamidegelelectrophoresis(PAGE)anddeterminedthecompletenucleotidesequenceoftheS1genesegmentofBYD1bysingleprimeramplificationtechnique.TheelectropherogramofBYD1wasdifferentfromthoseofthe3prototypestrainsandanyotherreovirusisolatesreportedbefore.TheentireS1segmentsequenceofBYD1is1437bplongwithtwomeaningfulopenreadingframes(ORFs).ThelongestORFencodesσ1,thecellattachmentprotein,andthesecondlongestORFsupposedlyencodesσ1s,animportantnonstructuralvirulencefactor.TheterminalsequencesofS1segmentare5'GCUAand3'UCAUC,whichareconsistentwiththoseofothermammalianreoviruses.Thehighesthomologyofdeducedσ1aminoacidsequenceis64%identitywithknownmammalianreoviruses.PhylogeneticanalysisofbothS1nucleotidesequenceandσ1aminoacidsequenceindicatedtheBYD1isolatebelongedtoanewcladeofserotype2group.TheresultsofthisstudyshowedthattheBYD1S1segmentwasmarkedlydifferentfromthoseofisolatesreportedbeforeandBYD1wasanovelhumanreovirusisolate.

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简介：ToconstructanexpressionvectorcontainingtheE1glycoproteingeneofrubellavirusforthestudyontheeffectofmutationoftheE1geneglycoproteinandtheanalysisofphylogeneticdifferencesofsequences,thegeneencodingtheE1envelopeglycoproteinwasamplifiedfromrubellavirus,JinanstrainJR23,byRT-PCRandligatedintoPMD-18Tvector.TheclonesthatcarriedtheE1genewereidentifiedafteramprselectionandanalysisofrestrictionenzymedigestion.AftersequencingthisgenewasanalyzedbyDanstarandWinstarprograms,andthemapofphylogenetictreewasdrawn.ThecloneofE1glycoproteinwasthusconstructed.ItwasfoundthatthesequencedifferencesbetweenJR23strainandtheTCRBstrainfromJapanandthosebetweenJR23strainandThomasstrainofEnglandwererathersmallwithdifferencevaluesof0.9%and1.2%respectively.YetthosebetweenJR23strainandBRD2strainfromBeijingandthosebetweenJR23strainandXG379strainfromHongKongwerecomparativelylargerwithdifferencevaluesof7.6%and7.3%respectively.ThesequenceofJR23strainwithotherstrainswaslessthan3%excepttheNCstrain(3.7%).ItconcludesthattheconstructionofE1glycoproteingeneoffersanapproachtostudytherelationshipbetweenstructuresandfunctionsofE1geneanditsgeneproducts.Inthephylogenetictree,itshowsthattherearesignificantdifferencesinthesequencesofrubellavirusisolatedinChina,andthismightbehelpfultodevelopaneffectivesubunitvaccine.

简介：Theimmuneefficiencyofarecombinantadenovirustype5withtype35fibercontainingHIV-1gaggene(rAd5/F35-mod.gag)wasinvestigatedinBALB/cmice,inwhichtherAd5/F35-mod.gagwasfirstlyidentifiedwithPCR,thentransfectedto293cellsandtheinvitroexpressionlevelofGagproteinwasdeterminedbyWesternblottingandindirectimmuno-fluorescentassay.MicewereimmunizedwithintramuscularinjectionsofrAd5/F35-mod.gag,rAd5-mod.gagorDNAandwereboostedafter3weeks.Totesttheeffectofpre-existinganti-viralimmunityonimmunization,micewerealsoinjectedwithAd5-GFPvectorandthenimmunized4and7weekslaterwithAd5/F35-mod.gagvector.TheP24-specificIgGantibodyinseraofimmunizedmicewasdeterminedbyELISAandthespecificcytotoxicTlymphocyte(CTL)responsewasassayedbyintracellularcytokinestaining.ItwasdemonstratedthattherAd5/F35-mod.gagvectorcouldexpressefficientlytheHIVGagproteinin293cellsinvitroandinducestrongHIV-specificimmuneresponsesinvivo.ThestrongestCTLandserumIgGresponseoccurredwhenmicewereimmunizedtwicewithinjectionofrAd5/F35alone,buttheanti-Ad5antibodyafterprimaryinfectionwithadenoviruscouldinhibitthespecificimmuneresponsesinducedbyrAd5/F35vector.ItisconcludedthatsingleimmunizationwithrecombinantadenovirusrAd5/F35-mod.gagcaninducespecificCTLandserumIgGantibodyresponsesinmice,buttheimmunogenicityofrAd5/F35iscomparablyweakerthanthatofrAd5.

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