简介：ThisarticleisageneralreviewoftheevolvementofHIV/AIDS-relatedpublicpoliciesinChinasince1980's.Ittrackstheimportantlaws,regulationsandothergovernmentaldocumentsinregardtoHIV/AIDSpreventionmainlyatcentrallevel.

简介：FewerthanonemillionHIVinfectedindividualsarecurrentlyreceivinganti-retroviraltherapy.ThelimitationsofsuchtreatmenthaveunderscoredtheneedtodevelopmoreeffectivestrategiestocontrolthespreadandpathogenesisofHIV.Typically,naturallyoccurringprotectiveimmuneresponsesprovidetheparadigmforsuchdevelopment.ItisnowclearhoweverthatHIVcanutilisethemillieuofanactivatedimmunesystemtoitsownreplicativeadvantage.Mobilisationoftheimmuneresponse,intendedtothwartofHIVcontributestolackofimmunecontrolandthedevelopmentofprogressivediseaseinthemajorityofinfected,untreatedindividuals.FurtherdelineationoftheintimateinteractionsbetweentheHIVandtheimmunesystemwillbecriticalandrecentadvancesinthisdirectionarediscussed.

简介：SmallinterferingRNA(siRNA)andmicroRNA(miRNA)aresmallRNAsof18-25nucleotides(nt)inlengththatplayimportantrolesinregulatinggeneexpression.TheyareincorporatedintoanRNA-inducedsilencingcomplex(RISC)andserveasguidesforsilencingtheircorrespondingtargetmRNAsbasedoncomplementarybase-pairing.ThepromiseofgenesilencinghasledmanyresearcherstoconsidersiRNAasananti-viraltool.However,inlong-termsettings,manyvirusesappeartoescapefromthistherapeuticalstrategy.Anexampleofthismaybeseeninthecaseofhumanimmunodeficiencyvirustype-1(HIV-1)whichisabletoevadeRNAsilencingbyeithermutatingthesiRNAtargetedsequenceorbyencodingforapartialsuppressorofRNAi(RNAinterference).Ontheotherhand,becausemiRNAtargetingdoesnotrequireabsolutecomplementarityofbase-pairing,mutationalescapebyvirusesfrommiRNAspecifiedsilencingmaybemoredifficulttoachieve.Inthisreview,wediscussstratagemsusedbyvariousvirusestoavoidthecells'antiviralsi/mi-RNAdefensesandnotionsofhowvirusesmightcontrolandregulatehostcellgenesbyencodingviralmiRNAs(vmiRNAs).

简介：Comparedwithhighinfectionareasoftheworld,thetotalHIVinfectionrateinChinaisrelativelylow.Nonetheless,becauseofChina'svastterritoryandlargepopulation,thepotentialinfectionriskmustbetakenseriously.Inthenextfewyears,needlesharingamonginjectiondruguserswillremainthemostcommonrouteoftransmissionfortheHIV/AIDSepidemicinChina.Unprotectedsexisgraduallybecomingamajorrouteoftransmission.ChinabegantoimplementHAARTin1999accordingtointernationalstandards.Priorto2003,therewereonlyabout150HIV/AIDSpatientsweretreatedwithHAARTinsomeclinicaltrialsandabout100HIV/AIDSpatientsweretreatedbyprivatesources.ResultsofthosetreatmentsarethescientificbasisfordevelopmentofthetherapeuticstrategiesinChina.InMarchof2003,theChinesegovernmentinitiatedChinaCARESprogram.InNovemberof2003,theChineseMinistryofHealthannouncedanationalpolicyoffreeARVtreatmenttoallHIV+ChinesecitizenswhowereinpovertyandrequiredARVtherapy.Therearetotalof19,456HIV/AIDSpatientsreceivedfreeARVdrugstodatein159regionsand441towns.Currentchallengesarehowtofollow-upandevaluatethosepatientsintheclinicalsettings.Thelongerthetherapyispostponed,themoresideeffectsandthehigherprobabilityofdrugresistancearegoingtooccur.Itremainsunclear,therefore,whenHAARTregimenshouldbestartedintheHIV/AIDSpopulationinChina.

简介：<正>Manyvirusesestablishlife-longinfectionsintheirnaturalhostwithfewifanyclinicalmanifestations.Therelationshipbetweenvirusandhostisadynamicprocessinwhichthevirushasevolvedthemeanstocoexistbyreducingitsvisibility,whilethehostimmunesystemattemptstosuppressandeliminateinfectionwithoutdamagetoitself.Wearenowbeginningtounderstandthatvirusescanemployavarietyofstrategiestoevadehostimmuneresponses.TheseincludeescapefromTcellrecognition,resistanceto

简介：Chinesenongovernmentalorganizations(NGOs)haveplayedasignificantroleinthebattleagainstAIDSinthePeople'sRepublicofChina.Thisarticleprovidesabriefoverviewofthestructureoftheseorganizations,aswellasananalysisoftheirprincipleaccomplishments.OfgreatsignificanceinthisanalysisisthefactthatChineseNGOshaveeffectivelydealtwithmanysensitivehealtheducationareasthatgovernmentauthoritieshavefeltreluctanttohandledirectly.Assuch,theyhaveprovidedanindispensablecomponentintheHIV/AIDSpreventionandcontrolcalculusonthemainland.

简介：Internationalnon-governmentalorganizationswereamongthefirstinternationalactorsthatrespondedtotheemergenceofAIDScrisisinChina.Since1994,thenumberofinternationalnon-governmentalorganizationsandcharitablefoundationsworkinginAIDSrelatedissueareasinChinahasgrownsteadilyandsubstantially.Despitetheirorganizationaldifferences,mostofthesenon-governmentalactorspresentthecharacteristicsofindependentmission,localizedpracticeanddiverseworkingfocus.Eventhoughtheyareconstrainedbyfinancialandotherfactorscomparedwithmultilateralandbilateralofficialassistanceagencies,theyhavestillplayedauniqueroleinfightingagainstAIDSinChinaastechnicalexperts,publiceducators,andcivilsocietysupporters.

简介：生长因素midkine(MK)是由堵住HIV粒子的附件到容许的细胞在autocrine和paracrine举止在细胞文化禁止HIV感染的cytokine。MKmRNA系统地从健康施主在成年的外部血淋巴细胞被表示，当它的表示显著地变得时，但是短暂地增加了在之上在有由公众房产管理局或通过CD28抗原的约会的T淋巴细胞的IL-2或IFN-gamma和激活的淋巴细胞的vitro治疗。到房间的MK的绑定在高度和一个低亲密关系绑定地点明确地发生。这个低亲密关系绑定地点是房间表面表示了nucleolin，它在HIV粒子的起始的附件的机制被含有到房间。因此，而它阻止MK的绑定到低亲密关系绑定地点，nucleolin有约束力的HB-19假肽没在MK绑定上有效果到高亲密关系绑定地点，因此建议MK的低亲密关系受体是cell-surface-expressednucleolin。共焦的免疫荧光激光显微镜学在不同的点揭示了MK和cell-surface-expressednucleolin的colocalization。nucleolin的各种各样的删除构造的使用然后显示极端C终端nucleolin结束，包含氨基酸主题RGG的重复，作为绑MK的领域。到表面nucleolin的MK的特定的绑定独立于heparan硫酸盐和chondroitin硫酸盐proteoglycans。在到房间的绑定以后，MK由nucleolin和类脂化合物椽子在看起来被含有的一个活跃过程进入房间。有势力和与它在由各种各样的生理的刺激的淋巴细胞的提高的表示一起的MK的不同anti-HIV行动，指出MK是能涉及HIV的cytokine致病。

简介：人的免疫不全病毒类型1(HIV-1)Vpr导致房间死亡在哺乳动物并且分裂酵母房间，建议那Vpr可以影响一个保存细胞的过程。然而，导致Vpr的酵母房间死亡是否在哺乳动物的房间模仿调停Vpr的apoptosis，是不清楚的。我们最近识别了很多Vprsuppressors不仅在分裂酵母压制导致Vpr的房间死亡，而且在哺乳动物的房间堵住导致Vpr的apoptosis。这些调查结果建议在酵母的导致Vpr的房间死亡可以类似于一些哺乳动物的房间的apoptotic过程。这研究的目标是为apoptosis的未来研究开发并且验证一个分裂酵母模型系统。类似于在哺乳动物的房间的导致Vpr的apoptosis，我们这里证明在分裂酵母的Vpr支持phosphatidylserine外表表现并且导致线粒体的hyperpolarization，导致mitochondrial膜潜力的变化。而且，反应的氧种类(ROS)的Vpr扳机生产，显示象apoptotic一样细胞死亡可能被ROS调停。有趣地，Vpr在可以为在分裂酵母测量象apoptotic一样过程提供一个简单标记的线粒体导致唯一的词法变化。验证这可能性，我们测试了二Vprsuppressors(EF2和Hsp16)除了最新识别的Vprsuppressor(Skp1)在哺乳动物的房间压制导致Vpr的apoptosis。所有三蛋白质废除了房间死亡由Vpr调停了并且在酵母房间恢复了正常mitochondrial形态学。在结论，在分裂酵母的导致Vpr的房间死亡类似于哺乳动物的apoptotic过程。分裂酵母可以潜在地因此为Vpr和另外的proapoptotic代理人导致的象apoptotic一样过程的未来学习被用作一个简单模型有机体。

简介：Activehost-pathogeninteractionstakeplaceduringinfectionofhumanimmunodeficiencyvirustype1(HIV-1).Outcomesoftheseinteractionsdeterminetheefficiencyofviralinfectionandsubsequentdiseaseprogression.HIV-infectedcellsrespondtoviralinvasionwithvariousdefensivestrategiessuchasinnate,cellularandhumoralimmuneantiviralmechanisms.Ontheotherhand,thevirushasalsodevelopedvariousoffensivetacticstosuppressthesehostcellularresponses.Amongmanyoftheviraloffensivestrategies,HIV-1viralauxiliaryproteins(Tat,Rev,Nef,Vif,VprandVpu)playimportantrolesinthehost-pathogeninteractionandthushavesignificantimpactsontheoutcomeofHIVinfection.OneofthebestexamplesistheinteractionofVifwithahostcytidinedeaminaseAPOBEC3G.AlthoughspecificrolesofotherauxiliaryproteinsarenotaswelldescribedasVif-APOBEC3Ginteraction,itisthegoalofthisbriefreviewtosummarizesomeofthepreliminaryfindingswiththehopetostimulatefurtherdiscussionandinvestigationinthisexhilaratingareaofresearch.