慢性乙型肝炎患者血清抗卯抗体检测及其与年龄变化、病毒载量和病毒基因型的关系分析

目的探讨幽门螺杆菌（HP）在慢性乙型肝炎中的作用。方法采用病例对照研究的方法分析376例慢性乙型病毒性肝炎患者的HP感染状况与年龄、乙型肝炎病毒（HBV）DNA定量和分型的关系。结果HP感染率随年龄变化无明显差异（P〉0．05），HP感染率在慢性乙型肝炎组（56．2％）、乙型肝炎肝硬化组（69．9％）、乙型肝炎合并肝癌组（75．0％）明显高于健康对照组（43．4％）（P〈0．01），各组与慢性胃炎组（57．9％）相比较无明显差异（P〉0．05），其中肝硬化组和合并肝癌组HP感染率均高于肝炎组（P〈0．05）。不同病毒载量慢性乙型肝炎患者的HP感染率均明显高于健康对照组（P〈0．01），但不同病毒载量之间无明显差异（P〉0．05）。慢性乙型肝炎患者B基因型、C基因型和D基因型HP感染率分别为61．3％、63．3％和50．0％，三组之间比较无统计学意义（P〉0．05）。结论慢性乙型肝炎患者HP感染率明显增加，且HP感染率随着肝病病变程度的进展而增加。     

慢性乙型肝炎患者幽门螺杆菌感染状况及其相关因素分析

目的探讨慢性乙型肝炎患者幽门螺杆菌（HP）感染状况。方法采用病例对照研究对502例慢性乙型肝炎患者的抗-HP-IgG和乙型肝炎病毒（HBV）DNA定量及分型进行检测。结果HP感染率在慢性乙型肝炎组（59．5％）、乙型肝炎肝硬化组（77．1％）及合并肝癌组（80．6％）均明显高于健康对照组（43．4％），且随着病变程度的加重，HP感染率亦增加。HBVDNA阳性组的慢性乙型肝炎患者HP感染率高于HBVDNA阴性组（P〈0．05）和健康对照组（P〈0．001），但不同病毒载量组之间比较差异无统计学意义。不同HBV基因型之间HP感染率无明显差异。肝硬化合并肝性脑病、消化性溃疡和消化道出血等并发症者HP感染率较高。结论慢性乙型肝炎患者幽门螺杆菌感染率明显增加，且随着病变程度的加重，HP感染率亦增加。乙型肝炎肝硬化患者并发症的发生可能与HP感染有关。     

慢性丙型肝炎患者血清抗Hp抗体与临床特征的关系

目的探讨幽门螺杆菌（Helicobacter pylori,Hp）在慢性丙型肝炎中的作用。方法采用病例对照研究的方法分析282例慢性丙型肝炎患者的Hp感染状况与年龄变化、HCV RNA载量和HCV RNA分型的关系。结果Hp感染率随年龄变化无明显差异（P〉0.05）,Hp感染率在慢性丙型肝炎组（55.6%）、丙型肝炎肝硬化组（76.5%）和丙型肝炎合并肝癌组（78.6%）明显高于健康对照组（43.4%）（均P〈0.01）,各组与慢性胃炎组（57.9%）相比较无明显差异（P〉0.05）,其中肝硬化组和合并肝癌组Hp感染率均高于肝炎组（P〈0.05）。不同病毒载量的慢性丙型肝炎患者的Hp感染率均明显高于健康对照组（P〈0.01）,但不同病毒载量之间无明显差异（P〉0.05）。慢性丙型肝炎患者基因1a型、1b型、2a型和2b型患者Hp感染率分别为60.0%、64.8%、61.0%和62.7%,各基因型之间比较无明显差异（P〉0.05）。结论慢性丙型肝炎患者Hp感染率明显增加,且Hp感染率随着肝病病变程度的进展而增加。     

乙型肝炎病毒X抗原表达与肝细胞凋亡的相关性

目的 探讨乙型肝炎病毒X蛋白(HBxAg)在HBV感染相关性肝病患者病情进展和癌变过程中的作用. 方法 用免疫组织化学方法检测38例HBV慢性感染者(HBV携带者14例及慢性乙型肝炎患者24例)、20例乙型肝炎肝硬化(LC)和20例HBV相关性肝细胞癌(HCC)患者肝组织中HBxAg、Fas及其配体(FasL)的表达,分析HBxAg与Fas、FasL表达的相关性及其与患者病毒学指标和肝脏病理学改变的关系.肝脏炎症分级及纤维化分期按照Knodell标准.计数资料用x2检验及Fisher精确概率法,多个样本间的两两比较用x2分割法,等级资料用秩和检验,相关性分析采用Spearman等级相关分析. 结果 HBV慢性感染者、LC及HCC患者肝组织中HBxAg阳性率分别为71.1％、60.0％、65.0％,差异无统计学意义(x2=0.754,P＞0.05).肝细胞中Fas和FasL阳性率分别为28.9％、20.0％、5.0％和36.8％、50.0％、60.0％,各组间差异均无统计学意义(x2值分别为4.667和2.988,P值均＞0.05).三组患者肝组织淋巴细胞Fas表达的阳性率分别为68.4％、60.0％和90.0％,其中,肝癌患者的表达强度显著高于HBV慢性感染者(Z=-4.360,P＜0.01).在LC重症炎症区域及部分HCC患者中可见HBxAg与FasL在同一区域表达.相关性分析显示,HBV慢性感染和LC患者中,HBxAg与Fas、FasL表达强度均具有相关性(r值分别为0.304和0.368,P值均＜0.05),Fas与FasL的表达也存在相关性(r=0.448,P＜0.01).HBxAg阳性率在高、中病毒载量组(分别为88.9％和69.2％)均明显高于低病毒载量组(为26.7％,P＜0.05). 结论 HBxAg在HBV感染各期均起重要作用,早期主要上调肝细胞Fas表达并诱导肝细胞凋亡,使肝脏炎症坏死加重;后期主要上调肝细胞FasL表达并诱导免疫逃避.HBxAg和高病毒载量在HBV慢性感染者病情发展和癌变中起重要作用.     

丙型病毒性肝炎肝硬化患者抗病毒疗效及影响因素分析

目的 研究丙型病毒性肝炎肝硬化患者抗病毒治疗耐受及应答情况,探讨丙型肝炎抗病毒疗效的影响因素.方法 收集慢性丙型肝炎患者52例,其中肝硬化患者13例,菲肝硬化患者39例,均给予干扰素(IFN)联合利巴韦林抗病毒治疗后,观察两组患者病毒学应答、生化学应答及不良反应发生情况.结果 丙型肝炎肝硬化组平均年龄为(58.31±8.72)岁,非肝硬化组平均年龄为(36.95±15.30),两组比较差异无统计学意义(P＞0.05).肝硬化患者快速病毒学应答率(RVR)、早期病毒学应答率(EVR)和持续病毒学应答率(SVR)分别为84.62％、100.00％和53.85％,非肝硬化患者RVR、EVR和SVR分别为92.31％、100.00％和71.79％,两组比较差异均无统计学意义(P＞0.05).两组生化学应答比较差异均无统计学意义(P＞0.05).肝硬化组患者中性粒细胞减少、血小板减少和贫血的发生率均明显高于非肝硬化组,两组比较差异均有统计学意义(P＜0.05).肝硬化组患者中有2例出现白蛋白下降和腹水,其中1例中断治疗.老年(年龄≥60岁)和采用普通IFN联合利巴韦林抗病毒治疗的患者获得SVR率明显低于中青年患者(年龄＜60岁)和采用长效IFN联合利巴韦林抗病毒治疗的患者(P＜0.05).基因1型患者的SVR率低于非基因1型,但差异无统计学意义(P＞0.05).结论 代偿期丙型病毒性肝炎肝硬化患者多能耐受抗病毒治疗,且远期疗效较好.     

拉米夫定治疗无良好应答患者乙型肝炎病毒P区突变与基因型的关系

目的 观察拉米夫定治疗后无良好应答的慢性乙型肝炎患者HBV P区变异情况与基因型的关系.方法 对631例拉米夫定治疗后无良好应答的慢性乙型肝炎患者进行研究.通过荧光定量PCR或核酸测序确定HBV基因型,直接测序观察P区突变,实时荧光定量PCR方法检测患者病毒载量,比较不同基因型患者的HBV DNA水平及HBV P区变异情况.计量资料采用成组设计资料t检验,计数资料采用x~2检验或Fisher精确检验.结果 631例慢性乙型肝炎患者中,B基因型HBV感染者272例,C基因型感染者359例,C基因型感染者患者年龄为(39.1±11.4)岁,明显大于B基因型感染患者的(33.7±9.7)岁(t=-6.55,P<0.01).C基因患者病毒载量为(5.96±1.22)log_(10)拷贝/ml,高于B基因型患者的(5.58±1.21)log_(10)拷贝/ml,t=-2.01,P<0.05.A181V/T变异在C基因型的发生率高于B基因型(0.4%比5.3%,χ~2=12.23,P<0.01),M204I/V,L180M、T184A/G/I/S、S202G/I和V173L变异发生率在B、C基因型之间差异无统计学意义(P值均>0.05).M204I在B基因型的发生率为20.6%,高于C基因型的13.9%(χ~2=4.91,P<0.05);M204V和M201Ⅳ变异在B、C基因型中的发生率差异无统计学意义(χ~2值分别为1.70和2.21,P值均>0.05).拉米夫定耐药发生率在B、C基因型间差异无统计学意义(χ~2=0.00,P>0.05).结论 拉米夫定常见耐药位点在B、C基因型之间无明显差异,但是C基因HBV感染患者病毒载量高于B基因型HBV感染患者;M204I变异在B基因型中出现频率高于C基因型,拉米夫定加用或改用阿德福韦酯后可能会使A181V/T变异在C基因型出现的概率高于B基因型;年龄、免疫因素和非常见位点的变异或许是影响拉米夫定疗效的重要因素.     

人微小病毒B19与乙肝病毒相关肝病的临床关系

目的 探讨人微小病毒B19在乙肝病毒相关肝病患者中的感染情况及其对这些疾病的影响.方法 应用ELISA技术检测原发性肝癌、肝硬化、慢性乙型肝炎三组患者(各50例)和健康对照组(50例)血清中HPV B19特异性抗体IgM(B19-IgM),同时检测其丙氨酸氨基转移酶、天冬氨酸氨基转移酶、肝功能Child-Pugh评分,分析HPV B19感染对肝脏功能的影响.结果 乙肝病毒相关肝病组人微小病毒B19感染率(16.7%)远高于正常对照组(2%),差别有显著性(P<0.05);原发性肝癌人微小病毒B19-IgM阳性率(28%)远高于慢性乙型肝炎组(10%)、肝硬化组(12%)及正常对照组(2%)(P<0.05);肝硬化组人微小病毒B19-IgM抗体阳性率明显高于正常对照组(P<0.05);原发性肝癌组中人微小病毒B19-IgM阳性患者转氨酶(ALT、AST)水平、肝功能Child-Pugh评分及肝癌分期较阴性者高,差异有统计学意义(P<0.05).结论 乙肝病毒相关肝病患者合并人微小病毒B19的感染常见,其中原发性肝癌组感染率最高;且转氨酶的水平及肝功能Child-Pugh评分高于未感染者,提示受人微小病毒B19感染的原发性肝癌患者肝功能受损将更严重.     

延边地区朝鲜族乙型肝炎病毒感染者病毒基因型的检测与分析

目的:分析延边地区朝鲜族HBV感染者HBV基因类型分布及其临床意义.方法:延边地区朝鲜族HBV感染者215例分为无症状携带者36例,急性乙型肝炎5例,慢性乙型肝炎106例,肝炎肝硬化50例,原发性肝癌18例.利用特异性引物聚合酶链反应法(PCR),对患者血清标本进行基因型检测.结果:215例HBV感染者中检出B基因型61例(28.0%),C基因型154例(72.0%),未检出其他基因型.在慢性乙型肝炎、肝炎肝硬化、肝细胞癌患者中,C基因型比例(79.0%、84.0%、89.0%)明显高于无症状携带者及急性乙型肝炎(25.0%、60.0%,P<0.01),在无症状携带者中,B基因型比例高于C基因型(75.0%vs 25.0%,P<0.01).HbeAg阳性组C基因型比例高于HBeAg阴性感染组(73.0% vs 54.0%,P<0.05),HbeAg阴性组的B基因型比例高于HBeAg阳性组(46.0% vs 27.0%,P<0.01).结论:延边地区朝鲜族HBV感染主要为C基因型,其次为B基因型.C基因型在临床上以慢性乙型肝炎、肝炎肝硬化、肝细胞癌多见.其发生率显著高于B基因型.     

老年慢性病毒性肝炎患者中幽门螺杆菌感染情况研究

目的研究慢性乙型肝炎、丙型肝炎患者幽门螺旋杆菌(Helicobacterpylori,Hp)感染情况,探讨Hp在其发展中的作用。方法选取慢性乙肝患者215例,丙肝患者104例,健康对照147例,采用酶联免疫吸附(ELISA)法检测抗体阳性为感染判断标准。对3组人群Hp感染情况进行比较分析。结果慢性乙型肝炎患者中有113例感染了Hp(感染率为52.6%),明显高于健康对照者(66例,感染率为44.9%);慢性丙型肝炎患者Hp感染67例,感染率为64.4%,显著高于健康对照者和慢性乙型肝炎患者。2种肝炎合并肝硬化组Hp感染率均高于无肝硬化组。结论慢性乙型和丙型肝炎患者Hp感染率明显增加,Hp在慢性乙型或丙型肝炎向肝硬化的发展过程中可能与HBV/HCV发挥协同作用;对患者进行Hp根除治疗有益于控制病情。     

新疆地区HBV基因型分布特点及其与肝硬化的相关性分析

目的探讨新疆地区HBV基因分型构成特点及其与肝硬化之间的关系。方法收集2011年10月至2013年6月新疆维吾尔自治区中医医院收治的慢性HBV感染者1018例。其中检测出基因型、资料完整的828例。根据实验室检查及彩超或CT结果将患者分为慢性乙型肝炎组、肝硬化组、原发性肝癌组。采用PCR法对HBV基因分型,运用列联卡方、秩和检验、多因素Logistic回归分析等方法对HBV基因型与临床病情及相关慢性肝病结局进行分析。结果 828例患者中,以C型为主,占总样本的54.11%(448/828),B型占25.15%(200/828),D型占16.18%(134/828);各基因型病情程度构成差异无统计学意义(H=0.1689,P0.05);116例肝硬化患者中基因C型占20.84%,与B型和D型相比较差异均有统计学意义(χ2值分别为25.486、20.947,P值均为0.000);乙型肝炎病程10年以上、基因C型、HBV DNA高病毒载量、ALTULN进入回归模型(P0.05)。其中基因C型与肝硬化的相关度最高(OR=2.819,95%CI:1.582~5.021)。结论新疆地区HBV基因分型以C型为主,其次为B型、D型。基因C型是HBV相关肝硬化患者的独立危险因素。     

慢性肝病患者乙型肝炎病毒BCP变异对HBV DNA复制水平影响的研究

目的探讨乙型肝炎病毒慢性感染中C基因启动子(BCP)变异对HBV DNA复制水平的影响及其临床意义。方法采用PCR微板核酸杂交结合ELISA检测显示技术,检测74例乙型肝炎病毒慢性感染者BCP区核苷酸(nt)1762碱基A→T和1764碱基G→A联合突变。结果在74例乙型肝炎病毒慢性感染者中检出BCP区T1762 A1764突变24例(32.4％),BCP变异阳性组的HBV DNA含量(10~(8.2992±0.8665)拷贝/ml)显著高于BCP变异阴性组的含量(10~(7.1737±1.1539)拷贝/ml ) P<0.001)。结论 BCP变异可引起HBV致病力增强,复制水平提高。     

乙型肝炎孕妇HBV血清标志物与HBVDNA载量及ALT的相关性分析

目的 分析乙型肝炎(乙肝)孕妇HBV血清标志物、HBVDNA载量及ALT检测结果,为HBV感染孕妇的诊治提供参考。方法 回顾性分析2016年11月—2017年11月在我区孕检的120例乙肝孕妇的临床资料,应用酶联免疫吸附法检测血清五项HBV标志物,同时采用荧光实时定量PCR技术检测HBVDNA水平,酶速率法检测ALT,并对检测结果进行统计分析。结果 120例孕妇血清中,感染模式Ⅰ(大三阳)HBsAg(+)、HBeAg(+)、HBcAb(+)58例,占48.33%;HBVDNA(+)49例,占84.48%,其中HBVDNA>106IU/ml42例,占72.41%;ALT增高39例,异常率为67.24%。感染模式Ⅱ(小三阳)HBsAg(+)、HBeAb(+)、HBcAb(+)45例,占37.50%;HBVDNA(+)27例,占60.00%,其中HBVDNA>106IU/ml15例,占33.33%;ALT增高20例,异常率为44.44%。感染模式Ⅰ孕妇HBVDNA阳性率、HBVDNA>106IU/ml率和ALT异常率最高,感染模式Ⅱ孕妇次之。结论 HBV血清标志物与HBVDNA高载量和ALT水平密切相关,三者相结合能为孕妇的临床诊断、围产期干预措施以及疗效观察提供参考依据。     

HBV endemicity in Mexico is associated with HBV genotypes H and G

Hepatitis B virus(HBV)genotypes have distinct genetic and geographic diversity and may be associated with specific clinical characteristics,progression,severity of disease and antiviral response.Herein,we provide an updated overview of the endemicity of HBV genotypes H and G in Mexico.HBV genotype H is predominant among the Mexican population,but not in Central America.Its geographic distribution is related to a typical endemicity among the Mexicans which is characterized by a low hepatitis B surface antigen seroprevalence,apparently due to a rapid resolution of the infection,low viral loads and a high prevalence of occult B infection.During chronic infections,genotype H is detected in mixtures with other HBV genotypes and associated with other co-morbidities,such as obesity,alcoholism and co-infection with hepatitis C virus or human immunodeficiency virus.Hepatocellular carcinoma prevalence is low.Thus,antiviral therapy may differ significantly from the standard guidelines established worldwide.The high prevalence of HBV genotype G in the Americas,especially among the Mexican population,raises new questions regarding its geographic origin that will require further investigation.     

HBV感染对孕妇产后母乳喂养的影响及护理策略

目的 了解HBV感染产妇乳汁HBV DNA水平状况,为决定是否给予母乳喂养提供依据。方法 2016年2月~2017年1月在我院分娩的135例HBV携带孕妇,采用时间分辨免疫荧光法检测HBV标志物,采用荧光定量PCR法检测HBV DNA。结果 64例血清HBV DNA载量<1×106 copies/ml组、15例1×106~1×107copies/ml组、21例1×107~1×108copies/ml组、32例1×108~1×109copies/ml组和3例≥1×109copies/ml组乳汁HBV DNA检出率分别为0.0%、13.3%、28.6%、35.7%和66.7%;19例血清HBsAg/HBeAg/抗-HBc阳性产妇乳汁HBV DNA检出率为68.4%,显著高于27例血清HBsAg/抗-HBe/抗-HBc阳性组的25.9%、或12例抗-HBe/抗-HBc阳性组的8.3%、或77例血清抗-HBs/抗-HBe/抗-HBc阳性组的1.3%（P<0.05）。结论 血清HBsAg/HBeAg/抗-HBc阳性或血清HBV DNA水平>1×107copies/ml的产妇乳汁HBV DNA阳性率较高,不建议这些人群进行母乳喂养。     

Quantification of HBV core antibodies may help predict HBV reactivation in patients with lymphoma and resolved HBV infection

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HBV DNA vaccine with adjuvant cytokines induced specific immune responses against HBV infection

AIM: To seek for an effective method to improve the immuneresponses induced by DNA vaccine expressing HBV surfaceantigen (pCR3.1-S) in Balb/c mice (H-2d).METHODS: The pCR3.1-S plasmid and the eukaryoticexpression vectors expressing murine IL-2 (pDOR-IL-2) orIL-12 (pWRG3169) were injected into mice subcutaneously.The immune responses to pCR3.1-S and the adjuvant effectof the cytokines plasmid were studied. Meanwhile the effectof pCR3.1-S on anti-translated subcutaneous tumor of P815mastocytoma cells stably expressing HBsAg (P815-HBV-S)was also studied. Anti-HBs in serum was detected by enzyme-linked immunoadsordent assay (ELISA) and HBsAg specificcytotoxic T lymphocytes (CTLs) activity was measured by 51Crrelease assay. After three weeks of DNA immunization, thecells of P815-HBV-S were inoculated into mice subcutaneouslyand the tumor growth was measured every five days. Thesurvival rate and living periods of mice were also calculated.RESULTS: After 8 wk DNA immunization, the ,4 450 nmvalues of sera in mice immunized with pCR3.1, pCR3.1-Sand pCR3.1-S codeliveried with IL-2 or IL-12 plasmids were0.03±0.01, 1.24±0.10, 1.98±0.17 and 1.67±0.12respectively. Data in mice codeliveried pCR3.1-S with IL-2or IL-12 plasmids were significantly higher than that of miceinjected pCR3.1 or pCR3.1-S only. The HBsAg specific CTLactivities in mice coinjected with pCR3.1-S and IL-2 or IL-12 eukaryotic expression vectors were (61.9±7.1) % and(73.3±8.8) %, which were significantly higher than that ofmice injected with pCR3.1 (10.1±2.1) % or pCR3.1-S (50.5±6.4) %. The HBsAg specific CTL activities in mice injectedwith pCR3.1, pCR3.1-S, pCR3.1-S combined with IL-2 or IL-12 eukaryotic expression vectors decreased significantly to(3.2±0.8) %, (10.6±1.4) %, (13.6±1.3) % and (16.9±2.3)% respectively after the spleen cells were treated by anti-CD8+ monoclonal antibody, but presented no significantchange to anti-CD4+ monoclonal antibody or unrelated tomonoclonal antibody. The HBV-S DNA vaccine (pCR3.1-S)could evidently inhibit the tumor growth, prolong the survivalperiod of mice and improve the survival rate of mice andthese effects could be improved by IL-12 gene codeliveried.CONCLUSION: HBV DNA vaccine has a strong antigenicityin humoral and cellular immunities, which can be promotedby plasmid expressing IL-2 or IL-12. CD8+ cells executedthe CTL activities. DNA vaccine may be useful for bothprophylaxis and treatment of HBV infection.     

乙肝病毒基因型与患者临床预后关系的研究

研究不同HBV基因型感染者临床特征的异同。选取慢性HBV感染者297例,用特异性引物PCR法测定其HBV基因型,并比较不同基因型者在临床各方面表现有何异同。297例样本中B型占12．8％,C型占87.2％, 未发现其他基因型。B型者与C型者相比,年龄≤35岁者较多,血清ALT、AST水平较低,两组的血清HBVDNA水平无明显差异。B型在慢性HBsAg携带者、慢性肝炎、肝硬化及肝癌患者中所占比例逐步下降,而C型所占比例则逐步上升。B型者HBeAg阳性率低,HBeAg血清学转换率高。B型、年龄小者及女性者容易呈慢性HBsAg携带者状态。在17例死于肝病者中,B型者死亡时感染HBV时间较长。B型者对抗病毒治疗应答比C型者好。C型HBV 感染与严重肝脏疾病的发生有关,感染B型HBV者临床预后较好,对抗病毒治疗的应答较好。     

HBV DNA vaccine with adjuvant cytokines induced specific immune responses against HBV infection

AIM: To seek for an effective method to improve the immuneresponses induced by DNA vaccine expressing HBV surfaceantigen (pCR3.1-S) in Balb/c mice (H-2d).METHODS: The pCR3.1-S plasmid and the eukaryoticexpression vectors expressing murine IL-2 (pDOR-IL-2) orIL-12 (pWRG3169) were injected into mice subcutaneously.The immune responses to pCR3.1-S and the adjuvant effectof the cytokines plasmid were studied. Meanwhile the effectof pCR3.1-S on anti-translated subcutaneous tumor of P815mastocytoma cells stably expressing HBsAg (P815-HBV-S)was also studied. Anti-HBs in serum was detected by enzyme-linked immunoadsordent assay (ELISA) and HBsAg specificcytotoxic T lymphocytes (CTLs) activity was measured by 51Crrelease assay. After three weeks of DNA immunization, thecells of P815-HBV-S were inoculated into mice subcutaneouslyand the tumor growth was measured every five days. Thesurvival rate and living periods of mice were also calculated.RESULTS: After 8 wk DNA immunization, the ,4 450 nmvalues of sera in mice immunized with pCR3.1, pCR3.1-Sand pCR3.1-S codeliveried with IL-2 or IL-12 plasmids were0.03±0.01, 1.24±0.10, 1.98±0.17 and 1.67±0.12respectively. Data in mice codeliveried pCR3.1-S with IL-2or IL-12 plasmids were significantly higher than that of miceinjected pCR3.1 or pCR3.1-S only. The HBsAg specific CTLactivities in mice coinjected with pCR3.1-S and IL-2 or IL-12 eukaryotic expression vectors were (61.9±7.1) % and(73.3±8.8) %, which were significantly higher than that ofmice injected with pCR3.1 (10.1±2.1) % or pCR3.1-S (50.5±6.4) %. The HBsAg specific CTL activities in mice injectedwith pCR3.1, pCR3.1-S, pCR3.1-S combined with IL-2 or IL-12 eukaryotic expression vectors decreased significantly to(3.2±0.8) %, (10.6±1.4) %, (13.6±1.3) % and (16.9±2.3)% respectively after the spleen cells were treated by anti-CD8+ monoclonal antibody, but presented no significantchange to anti-CD4+ monoclonal antibody or unrelated tomonoclonal antibody. The HBV-S DNA vaccine (pCR3.1-S)could evidently inhibit the tumor growth, prolong the survivalperiod of mice and improve the survival rate of mice andthese effects could be improved by IL-12 gene codeliveried.CONCLUSION: HBV DNA vaccine has a strong antigenicityin humoral and cellular immunities, which can be promotedby plasmid expressing IL-2 or IL-12. CD8+ cells executedthe CTL activities. DNA vaccine may be useful for bothprophylaxis and treatment of HBV infection.     

HBV/HIV coinfection is associated with poorer outcomes in hospitalized patients with HBV or HIV

We examined the impact of HBV/HIV coinfection on outcomes in hospitalized patients compared to those with HBV or HIV monoinfection. Using the 2011 US Nationwide Inpatient Sample, we identified patients who had been hospitalized with HBV or HIV monoinfection or HBV/HIV coinfection using ICD‐9‐CM codes. We compared liver‐related admissions between the three groups. Multivariable logistic regression was performed to identify independent predictors of in‐hospital mortality, length of stay and total charges. A total of 72 584 discharges with HBV monoinfection, 133 880 discharges with HIV monoinfection and 8156 discharges with HBV/HIV coinfection were included. HBV/HIV coinfection was associated with higher mortality compared to HBV monoinfection (OR 1.67, 95% CI 1.30–2.15) but not when compared to HIV monoinfection (OR 1.22, 95% CI 0.96–1.54). However, the presence of HBV along with cirrhosis or complications of portal hypertension was associated with three times greater in‐hospital mortality in patients with HIV compared to those without these complications (OR 3.00, 95% CI 1.80–5.02). Length of stay and total hospitalization charges were greater in the HBV‐/HIV‐coinfected group compared to the HBV monoinfection group (+1.53 days, P < 0.001; $17595, P < 0.001) and the HIV monoinfection group (+0.62 days, P = 0.034; $8840, P = 0.005). In conclusion, HBV/HIV coinfection is a risk factor for in‐hospital mortality, particularly in liver‐related admissions, compared to HBV monoinfection. Overall healthcare utilization from HBV/HIV coinfection is also higher than for either infection alone and higher than the national average for all hospitalizations, thus emphasizing the healthcare burden from these illnesses.