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。     

慢性乙型肝炎患者血清抗HP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.     

乙型肝炎病毒前C区和/或核心启动子区突变的临床意义

目的探讨乙型肝炎病毒前C区和／或核心启动子区突变的临床意义。方法应用全自动DNA基因测序仪检测91例慢性乙型肝炎及肝硬化患者乙型肝炎病毒前C区和／或核心启动子区位点变异情况，并观察发生突变组与未发生突变组在HBVDNA载量和肝脏病理改变等方面有无差异。结果HBeAg阳性慢性乙型肝炎患者的变异率为10．7％，HBeAg阴性慢性乙型肝炎患者的变异率为65．2％（P〈0．05）；肝硬化代偿期组变异率为46．2％，失代偿期组变异率为35．7％（P〉0．05）；35例基因变异患者HBVDNA载量（取1g值）为4．98±1．38，与56例未变异患者的6．36±1．31无显著差异（P〉0．05）；基因变异的慢性乙型肝炎患者肝组织病理损害较未变异患者为重。结论乙型肝炎病毒前C区和／或核心启动子区突变多见于HBeAg阴性慢性乙型肝炎患者中，但似乎与肝硬化的发生无明显的关系。     

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。     

病毒性肝炎与糖尿病关系的临床研究

目的探讨病毒性肝炎与糖尿病发病的关系。方法对84例慢性乙型肝炎与83例慢性丙型肝炎患者,76例同期住院患者（对照组）进行病例分析研究,明确其是否合并糖尿病。结果慢性乙型肝炎患者糖尿病并发率为5．9％,慢性丙型肝炎患者糖尿病并发率为13．3％,对照组患者糖尿病并发率为7．9％,慢性丙型肝炎组糖尿病的并发率明显高于慢性乙型肝炎组和对照组患者（P〈0．05）,慢性乙型肝炎组和对照组患者糖尿病并发率差异无统计学意义（P〉0．05）。慢性肝炎合并糖尿病男女比例为2．2：1。三组中合并糖尿病与未合并糖尿病的患者均为中老年人,在年龄、体质量指数、空腹血糖方面差异无统计学意义。合并糖尿病的慢性乙型肝炎和慢性丙型肝炎患者血清丙氨酸氨基转移酶、门冬氨酸氨基转移酶及总胆红素水平高于未合并糖尿病者（P〈0．05）。结论慢性丙型肝炎病毒感染易合并糖尿病,丙型肝炎病毒感染可能是糖尿病的发病因素之一。     

AAR和API评估慢性乙型病毒性肝炎肝纤维化临床价值的比较

目的比较谷草转氨酶-谷丙转氨酶的比值（AAR）和年龄-血小板指数（API）对慢性乙型病毒性肝炎肝纤维化的临床价值。方法172例慢性乙型病毒性肝炎患者均接受肝组织病理检查，并同时检测肝功能和血常规，用ROC曲线评价AAR和API诊断慢性乙型病毒性肝炎肝纤维化的能力。结果肝纤维化S0、S1、S2、S3和S4的AAR无显著差异（P〉0．05），肝纤维化分期与AAR的相关系数（rs）=0．107（P〉0．05），ROC曲线分析显示AAR诊断显著肝纤维化和肝硬化的AUC均〈0．7；肝纤维化S4的API高于S0、S1、S2和s3（P〈0．01），肝纤维化分期与API的rs=0．314（P〈0．01），ROC曲线分析显示API诊断显著肝纤维化的AUC〈0．7（P〉0．05），但诊断肝硬化的AUC达到0．773（P〈0．01），敏感度（SN）达到70．83％，特异度（sP）达到72．18％。结论AAR对于评估慢性乙型病毒性肝炎肝纤维化的临床价值不大；API与肝纤维化分期有一定的相关性，可以用于肝纤维化S4的诊断，但对肝纤维化s1、s2和s3的区分能力有限。     

对拉米夫定耐药患者乙型肝炎病毒基因型与病毒载量及其核苷酸序列分析

目的探讨对拉米夫定耐药患者HBVB、C基因型的病毒载量及其核苷酸序列突变等病毒学特性的差异。方法采用ELISA、实时荧光定量PCR和DNA序列分析的方法，检测53例对拉米夫定耐药患者的HBV基因型、病毒载量及其C、P基因核苷酸序列，并将测序结果与基因库中标准HBV基因型序列进行比较分析。结果53例拉米夫定耐药患者中，B基因型22例，C基因型31例；C基因型的YIDD突变率明显高于B基因型（87．1％比36．4％，P〈0．01），且C基因型的病毒载量为（7．71±0．80）lg拷贝／mL，明显高于B基因型的（6．97±0．77）lg拷贝／mL（P〈0．01）；而B基因型的YVDD突变率和前C区突变（G1896A）明显高于C基因型（分别为63．6％比12．9％、77．3％比32．3％，P值均〈0．01）。B、C基因型的核心启动子突变（T1762／A1764）比较，差异无统计学意义（31．8％比35．5％，P〉0．05）。前C区／核心启动子的突变影响拉米夫定耐药患者的病毒水平。结论拉米夫定耐药患者HBV B、C基因型的YMDD基序分别以YVDD和YIDD变异为主，且基因型C的病毒载量比B基因型要高；B基因型易出现前C区突变（G1896A）。     

乙型肝炎病毒前C区基因及核心启动子双变异临床研究

目的探讨乙型肝炎病毒（HBV）前C区基因及基本核心启动子（BCP）变异在慢性肝病中出现的规律。揭示HBV前C基因变异及BCP双变异与慢性肝病的病情进展及预后的相关性。方法通过DNA扩增、基因序列分析检测21例慢性乙型肝炎（CHB）、18例肝硬化（LC）和15例肝癌（HCC）血清的HBV前C区和BCP的基因序列。结果前C区终止变异（nt1896G→A）在慢性乙肝重度、中度组中的发生率显著高于慢性乙肝轻度组、肝硬化和肝癌组（75％、42．86％和10％、22．22％、20％）（P〈0．01）；BCP双变异（nt162A→T和nt1764G→A）则在肝硬化和肝癌组中的发生率显著高于慢性乙肝组（55．56％、60％和10％、28．57％、25％）（P〈0．05）。结论前C区终止变异与慢性肝病病情进展密切相关，BCP双变异促进肝硬化和肝癌的产生。     

慢性乙型肝炎肝硬化结节样变与病毒变异的关系

目的：分析慢性乙型肝炎肝硬化结节样变与 HBV 变异的关系以及 HBV 变异在慢性肝硬化、肝癌进展中的作用。方法收集临床诊断慢性乙型肝炎肝硬化患者104例,其中不典型结节样增生病例43例,单纯肝硬化患者41例,肝癌患者20例。采用荧光探针实时定量 PCR 试剂盒提取 HBV 基因组,选取 PCR 强阳性产物用 Sanger 双脱氧链末端终止法对 HBV 前 C 区变异基因 G1896A ,BCP 区 G1764A、A1762T 位点在全自动核苷酸分析仪上测序,测序结果与 Gene Bank 中 pADR 标准株序列作对比分析。结果结节性增生组、单纯肝硬化组、肝癌组患者 HBV 前 C Gl896A 变异检出率分别是52．3％、40．1％和37．4％,差异无统计学意义（χ2＝0．547,P ＝0．05）;结节性增生组 BCP A l762T 变异率68．4％,与单纯硬化组36．3％比较,差异有统计学意义（P ＝0．038）,与肝癌组 G1764A 变异检出率分别是73．0％,与对照组比较具有显著性差异（P ＝0．0411）。单纯肝硬化组、结节性增生组 BCP 基因变异（＋）组,HBV DNA 载量2．18×107、1．2×106高于基因变异（-）组1．18×104、2．95×103,差别有统计学意义（P ＝0．0451,P ＝0．0412）;结节性增生组、肝癌组 BCP 基因变异（＋）组HBeAg 定量750．00 IU／mL,1300．00 IU／mL 高于基因变异（-）组416．13 IU／mL,927．60 IU／mL 差别有统计学意义（P ＝0．0451,P ＝0．0073）。结论前 C 区变异与乙肝肝硬化结节样变临床进展为肝癌无关,而 BCP 区变异与乙肝结节样变临床进展为肝癌有关。     

细胞因子与乙型肝炎肝硬化肝功能分级的相关性

目的：研究观察慢性乙型病毒性肝炎（CHB）肝硬化Child-Putgh分级与血清转化生长因子-β1（TGF—β1）、血小板衍生生长因子（PDGF）和γ干扰素（IFN-γ）水平的关系。方法：采用ELISA法检测28例乙型肝炎肝硬化（简称肝硬化）患者和29例健康体检者血清TGF—β、PDGF和IFN-γ水平。肝硬化患者按Child．Pu-gh肝功能分级标准分成A、B、c3级。结果：肝硬化组患者血清TGF-β1和PDGF水平均明显高于正常对照组（P〈0．05），并且ChildB级和ChildC级患者TGF—β1和PDGF水平明显高于ChildA级（P〈0．05）；IFN．1水平明显低于正常对照组（P〈0．05），并且ChildB级和ChildC级IFN-γ水平明显低于ChildA级（P〈0．05）。结论：血清TGF—β1、PDGF和IFN-γ水平在乙型肝炎肝硬化的发生发展过程中有着重要意义，并在一定程度上反应肝硬化患者肝功能损害程度，有利于临床上对该类患者病情和预后的判断。     

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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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/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.     

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 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.