乙型肝炎表面抗原阳性者胃癌术后以顺铂为基础的辅助化疗中乙型肝炎的再激活

目的 了解HBsAg阳性者胃癌术后以顺铂为基础的辅助化疗中乙型肝炎的复发、转归及危险因素.方法 回顾性分析了2005年1月到2010年12月接受辅助化疗的2538例胃癌术后患者,观察HBsAg阳性患者乙型肝炎的再激活情况.所有入组患者进行HBV血清学和生物化学检测及接受以顺铂为基础的辅助化疗方案.数据进行X2检验.结果 146例HBsAg阳性胃癌术后患者中,43例(29.5％)进展为乙型肝炎,29例(19.9％)由于HBV复制激活而乙型肝炎复发.单因素分析表明患者年龄≥51岁(P=0.029)、肝脏超声为脂肪肝或早期肝硬化(P =0.031)是辅助化疗中HBV复制激活的相关因素;性别、HBeAg阳性、化疗期间使用皮质类固醇激素与HBV复制激活无关联.结论 胃癌术后的辅助化疗中,在无症状HBsAg阳性患者有一定比例可以发生HBV的复制激活,检测到HBV复制激活再进行拉米夫定干预治疗后仍有大多数患者无法完成既定的化疗计划,因此在此类患者中有必要在辅助化疗开始前预防性的使用拉米夫定阻止乙型肝炎复发.     

未抗病毒治疗人类免疫缺陷病毒感染者隐匿性乙型肝炎的调查及其临床特点

目的 观察未经抗病毒治疗(ART)的人类免疫缺陷病毒(HIV)感染者和普通人群隐匿性乙型肝炎流行状况,评估HIV感染者合并隐匿性乙型肝炎的临床特点.方法 通过酶联免疫分析法检测未经ART治疗的HIV感染者和普通人群血浆HBsAg、抗-HBs、HBeAg、抗-HBe和抗-HBc水平,筛查出HBsAg阴性的HIV感染者(感染组)249例,健康体检者HBsAg阴性者121例(健康组),再采用罗氏COBASAmpliPrep/COBAS TaqManHBVTest,version2.0试剂盒检测外周血HBV DNA水平.统计分析用STATA 10软件处理本实验各组数据.用Fisher's精确概率检验、秩和检验.结果 感染组HBV DNA阳性者24例,隐匿性乙型肝炎占9.7％;健康组HBV DNA阳性者4例,隐匿性乙型肝炎占3.3％,两组比较,P=0.035,差异有统计学意义.感染组24例HBVDNA阳性者,HBV DNA载量最低者血中能测到,但在检测值水平以下,(即＜20 IU/ml),最高者3.22×105 IU/ml.大于100 IU/ml占37.5％(9/24),20 ～ 99 IU/ml占16.7％ (4/24),＜20IU/ml,但可测出HBV DNA占45.8％ (11/24).HIV感染者抗-HBc(+)/抗-HBs(+)组、抗-HBc(+)/抗-HBs(-)组、抗-HBc(-)/抗-HBs(+)组、抗-HBc(-)/抗-HBs(-)组DNA阳性率分别为7.3％ (8/110),20.8％ (11/53),14.3％ (3/21),3.1％(2/64),抗-HBc(+)/抗-HBs(-)组分别与抗-HBc(+)/抗-HBs(+)组、抗-HBc(-)/抗-HBs(-)组两组比较,P值分别为0.018和0.003,差异有统计学意义.四组间HBV DNA病毒载量比较,P=0.805,差异无统计学意义.感染组HBV DNA(+)组与HBV DNA(-)组比较,CD4计数(Z=1.902,P=0.0586)和ALT水平(Z=1.401,P=0.1611)差异无统计学意义.结论 在未经ART治疗HIV感染者中,隐匿性乙型肝炎高于普通人群,HIV感染者抗-HBc(+)/抗-HBs(-)组隐匿性乙型肝炎最高.     

慢性乙型肝炎病毒感染者家族隐匿性乙型肝炎病毒感染的调查

目的 了解慢性HBV感染者家族隐匿性HBV感染的发生率及其与HBV标志物、年龄和性别等的关系.方法 ELISA方法检测慢性HBV感染者家族成员的HBV血清学标志物,套式PCR法检测136例HBsAg阴性家族成员的血清HBV DNA,并将隐匿性HBV感染者和HBsAg、HBV DNA均阴性者分别作为试验组和对照组进行HBV标志物、年龄、性别和生物化学检测结果的比较.两组均数比较采用t检验.率的比较采用χ~2检验或Fisher确切概率法检验.结果 在52个慢性HBV感染者家族中共检测到92例HBsAg阳性者和136例HBsAg阴性者,其中15例为隐匿性HBV感染者,慢性HBV感染者家族HBsAg阳性率和隐匿性HBV感染的发生率分别为40.4%和11.0%,15例隐匿性HBV感染者中有7例抗-HBc阳性(χ~2=5.341,P=0.02),但隐匿性HBV感染的存在与年龄、性别等无关.结论 HBV感染存在家庭聚集现象,且在其家族中存在隐匿性HBV感染,并在抗-HBc阳性者中发生率较高.     

HBsAg与抗-HBs同时阳性的慢性乙型肝炎患者临床特点分析

目的分析HBsAg与抗-HBs同时阳性的现象及其临床特点,并探讨其产生的原因。方法收集2011年2月-2014年2月东南大学附属第二医院体检者2260例,其中被诊断为慢性乙型肝炎的患者830例。采用化学发光微粒子免疫分析法筛选HBsAg与抗-HBs同时阳性的患者188例,分为HBeAg阳性组(n=101)和HBeAg阴性组(n=87)。同时选取200例HBsAg阳性、抗-HBs阴性者作为对照,其中HBeAg阳性组80例,HBeAg阴性组120例。检测HBV血清学标志物、肝功能、病毒载量并结合临床进行分析。计数资料组间比较采用χ2检验。结果 HBV血清学标志物在HBsAg与抗-HBs双阳性情况下共有5种模式,其中以HBsAg、抗-HBs、HBeAg及抗-HBc阳性,且抗-HBe阴性多见,占47.9%(90/188),肝功能指标总异常率为69.1%(130/188),HBV DNA总阳性率为56.9%(107/188)。HBeAg阳性的2组HBV DNA均存在高水平复制,其中HBsAg与抗-HBs双阳性组HBV DNA阳性率与对照组比较,差异无统计学意义(χ2=2.632,P0.05);HBeAg阴性组中,HBsAg与抗-HBs双阳性组HBV DNA定量1×105IU/ml的比例与对照组比较,差异有统计学意义(χ2=10.740,P0.05)。对HBV S区进行测序分析发现,测序的80例HBsAg与抗-HBs双阳性患者中有27例患者的HBV S区发生变异,突变率33.7%,且S区变异位点主要有P29L、S61L、P62L、I126T/S、Q129N、M133K、F134L、G145R/K、L175S和L186H等。结论 HBsAg与抗-HBs同时阳性者在乙型肝炎患者中有一定比例,其主要原因可能是病毒株变异所致。这种情况并不代表疾病好转,且抗-HBs出现并不一定能完全有效清除HBsAg,病毒DNA往往存在持续复制,需引起重视。     

乙型肝炎相关性肝衰竭患者HBV DNA低水平复制及特异性抗体表达的临床意义

目的探讨乙型肝炎相关性肝衰竭患者血清HBV DNA低水平复制及HBV特异性抗体表达的相关因素及临床意义。方法收集2008年6月至2013年12月于天津市第二人民医院住院治疗的391例乙型肝炎相关性肝衰竭患者及394例慢性乙型肝炎患者的病历资料。比较乙型肝炎相关性肝衰竭与慢性乙型肝炎患者HBV DNA表达的不同及影响因素分析。根据HBV血清学标志物(HBV M)特异性表达的不同将肝衰竭患者分为特异性抗体阳性(指抗-HBs、抗-HBe和抗-HBc同时阳性)和特异性抗体阴性(无抗-HBs、抗-HBe和抗-HBc同时阳性)2组,分析2组患者HBV DNA水平的变化和生存情况。组间比较采用独立样本t检验或MannWhitney秩和检验,计数资料比较采用χ2检验。结果乙型肝炎相关性肝衰竭患者HBV DNA水平低于慢性乙型肝炎组,差异有统计学意义(Z=-16.469,P0.05);HBeAg阳性和阴性的肝衰竭患者HBV DNA水平均低于相应的慢性乙型肝炎患者,差异有统计学意义(Z分别为-11.665和-12.853,P0.05)。在391肝衰竭病例中,HBV特异性抗体阳性组29例(7.42%),死亡25例(86.21%),HBV特异性抗体阴性组362例(92.58%),死亡157例(43.37%),2组病死率差异有统计学意义(P0.05)。特异性抗体阳性组患者HBV DNA水平明显低于特异性抗体阴性组,差异有统计学意义(Z=-3.594,P0.05)。2组HBeAg阴性患者HBV DNA水平均低于HBeAg阳性患者,差异有统计学意义(Z分别为7.427和7.513,P0.05)。结论 HBV M表达形式及机体免疫状态的动态变化在乙型肝炎相关性肝衰竭的发生发展过程中起着一定作用,HBV DNA低水平复制系机体处于免疫清除期所致,而同时伴抗-HBs、抗-HBe、抗-HBc 3个抗体同时阳性则提示机体对HBV的超强免疫反应,致使病情恶化、发展迅速,病死率高。     

经血液(非静脉吸毒者)和性途径传播的HIV感染者合并HBV和HCV感染的现状

目的 探讨我国经血液(非静脉吸毒者)和性途径传播的HIV感染者合并乙型肝炎和丙型肝炎的状况.方法 回顾性分析2005年1至9月在全国13个研究中心就诊的362例HIV/AIDS患者(静脉吸毒者除外),应用酶联免疫试剂盒分别测定其HBsAg、抗-HBs,HBeAg、抗-Hbe、抗-HBc和抗-HCV.采用t检验和X2检验分别对计量和计数结果进行统计学分析.结果 315例检测血HBV和HCV的患者中,HBsAg阳性14例,占4.4%;抗-HCV阳性158例,占50.2%,抗-HCV阴性157例,占49.8%;HIV、HBV、HCV共感染2例,占0.6%.抗-HCV阳性组中经血液和性传播的比例分别占92%和4%,以血液传播为主;抗-HCV阴性组中经血液和性传播的比例分别占11%和66%,以性传播为主.抗-HCV阳性组的HIV确诊时间、CD4+T淋巴细胞绝对计数、ALT和AST均高于抗-HCV阴性组.两组患者的HBV标志物表达也存在差异,其中抗-HCV阳性组中HBsAg阳性2例,占1.3%,抗-HCV阴性组中HBsAg阳性12例,占7.6%,两组比较差异有统计学意义(X2=7.542,P<0.01).10例HBsAg阳性者进行HBV DNA检测,其中4例阳性,抗-HCV均为阴性.57例抗-HCV阳性患者进行HCV RNA检测,阳性者占63.2%.结论 我国输血和性传播途径的HIV感染合并HBV或HCV感染,以合并HCV感染为主,并多见于经输血感染者.合并HCV感染可加重HIV患者的肝脏损伤,同时也可能存在干扰HBV复制的情况.     

HBsAg阳性恶性肿瘤患者化疗后肝损伤及HBV再激活的临床分析

目的探讨HBsAg阳性肿瘤患者化疗后肝损伤情况及HBV再激活的相关危险因素。方法收集2011年1月-2013年12月在汕头市中心医院接受化疗的HBsAg阳性的恶性肿瘤患者共150例。其中43例行预防性抗病毒治疗,即化疗前、化疗期间和化疗结束后半年使用抗病毒治疗(试验组),107例未行预防性抗病毒治疗(对照组)。回顾性分析2组患者化疗后肝损伤情况。计数资料组间比较采用χ2检验,使用Logistic回归分析法分析影响化疗后HBV再激活的相关因素。结果所有患者经过化疗,63例(42.0%)出现肝损伤,其中肝脏不良反应分级:Ⅰ度13例(8.7%)、Ⅱ度29例(19.3%)、Ⅲ度15例(10.0%)、Ⅳ度6例(4.0%),2组肝损伤程度差异具有统计学意义(χ2=19.498,P=0.001)。试验组肝损伤发生率为18.6%(8例),比对照组51.4%(55例)明显降低,差异有统计学意义(χ2=25.864,P0.001)。Logistic单因素回归分析显示,化疗前乙型肝炎六项状态、HBV定量、是否使用激素及是否预防性使用抗病毒治疗差异具有统计学意义,将其纳入Logistic多因素回归分析显示,这4项指标均是患者化疗后HBV再激活的独立影响因素,其中预防性抗病毒治疗是患者化疗后HBV再激活唯一保护性因素。结论 HBsAg阳性肿瘤患者化疗后肝损伤发生率较高,预防性使用抗病毒治疗可以有效降低HBV再激活的发生率,从而减少肝损伤的发生。     

核苷类似物预防乙型肝炎病毒再激活的临床分析

目的 探讨非活动性HBsAg携带者,因肿瘤或其他疾病,在接受化学治疗或免疫抑制剂治疗后,HBV再激活的发生情况和其临床特点以及用核甙类似物预防和治疗后疾病发生及发展的规律,为临床防治该类疾病提供依据. 方法选择患有肿瘤、自身免疫性疾病需进行细胞毒性药物化学治疗或免疫抑制剂治疗的非活动性HBsAg携带者为研究对象.对照组为2002年6月-2007年4月在我院符科室住院的患者,观察患者在免疫状态改变下病毒活跃复制、肝功能损害的临床特点和应用核甙类似物治疗后的效果及其最终临床转归.预防组为2007年4月-2008年7月在我院门诊或住院部治疗的患者,在基础疾病治疗前应用核苷类似物治疗,观察HBV再激活的情况和I临床表现.统计学分析采用两种属性独立性的χ2检验和相对危险度估计. 结果预防组患者共32例,在服用核苷类似物治疗后的第1、3、6、12个月定量检测HBV DNA,只有9.4%(3/32)患者出现了HBV冉激活,表现为HBV DNA阳转,肝功能异常.对照组患者共77例,化学治疗或使用免疫抑制剂前未使用核苷类似物,其中58.4%(45/77)的患者出现HBV再激活,χ2=22.083,P<0.01.对照组中有5例患者发展为重型肝炎,其中4例患者死亡,1例行活体肝移植.结论 非活动性HBsAg携带者接受化学治疗或免疫抑制剂治疗后HBV冉激活的发生率高,应早期使用拉米夫定等核苷类似物预防性抗病毒治疗,减少HBV再激活的概率,从而改善临床预后.     

核苷类似物预防乙型肝炎病毒再激活的临床分析

目的 探讨非活动性HBsAg携带者,因肿瘤或其他疾病,在接受化学治疗或免疫抑制剂治疗后,HBV再激活的发生情况和其临床特点以及用核甙类似物预防和治疗后疾病发生及发展的规律,为临床防治该类疾病提供依据. 方法选择患有肿瘤、自身免疫性疾病需进行细胞毒性药物化学治疗或免疫抑制剂治疗的非活动性HBsAg携带者为研究对象.对照组为2002年6月-2007年4月在我院符科室住院的患者,观察患者在免疫状态改变下病毒活跃复制、肝功能损害的临床特点和应用核甙类似物治疗后的效果及其最终临床转归.预防组为2007年4月-2008年7月在我院门诊或住院部治疗的患者,在基础疾病治疗前应用核苷类似物治疗,观察HBV再激活的情况和I临床表现.统计学分析采用两种属性独立性的χ2检验和相对危险度估计. 结果预防组患者共32例,在服用核苷类似物治疗后的第1、3、6、12个月定量检测HBV DNA,只有9.4%(3/32)患者出现了HBV冉激活,表现为HBV DNA阳转,肝功能异常.对照组患者共77例,化学治疗或使用免疫抑制剂前未使用核苷类似物,其中58.4%(45/77)的患者出现HBV再激活,χ2=22.083,P<0.01.对照组中有5例患者发展为重型肝炎,其中4例患者死亡,1例行活体肝移植.结论 非活动性HBsAg携带者接受化学治疗或免疫抑制剂治疗后HBV冉激活的发生率高,应早期使用拉米夫定等核苷类似物预防性抗病毒治疗,减少HBV再激活的概率,从而改善临床预后.     

核苷类似物预防乙型肝炎病毒再激活的临床分析

目的 探讨非活动性HBsAg携带者,因肿瘤或其他疾病,在接受化学治疗或免疫抑制剂治疗后,HBV再激活的发生情况和其临床特点以及用核甙类似物预防和治疗后疾病发生及发展的规律,为临床防治该类疾病提供依据. 方法选择患有肿瘤、自身免疫性疾病需进行细胞毒性药物化学治疗或免疫抑制剂治疗的非活动性HBsAg携带者为研究对象.对照组为2002年6月-2007年4月在我院符科室住院的患者,观察患者在免疫状态改变下病毒活跃复制、肝功能损害的临床特点和应用核甙类似物治疗后的效果及其最终临床转归.预防组为2007年4月-2008年7月在我院门诊或住院部治疗的患者,在基础疾病治疗前应用核苷类似物治疗,观察HBV再激活的情况和I临床表现.统计学分析采用两种属性独立性的χ2检验和相对危险度估计. 结果预防组患者共32例,在服用核苷类似物治疗后的第1、3、6、12个月定量检测HBV DNA,只有9.4%(3/32)患者出现了HBV冉激活,表现为HBV DNA阳转,肝功能异常.对照组患者共77例,化学治疗或使用免疫抑制剂前未使用核苷类似物,其中58.4%(45/77)的患者出现HBV再激活,χ2=22.083,P<0.01.对照组中有5例患者发展为重型肝炎,其中4例患者死亡,1例行活体肝移植.结论 非活动性HBsAg携带者接受化学治疗或免疫抑制剂治疗后HBV冉激活的发生率高,应早期使用拉米夫定等核苷类似物预防性抗病毒治疗,减少HBV再激活的概率,从而改善临床预后.     

慢性乙型肝炎患者肝细胞内乙型肝炎核心抗原阳性的临床意义

目的探讨CHB患者肝组织HBcAg阳性的意义。方法对200例CHB患者应用荧光聚合酶链反应（FQ-PCR）法精确定量检测血清HBV DNA含量。患者均检测血清中HBeAg含量,同时进行肝活组织检查,应用免疫组织化学技术检测HBcAg情况,并进行相关性分析。结果按测定血清HBV DNA水平,分为A组（＜3 log10拷贝/ml）20例,B组（≥3 log10拷贝/ml-＜5 log10拷贝/ml）13例,C组（≥5 log10拷贝/ml～＜6 log10拷贝/ml）24例,D组（≥6 log10拷贝/ml～＜8 log10拷贝/ml）116例,E组（≥8 log10拷贝/ml）27例。肝组织HBcAg阳性者175例,占87．5％,A组HBcAg阳性率55．0％（11/20）,B组53．8％（7/13）,C组75．0％（18/24）,D组96．6％（112/116）,E组100．0％（27/27）,HBcAg阳性率与血清HBV DNA水平之间呈显著正相关（r=0．80,P＜0．01）。血清HBV DNA水平高低与HBeAg阳性率之间呈显著正相关（r=0．47,P＜0．01）。其中20例HBV DNA阴性者中（A组）,HBeAg阳性者5例（25％）,HBcAg阳性者11例（55％）；15例HBV DNA阴性且HBeAg阴性者中有7例HBcAg阳性,占46．7％。结论CHB患者肝组织HBcAg阳性能更可靠地反映肝细胞内HBV复制状态。检测肝组织内HBcAg对CHB患者疗效评价和对治疗反应性的预测更具有临床意义。     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.