有偿献血员中艾滋病病毒、乙型肝炎和丙型肝炎病毒感染状况的研究

目的 探讨有偿献血员艾滋病病毒(HIV)、丙型肝炎(丙肝)病毒(HCV)、乙型肝炎(乙肝)病毒(HBV)感染的特点。方法61份HIV阳性献血员及89份HIV阴性献血员的血清,经酶联免疫吸附试验(ELISA)检测HCV抗体(抗-HCV)及HBV血清学标志物,比较两组人群的HCV、HBV及HCV/HBV感染情况。结果HIV阳性献血员的抗-HCV阳性率为70.49％。乙肝病毒表面抗原(HBsAg)与抗体(抗-HBs)、乙肝病毒e抗原(HBeAg)与抗体(抗-HBe)、乙肝病毒核心抗体(抗-HBc)和HBV的阳性率分别为8.20％、29.51％、3.28％、44.26％、11.4896、47.54％;而HIV阴性献血员的抗-HCV阳性率为19.10％,HBsAg、抗-HBs、HBeAg、抗-HBe、抗-HBc、HBV的阳性率分别为2.25％、38.20％、1.12％、47.19％、6.74％、47.19％。经统计学分析,两组人群的HCV、HCV/HBV感染率的差异有显著的统计学意义,而HBV血清学标志物则无显著性差异。结论 与HIV阴性献血员相比。HIV阳性献血员的HCV感染率很高,而HBV血清学标志物则无显著性差异。对献血员进行HBV检测而未检测HIV、HCV造成的选择偏倚,可能是中国中部一些省份HIV感染者HCV感染率高而HBV感染并不相应增高这一现象的原因之一。     

HIV感染者中HCV及HBV感染状况的研究

目的 了解HIV感染者中HCV、HBV的感染状况。方法 对197例HIV感染者中的HCV、HBV感染情况进行了血清流行病学调查研究。结果 HIV感染者中HCV的感染率为90.35％,HBV的总感染率为51.94％,HIV、HCV、HBV三重感染率为49.35％。结论 HIV感染者中有极高的HCV感染率,有较高的HBV感染率。     

饮酒与原发性肝癌关系的调查--附吉林省1057例原发性肝癌病因学分析

明确饮酒与肝炎病毒感染是否有协同致原发性肝癌的作用.采用病例对照研究的方法对吉林省1057例原发性肝癌患者及3171例非肝病患者的饮用酒精量和HBV/HCV感染状况进行比较.结果表明饮酒可增加患原发性肝癌的危险性,饮酒(40-100)g/d者OR值为1.41,＞100g/d为3.04.饮酒可增加HBV、HCV感染者患原发性肝癌的危险性,饮酒(40-100)g/d的HBV感染者OR值为18.82,＞100g/d为31.15;饮酒(加-100)g/d的HCV感染者OR值为32.02,＞100g/d为47.63;饮酒(40-100)g/d的HBV、HCV重叠感染OR值为79.39,＞100g/d为121.42.452例行HBV-DNA检测的患者中,非嗜酒史者阳性率为26.15%,饮酒(40-100)g/d为49.07%,饮酒＞100g/d为70.56%;特别是HBsAg、抗-HBc、抗-HBe阳性的重度嗜酒者HBV-DNA阳性率最高为78.21%.嗜酒可增加HBV、HCV及重叠感染者患原发性肝癌的危险性,酒精对HBV、HCV在致肝细胞癌方面有协同和加强作用.     

有偿献血员中艾滋病病毒、乙型肝炎和丙型肝炎病毒感染状况的研究

目的：探讨有偿献血员艾滋病病毒（HIV）、丙型肝炎（丙肝）病毒（HCV）、乙型肝炎（乙肝）病毒（HBV）感染的特点，方法：71份HIV阳性献血员及89份HIV阴性献血员的血清，经酶联免疫吸附试验（ELISA）检测HCV抗体（抗－HCV）及HBV血清学标志物，比较两组人群的HCV、HBV及HCV／HBV感染情况，结果：HIV阳性献血员的抗－HCIV阳性率为70．49％，乙肝血清学标志物，比较两组人群的HCV、HBV及HCV／HBV感染情况。结果：HIV阳性献血员的抗－HCV阳性率为70．49％，地病毒表面抗原（HBsAg）与抗体（抗－HBs）、乙肝病毒e抗原（HBeAg）与抗体（抗－HBe)、乙肝病毒核心抗体（抗－HBc）和HBV的阳性率分别为8．20％、29．51％、3．28％、44．26％，11．48％、47．54％、1．12％、47．19％、6．74％、47．19％。经统计学分析，两组人群的HCV、HCV／HBV感染率的差异有显著的统计学意义，而HBV血清学标志物则无显著性差异。结论：与HIV阴性献血员相比，HIV阳性献血员的HCV感染率很高，而HBV血清学标志物则无显著性差异，对献血员进行HBV检测而未检测HIV、HCV造成的选择偏倚，可能是中国中部一些省份HIV感染者HCV感染率高而HBV感染并不相应增高这一现象的原因之一。     

肝病与乙型、丙型肝炎病毒感染关系的探讨

本文采用ELISA法对25例慢性肝炎，105例肝硬化，64例肝癌，以及8例急性黄疸型肝炎进行了HBV标志物及抗－HCV的检测，结果：HBV感染率为80．6％，抗－HCV检测阳性率为46％，二者均阳性的双重感染率为32％。其中肝癌组双重感染明显高于肝硬化组，P＜0．001。单纯抗-HCV检出率为10．8％，说明HBV是引起肝炎，肝硬化，肝癌的主要原因，而CV感染也是其致病因素。本文对有输血史的慢性肝炎，肝硬化，肝癌100例进行抗－HCV检测其阳性率为59％，而02例无输血史的肝病患者抗－HCV检出率为25％，输血组抗－HCV检出率明显高于无输血组，P＜0．001。其中慢性肝炎，肝硬化，肝癌病人输血组抗－HCV检出率亦明显高于无输血组，各组P＜0．001，故提示，HCV感染与输血有密切关系。50例HBV标志物阴性的健康献血员抗－HCV阳性率为6％。     

乙型、丙型和丁型肝炎病毒与肝细胞癌岛关系

采用 ELISA 法检测了140例肝癌患者的 HBV—M 和抗—HCV(其中38例检测了 HDV—M),并分别与56例非肝病患者和164例肝炎患者比较。结果肝癌病人中有91.2％检出 HBV—M 阳性,32.1％检出抗—HCV 阳性,HDV—M 无阳性检出。在抗—HCV 阳性的肝癌病人中,HBV—M 阳性率达95.6％。经X(?)检验分析,在 HCC 中,HBV—M、抗—HCV 和 HDV—M 的总体率两两之间均有极显著性差异。提示 HBV 与 HCC 关系最密切。HCV 次之,而 HDV 关系不明显。HCV 主要与 HBV 以重叠感染方式存在,因而推测 HCV 单独致癌的可能性不太,主要是通过调节和协同 HBV 而起促癌作用。     

HBV感染恢复期血清标志物与肝细胞HBV cccDNA检测对照

目的:了解肝组织乙肝病毒共价闭合环状脱氧核糖核酸(HBV cccDNA)与血清HBV复制指标的关系,以探索判定抗HBV的疗程终结点的观察方法。方法:既往HBV感染者、乙型肝炎肝硬化肝癌及慢性乙型肝炎(CHB)患者各13例,将血清HBV DNA、HBV-M及肝组织HBV cccDNA检测结果进行对照。结果:肝硬化肝癌及CHB患者抗-HBe阳性分别为12例和9例,血HBV DNA阳性分别为6例和8例,肝细胞HBV cccDNA均阳性;既往HBV感染13例中,HBsAg阴性,抗-HBs和/或抗HBc阳性各7和6例,有3例肝细胞中HBV cccDNA阳性。抗-HBs阳性的7例肝细胞HBV cccDNA阴性,抗-HBe阳性及抗HBs合并抗-HBe阳性者,肝细胞HBV cccDNA分别为105拷贝/ml和103拷贝/ml,与抗-HBs阳性组对照,t=4.5、4.0(P均<0.01),差异有非常显著性意义。CHB患者核苷类治疗后全应答,肝组织HBV cccDNA仍均为阳性。结论:抗-HBs阳性HBV感染后恢复期血清,肝组织HBV cccDNA阳性比率明显低于CHB抗HBe阳性HBV DNA阴性病例。抗病毒治疗CHB的终点,应是血清抗-HBs阳性的出现。     

原发性肝癌患者血清HBV基因型分析

目的了解本地区肝癌病人HBV感染情况和HBV基因型分布及意义。方法对92例肝癌患者进行HBVM和抗-HCV检测并对30例单纯HBV感染者和14例慢性乙型肝炎患者进行了HBV基因型检测。结果92例中单纯HBV感染67例(72.83%),HBV和HCV重叠感染6例(6.5%),单纯HCV感染1例(1.08%);在30例检测的患者中,B基因型20例(66.7%),C基因型9例(30%),F基因型1例(0.3%)。结论在肝癌患者中HBV感染率高达81.4%,说明原发性肝癌的发生与HBV有着非常密切的关系,主要是B和C基因型。     

丙型肝炎病毒与甲乙型肝炎病毒重叠感染的研究

对485例病毒性肝炎患者进行了抗HCV、抗HAV-IgM、HBV-M检测.各型病毒性肝炎患者中抗HCV阳性率15.05％,慢性肝炎、肝硬变和重型肝炎阳性率高于急性肝炎;抗HCV阳性者中,27.40％有输血或血浆史;57.53％HBV-M阳性,其中HBsAg阳性占54.76％,抗HBc阳性达88.10％;既往有HBV感染者占33.33％.HBV与HCV重叠感染中慢性肝炎占58.06％,IAV与HCV重叠感染以急性肝炎多见(94.44％),HCV与甲乙型肝炎病毒三重感染可加速肝炎重症化的进程。     

乙型肝炎患者重叠感染HCV及HDV临床意义探讨

本文对305例乙型肝炎患者的血清标本回顾性地检测了HCV及HDV感染标志,结果有48.2％的乙肝患者重叠感染了HCV和/或HDV,其中双重感染率:HBV/HCV 15.4％,HBV/HDV 21.0％;三重感染率:HBV/HCV/HDV同时感染占11.8％,急性盱炎(AH)、厄症状表面抗原携带者(ASC),慢迁肝(CPH).慢活肝(CAH)、肝硬化(CIR)、重型肝炎(SH)及原发性肝癌(PHC)患者的抗-HCV检出率分别为:6.7％、6.7％、22.5％.29.7％、36.4％、38.5％、33.3％:其DHV的检出率分别为:10.0％、13.3％、25.0％、35.9％、41.1％、53.8％、42.9％。肝病越严重,其HCV及HDV的感染率就越高,提示HBV重叠感染HCV及HDV时可以促使肝脏病变加重。合并HCV及HDV感染者的HBV复制率较低。     

TTV感染与原发性肝癌关系的病例对照研究

目的：了解ＴＴＶ与ＨＰＣ的关系。方法：对８２例ＰＨＣ、４０例非肝癌恶性肿瘤病人（对照组１）、４０例正常人（对照组２）进行病例对照研究。结果：ＰＨＣ组中．ＨＢｓＡｇ、ＨＢｅＡｇ、ＨＢＶ－ＤＮＡ,、ＨＢＶ－Ｍ的阳性率分别为７５．６％,５１．２％、１９．５％、２８．９％、８２．９％。显著高于两组照组,ＴＴＶ－ＤＮＡ阳性率２６．８％（２２／８２）也显著高于两对照组。ＨＢＶＣ感染率（８２．９％（）显著高于Ｔ     

PCR检测HBV感染患者血清HBV DNA的临床意义

目的探讨急、慢性乙型肝炎及与ＨＢＶ感染相关的肝硬变和肝癌患者血清ＨＢＶＤＮＡ的临床意义．方法应用ＰＣＲ技术检测不同ＨＢＶ感染２０５例，患者血清ＨＢＶＤＮＡ，并与正常人２０例作比较．结果ＨＢＶ感染患者２０５例血清ＨＢＶＤＮＡ阳性率为６９３％，慢性乙肝、乙肝后肝硬变和肝癌患者的阳性率分别为７６４％，７１９％和７００％，显著高于急性乙肝患者２１７％的阳性率（Ｐ＜００１）；ＨＢｅＡｇ（＋）患者血清ＨＢＶＤＮＡ阳性率为９３６％，显著高于ＨＢｅＡｇ（－）抗ＨＢｅ（＋）／（－）和ＨＢｓＡｇ（－）患者的阳性率（４５６％，２５０％和１２５％，Ｐ＜００１）；血清ＨＢＶＤＮＡ阳性和阴性两组患者的血清ＡＬＴ水平无明显差异（Ｐ＞００５）．结论血清中ＨＢＶＤＮＡ持续存在可能与乙型肝炎的慢性化有关，而与ＨＢＶ感染患者的肝损伤无明显关系     

Reactivation of hepatitis B but not hepatitis C in patients with malignant lymphoma and immunosuppressive therapy. A prospective study in 305 patients

BACKGROUNDS/AIMS: The aim of this prospective study was to determine the prevalence of hepatitis B (HBV) and hepatitis C viral (HCV) infection as well as to study the morbidity and mortality of viral reactivations in patients treated with corticosteroid containing chemotherapy. METHODOLOGY: From January 1991 to April 1996, 305 patients admitted for treatment of Hodgkin's disease and non-Hodgkin's lymphoma were tested for HBV, and 181 patients for HCV infection. They were followed-up regularly on a monthly basis with liver biochemistry and viral serology. RESULTS: The prevalence of HBs antigen and hepatitis C antibody was found to be 3.2% and 16% respectively. There were 9 reactivations of HBV among 8 HBs antigen positive patients (78%), one among 35 HBs antigen negative patients (2.8%) and none in HCV positive patients. In 83% of cases, reactivation was connected to chemotherapy and corticosteroids. The overall death rate of HBV reactivation was 37%; in severe hepatitis it was 60%. All fatal reactivations were in anti-HBe positive patients. CONCLUSIONS: The low prevalence of HCV failed to demonstrate an association between hepatitis C viral infection and lymphoma in Slovenia. Reactivation of HBV infection in HBsAg positive malignant lymphoma patients is a common and often fatal complication of treatment.     

Contribution of low level HBV replication to continuing inflammatory activity in patients with anti-HBe positive chronic hepatitis B virus infection

The relationship between the histological diagnosis and serological and tissue markers of HBV replication in 41 Greek and 29 British patients with chronic HBV infection were studied. All the nine Greek and 13 British patients who were HBeAg positive had HBV-DNA in serum and HBcAg expression in the hepatocytes. The majority (73%) of these patients had active liver disease. Forty seven per cent of the Greek and 19% of the British patients who were anti-HBe positive continued to display HBcAg in the liver with or without HBV-DNA detected in serum. All but three of these patients had persistently active liver disease. Continuing inflammatory activity in the liver, however, was also found in 31% of anti-HBe positive patients who had no evidence of HBV replication. In these patients, other factors such as delta agent, NANB viruses, alcohol abuse or an autoimmune reaction initiated by HBV may be contributory.     

Prevalence of hepatitis B or C virus infections in patients with non-Hodgkin's lymphoma

BACKGROUND: Hepatitis C virus (HCV) and hepatitis B virus (HBV) are not only hepatotropic, but also lymphotropic viruses. Recently, some reports suggested that these viruses may participate in the development of malignant lymphoproliferative disorders. METHODS: We investigated the prevalence of HCV or HBV infection in 348 patients with non-Hodgkin's lymphoma (NHL). We also compared these prevalences with those in blood donors as a control group representing the general population in our area (n= 1,513,358). Next, we evaluated the clinical and pathologic characteristics of HCV- or HBV-infected NHL cases. Non-Hodgkin's lymphoma was classified according to the Working Formulation classification. RESULTS: Thirty-seven cases (14.9%) were found to be infected with HCV or HBV; of these, 20 (8.1%) were infected with HCV, and 17 (6.9%) with HBV. In male NHL patients, the rate of HCV infection was significantly higher than in an age- and sex-matched population in the same area (P < 0.001, Mantel-Haenszel test). The rate of HBV infection also tended to be higher in the population (P = 0.0551). In contrast, in female NHL patients, the rate of HCV or HBV infection was not higher than in the general population. In HCV-infected cases, 15 cases (75%) had B-cell NHL and 16 cases (80%) were classified as being in the intermediate grade; B-cell NHL comprised 83% of all NHL cases. In HBV-infected NHL cases, 11 (65%) were of B-cell type and 10 (58%) were classified as being in the intermediate grade. CONCLUSIONS: The high prevalence of HCV or HBV infections in our study population provides epidemiologic evidence suggesting that HCV and HBV infections may be involved in the development of a subgroup of NHL in males. Our investigation also revealed that both HCV- and HBV-infected NHL patients showed certain similarities in clinical and pathologic manifestations.     

Prevalence of hepatitis B and C in the sera of patients with HIV infection in São Paulo, Brazil

The objective of this study was to evaluate the prevalence of hepatitis B and C viruses in a group of HIV infected patients, followed at a single institution since 1996. 1,693 HIV positive patients (1,162 male, 531 female) were tested for HBV infection. Virological markers for HBV included HBsAg and total anti-HBc by ELISA. 1,457 patients (1,009 male, 448 female) were tested for HCV infection. Detection of HCV antibodies was carried out by ELISA. A sample of HCV antibody positive patients was tested for HCV by PCR to confirm infection. Of 1,693 patients tested for HBV, 654 (38.6%) and 96 (5.7%) were anti-HBc and HBsAg positive, respectively. Of 1, 457 patients tested for HCV, 258 (17.7%) were anti-HCV positive. 82 of these patients were also tested by PCR and 81 were positive (98%). Of 1,411 patients tested for HBV and HCV 26 (1.8%) were positive for both viruses.     

Coinfection of hepatitis B and hepatitis C virus in HIV-infected patients in south India

AIM To screen for the co-infection of hepatitis B (HBV)and hepatitis C virus (HCV) in human immunodeficiency virus (HIV) infected patients insouthern India.METHODS Five hundred consecutive HIV infected patients were screened for Hepatitis B Virus (HBsAg and HBV-DNA) and Hepatitis C virus (anti-HCV and HCV-RNA)using commercially available ELISA kits; HBsAg, HBeAg/anti-HBe (Biorad laboratories, USA) and anti-HCV (Murex Diagnostics, UK). The HBV-DNA PCR was performed to detect the surface antigen region (pre S-S). HCV-RNA was detected by RT-PCR for the detection of the constant 5' putative non-coding region of HCV.RESULTS HBV co-infection was detected in 45/500 (9%)patients and HCV co-infection in 11/500 (2.2%) subjects.Among the 45 co-infected patients only 40 patients could be studied, where the detection rates of HBe was 55%(22/40), antiHBe was 45% (18/40) and HBV-DNA was 56% (23/40). Among 11 HCV co-infected subjects, 6(54.5%) were anti-HCV and HCV RNA positive, while 3(27.2%) were positive for anti-HCV alone and 2 (18%)were positive for HCV RNA alone.CONCLUSION Since the principal routes for HIV transmission are similar to that followed by the hepatotropic viruses, as a consequence, infections with HBV and HCV are expected in HIV infected patients.Therefore, it would be advisable to screen for these viruses in all the HIV infected individuals and their sexual partners at the earliest.     

Virological profiles in patients with chronic hepatitis C and overt or occult HBV infection

OBJECTIVES: The virological profiles of hepatitis B and C viruses (HBV and HCV) and their interplay in cases of coinfection are undefined. A suppressed and occult HBV infection may occur in hepatitis B surface antigen (HBsAg) negative patients with chronic hepatitis C. The HCV core protein is able to inhibit HBV "in vitro," and serines at positions 99 and 116 are essential for such inhibition. We aimed to assess the HBV and HCV virological profiles in cases of coinfection and to evaluate the relationship between HCV core gene variability and HBV activity. METHODS: Eighty-two anti-HCV positive patients were examined: 35 cases were HBsAg positive, 24 were HBsAg negative with "occult" HBV infection, and 23 were HBV negative. HBV and HCV viremia levels were evaluated in all cases. HCV genomic region coding for the aminoacid sequence 99-116 of core protein was amplified and sequenced in all HCV RNA positive cases. The entire core gene was amplified and sequenced in three randomly selected cases. RESULTS: Serum HCV RNA was detected in all cases but 13, all HBsAg positive individuals; HCV viremia levels of the other 22 HBsAg positive subjects were similar to those detected in HBsAg negative patients with or without occult HBV infection. Among the 35 HBsAg positive patients both HBV DNA and HCV RNA were detected in five cases, HCV RNA alone in 17, and HBV DNA alone in six, whereas seven cases had undetectable levels of both viruses. Sequencing analyses showed that the HCV core gene was highly preserved in all patients. CONCLUSION: A wide spectrum of HCV and HBV virological patterns may occur in a case of coinfection. HCV core variability is not related to HBV activity "in vivo."     

Markers of hepatitis viruses and human T-lymphotropic virus types I/II in patients who have undergone open-heart surgery: evidence of increased risk for exposure to HBV and HEV

BACKGROUND: Open-heart procedure is characterized by a high-risk for contracting blood-borne infections. We evaluated the prevalence of several markers of hepatitis viruses (B-E) and human T-cell lymphotropic virus types I/II (HTLV-I/II) in a consecutive series of patients who had undergone open-heart surgery. METHODS: 204 patients and 158 selected age- and sex-matched healthy volunteers were investigated. Samples were collected at least 6-12 months postoperatively. Commercial enzyme immunoassays and confirmatory immunoblot assays for HCV, HEV and HTLV-I/II were used. RESULTS: None of the subjects tested positive for antibodies to HTLV-I/II. Prevalence of markers of past HBV infection and antibodies to HEV (anti-HEV) were higher in patients than in healthy controls (anti-HBc: 45.1% vs. 31%, p=0.009; anti-HBs: 31.9% vs. 22.2%, p=0.02; anti-HBe: 32.4% vs. 10.1%, p=0.000; anti-HEV: 5.4% vs. 0%, p=0.008). HBsAg and antibodies to HCV did not differ between the groups. CONCLUSIONS: HTLV, HBsAg and HCV infection markers did not differ between patients and healthy controls. However, patients had significantly increased prevalence of markers of previous HBV infection suggesting that an intensive vaccination schedule against HBV preoperatively might be helpful in minimizing the risk. The increased prevalence of anti-HEV in cardiac patients requires further investigation. Prospective studies are needed in order to definitely address whether the high prevalence of exposure to HBV and HEV infections in patients who had undergone open-heart surgery is procedure-related or not and whether it has any impact on morbidity of these patients.