乙型及丙型肝炎病毒感染与原发性肝癌的临床研究

目的研究HBV DNA、HBsAg、HBeAg、HBeAb、HBcAb及抗-HCV与原发性肝癌发生的相关性。方法采用回顾性调查分析方法,对58例原发性肝癌患者（病例组）,同期收治的58例其他恶性肿瘤患者（对照组）HBV和HCV感染情况进行统计,并分析HBV血清标志物及HBV DNA与原发性肝癌发生发展的规律。结果两组资料的HBV感染率分别为82.76%和44.83%,病例组与对照组比较有显著性差异（P〈0.05）,单纯HCV感染及HBV/HCV混合感染率两组无明显差异（P〉0.05）;血清HBV DNA阳性率在病例组和对照组分别为72.92%、23.08%（P〈0.05）;HBsAg、HBeAb和HBcAb检出率病例组高于对照组（P〈0.05）;而HBeAg阳性率两组比较无显著性差异（P〉0.05）。结论在慢性HBV感染的肝癌高发人群中,HBV DNA、HBsAg、HBeAg、HBeAb及HBcAb所反映的HBV感染状态及不同临床演变过程与肝癌的发生发展密切相关,共同参与肝癌的发病机制。     

有受血史的肿瘤患者HBV、HCV感染状况分析

为了调查有受血史的肿瘤患者HBV、HCV感染状况 ,将 4 93例有受血史的肿瘤患者和 5 0 0例无受血史的肿瘤患者HBV、HCV感染情况进行调查分析。结果显示 ,有受血史的肿瘤患者HBV、HCV单纯感染率及HBV/HCV重叠感染率分别为 30 4 %、14 0 %、9 5 % ,显著高于对照组 (17 8%、3 8%、2 8% ) (均P <0 0 1) ,而且三种不同的感染类型均与输血量存在着关联 (均P <0 0 1)。由此可见 ,输血是引起HBV、HCV感染的高危因素 ,严格控制输血指征 ,大力提倡义务献血 ,同时对献血员采用高敏感性的筛选手段 ,是控制HBV、HCV血源性感染的有效措施     

2000例门诊和住院患者中HIV与HBV、HCV混合感染的血清学分析

目的分析医院对艾滋病病毒(HIV)抗体筛选结果,了解HIV感染与HBV、HCV肝炎病毒混合感染的关系.方法1998年6月～1999年6月采用ELISA法、MEIA(微粒子酶免法)对HIV、HBV、HCV检测.结果(1)抗HIV感染率为1.4%,其中男性占1.8%,女性占0.9%.民族分布维吾尔族占3.09%,汉族占0.27%,回族占0.77%;维吾尔族与汉族感染率有极显著性差异(χ2=25.34;P＜0.01).(2)在HIV阳性血清中抗HIV单一感染率14.29%;HIV、HCV双重感染率60.71%,HIV、HBV、HCV三重感染率25%;HIV、HCV与HIV、HBV、HCV混合感染率有极显著性差异(χ2=23.9;P＜0.01).结论在本组血清中HIV感染率高,HCV阳性在HIV/AIDS病人血清中混合感染率高,这与青年人静注毒品有关.HIV与HCV有共同传播途径--血液传播.     

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％。     

SEN病毒感染与慢性肝病的关系

目的 :揭示SEN病毒 (SEN V)感染与慢性肝病之间的关系。方法 :使用SEN VPCR引物 ,从 50例健康志愿者及 2 60例慢性肝病患者 (包括 45例不明原因肝炎、1 2 5例肝硬化和 90例原发性肝细胞肝癌患者 )血清中检测SEN VDNA ,每份DNA样本均取自lml血清。记录各组患者的临床特点 ,并分析其与SEN V感染的关系。结果 :SEN VDNA在健康志愿者、不明原因肝炎患者、肝硬化患者和原发性肝细胞肝癌患者中阳性检出率分别为 1 6 .0 0 %、2 2 .2 2 %、36 .80 %和 2 1 .1 1 % ,仅肝硬化组与健康对照组有显著差异 (P <0 .0 5)。肝硬化组中 ,丙型肝炎病毒 (HCV)感染、HCV和乙型肝炎病毒 (HBV)共感染及不明原因的肝硬化患者SEN V感染率分别为 63 .64 %、62 .50 %和 54 .55 % ,均与对照组有显著差异 (P <0 .0 5)。所有 2 60例慢性肝病患者中 ,共 75例SEN V阳性 ,感染率达 2 8.85 % ,与对照组相比有显著差异 (P <0 .0 5)。SEN V在HCV感染中阳性率为 43 .75 % ,与对照组相比有显著差异 (P <0 .0 5)。在各组患者中 ,SEN V感染与否同患者的临床特点无相关关系。SEN V感染与输血亦无显著关联。结论 :SEN V较其它肝炎病毒在健康人群中的检出率高。在肝硬化患者 ,特别是丙型肝炎肝硬化患者中检出率较高。SEN V和HCV可能有相似的传播途径     

劳教学员中静脉注射海洛因依赖者的乙型肝炎和丙型肝炎感染调查

目的了解海洛因依赖者的乙型肝炎(HBV)和丙型肝炎(HCV)感染情况,探讨其与感染有关的行为特征.方法采用ELISA法检测了152例海洛因依赖者和56例对照者的乙型肝炎和丙型肝炎感染情况,并调查了海洛因依赖者的成瘾史、不洁注射史、性伙伴情况等与肝炎传播有关的行为特征.结果发现海洛因依赖组与对照组的总感染率、HBV感染率、HCV感染率、HBV和HCV的混合感染率依次为46.7%,28.3%,27.6%和9.2%与10.7%,7.1%,3.6%和0.HBV和HCV的感染与海洛因依赖者的静脉注射、不洁注射史、成瘾时间及性别有关.结论提出在海洛因依赖者中预防HBV、HCV感染、减少药物滥用危害的重要性.     

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。     

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。     

579例原发性肝癌患者乙肝病毒与丙肝病毒血清学标志物分析

目的 探讨原发性肝癌(PHC)与乙肝病毒(HBV)、丙肝病毒(HCV)感染模式之间的关系.方法 用酶联免疫吸附试验(ELISA)检测579例PHC患者、1 013例非PHC患者血清的HBV表面抗原(HBsAg)、HBV表面抗体(抗-HBs)、HBV e抗原(HBeAg)、HBV e抗体(抗-HBe)、HBV核心抗体(抗-HBc)、HCV抗体免疫球蛋白G(抗-HCV IgG)等六项指标.结果 ①PHC组HBV感染率为86.53%,对照组HBV感染率为49.65%,两组比较差异有统计学意义(χ2=215.06,P＜0.01).PHC组HCV感染率为0.52%,对照组HCV感染率为0.30%,两组比较差异无统计学意义(χ2=0.204 5,P＞0.05).②PHC组乙肝两对半模式1、模式2、模式3、模式4、模式5、模式7、模式8的阳性率与对照组相比差异有统计学意义(P＜0.05,P＜0.01);而模式6、模式9的阳性率与对照组相比差异无统计学意义(均P＞0.05).③乙肝两对半"小三阳"与"小二阳"的PHC发病率差异有统计学意义(84.07% vs 67.17%,χ2=12.17,P＜0.01);"小三阳"与"大三阳"的PHC发病率差异无统计学意义(67.17% vs 64.00%,χ2=0.29,P＞0.05).结论 慢性HBV感染是本地区PHC的主要原因,乙肝两对半"小二阳"的致癌能力也不容忽视.     

中国东北丙型肝炎病毒感染基因特征及人群易感性分析

采用微板核酸杂交-ELISA法及基因芯片技术对5 79例HCV感染者的HCV基因型以及30例HCV感染者以及30例健康人HLA -DRB1等位基因分布情况进行分析,探讨中国东北丙型肝炎病毒(HCV)感染基因型特征及丙型肝炎病毒感染的人群易感性。5. 79例患者中Ⅳ/ 2b型HCV感染率最高,为5 1 .12 % ;约34 .72 %的HCV感染者ALT持续正常;Ⅱ/ 1b型和混合型HCV感染在ALT反复升高组中的感染率明显高于ALT持续正常组(P <0 .0 5 )。Ⅰ型和Ⅲ型HCV合并HBV感染的发生率较高,混合型HCV合并HBV感染的发生率较低,与单独感染比较差异显著(P <0 .0 5 ) ;混合型HCV感染主要见于有2次或2次以上输血史者。HLA -DRB1 0 4和DRB1 13在HCV感染者中的出现频率较高,与健康对照组相比差异显著(P <0. 0 5 )。因此,中国东北地区HCV感染以Ⅳ/ 2b型为主,约34 72 %的HCV感染者不表现出肝炎的症状,可能成为重要的传染源。Ⅱ/ 1b型和混合型HCV感染更容易导致肝细胞损伤。Ⅰ/ 1a型和Ⅲ/ 2a型HCV可能更易于同HBV共存,两种或两种以上基因型共存的HCV则不易于同HBV合并感染。反复接受血液或血制品可能是出现混合型HCV感染的主要原因。HLA -DRB1 0 4和DRB1 13等位基因可能与HCV的人群易感性有关。     

Comparison of recurrence after hepatic resection in patients with hepatitis B vs. hepatitis C-related small hepatocellular carcinoma in hepatitis B virus endemic area.

PURPOSE: Hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are two important factors in the development of hepatocellular carcinoma (HCC). The carcinogenic mechanism of HBV and HCV is considered to be different. It is interesting to compare the recurrence after hepatic resection in patients with small HCC who were infected with HBV or HCV. METHODS: From 1991 to 1995, 145 patients who were positive for hepatitis B surface antigen (HBsAg) or antibody to HCV (anti-HCV) and diagnosed as small HCC (< or =3 cm) in three medical centers in Taiwan were evaluated in this study. All patients underwent hepatic resection. Among them, 83 (57.2%) were infected by HBV, 51 (35.2%) were infected by HCV, and 11 (7.6%) had dual HBV and HCV infection. RESULTS: Anti-HCV+ HCCs were associated with older age, lower serum albumin, higher alanine transaminase (ALT) level and multi-nodular tumors during diagnosis. During the follow-up, 92 (63.4%) patients developed tumor recurrence. Anti-HCV + HCC had a higher cumulated recurrence rate than HBsAg+ HCC (72.4% vs 53.6 % at 5 year, P = 0.032). In multivariate analysis, the presence of vascular invasion and lower serum albumin levels (<3.9 g/dl) were the determinants for tumor recurrence. CONCLUSIONS: HCV infection, as compared with HBV infection, had a higher cumulated recurrence after hepatic resection in patients with small HCC. Low serum albumin level was significantly associated with recurrence among these patients.     

Viral hepatocarcinogenesis: from infection to cancer

Hepatocellular carcinoma (HCC) is a worldwide health issue that has started receiving attention but is still poorly understood. However, the hepatitis B virus (HBV) and the hepatitis C virus (HCV) are known to be two major causative agents of HCC. They differ in their modes of infection, their treatment options, their genomes and their carcinogenic abilities. However, both share a link with HCC through alterations of the host genome. In order to continue in our search for the mechanisms behind viral hepatocarcinogenesis, the individual entities (HBV, HCV, HCC and host), their natural history, treatment options and genomic properties must be further understood. Additionally, an understanding of the genomics, the link between the entities, is crucial for the success of the ongoing search for therapeutic options for HCC. Similar to most types of cancer, hepatocarcinogenesis is a multistep process involving different genetic alterations that ultimately lead to malignant transformation of the hepatocyte. As technology advances and research continues, the genetic changes and influences among these entities will prove essential to improved diagnostic and therapeutic options. It remains a challenge to provide a clear picture of the connection between virus and cancer. We review (i) the epidemiological link between HBV/HCV infection to HCC; (ii) prevention and control of chronic hepatitis B or C in reducing HCC risk; and (iii) genetic characters of viruses and hosts and the mechanisms associated with HCC susceptibilities, with the intention of providing a direction for future research and treatment.     

HCV and HBV coexist in HBsAg-negative patients with HCV viraemia: Possibility of coinfection in these patients must be considered in HBV-high endemic area

Hepatocellular carcinoma (HCC) is one of the most common cancers and is highly associated with hepatitis B virus (HBV) infection in Korea. The role of HBV and hepatitis C virus (HCV) in HCC patients who are negative for hepatitis B surface antigens (HBsAg) remains poorly defined. It has been suggested that HCV core protein may impair the polymerase activity of HBV in vitro, potentially lowering HBV titre in coinfected patients. Therefore, routine enzyme immunoassay may not detect HBV, in spite of the presence of HBV viraemia in low titres. The aim of this study was to confirm the coexistence of HBV viraemia in hepatitis C-infected patients with HCC who have apparent HBsAg seronegativity and to establish the need for clinical reinterpretation of enzyme immunoassay (EIA) serological tests of HBsAg in patients with HCV viraemia and HCC. The serological profiles of HBV and HCV in 616 patients with HCC were analysed and the coinfection rate of HCV and HBV investigated. Sera were obtained from 16 patients who were both anti-HCV and HCV-RNA positive but HBsAg negative, and tested for HBV by polymerase chain reaction (PCR). Eleven non-A and non-B chronic hepatitis patients without HCC who had the same profiles of anti-HCV, HCV-RNA, and HBsAg were tested for HBV by PCR. As a control group, sera were obtained from 15 patients with HCC and 30 non-A and non-B chronic hepatitis patients without HCC; both were anti-HCV, HCV-RNA, and HBsAg negative and tested for HBV PCR. Of the 616 patients with HCC, 450 (73.1%) had current HBV infection, 48 (7.8%) had anti-HCV antibodies, and nine (1.5%) had viral markers of both HCV and HBV by serological profiles. Of the 27 patients with HCV viraemia and HBsAg seronegativity (16 with HCC; 11 with non-A non-B chronic hepatitis), 14 (51.9%) showed HBV viraemia by PCR. In contrast, of the 75 patients in the control group (45 with HCC; 30 with non-A and non-B chronic hepatitis) who were both HCV PCR negative and HBsAg negative, five (11.1%) showed HBV viraemia by PCR. The PCR for HBV revealed coexistent HBV viraemia in HCV viraemia patients, despite HBsAg negativity by EIA. In HBV-endemic areas, the possibility of coinfection of HBV in HBsAg-negative patients with HCV viraemia should be considered and molecular analysis for HBV-DNA performed.     

Low‐level hepatitis C viremia and humoral immune response to NS4 in chronic hepatitis B virus‐hepatitis C virus coinfection

Background: There is a limited amount of published data on the interference of hepatitis B virus (HBV) on hepatitis C virus (HCV). The aim of this study was to investigate the effect of concurrent HBV infection on serum titers of HCV RNA and HCV antibody profiles in chronic HCV infection. Methods: The clinical and virological profiles (serum titers of HCV RNA, HCV genotypes and antibody profiles) of 25 patients with chronic HBV‐HCV coinfection were compared with those of 25 age‐ and sex‐matched patients with HCV infection alone. Results: Among the 25 patients with HBV‐HCV coinfection, only 3 were found hepatitis Be antigen (HBeAg) and HBV DNA positive by hybridization assays, and the other 11 were found HBV DNA positive by polymerase chain reaction. Genotype 1b was dominant in both HBV‐HCV coinfection and HCV infection alone (64% versus 84%, P?>?0.1). Patients with HBV‐HCV coinfection had significantly lower alanine aminotransferase (ALAT) levels and inflammatory scores but higher fibrosis scores than those with HCV infection alone. Serum titers of HCV RNA were significantly lower in HBV‐HCV coinfection than in HCV infection alone. The frequency and relative intensity of antibody response to core, E2/NS1, NS3, and NS5 showed no significant difference between the two groups, but antibody response to NS4 was diminished significantly in HBV‐HCV coinfection. Conclusions: In HBV‐HCV coinfection, serum levels of HBV DNA are usually low or undetectable. Concurrent HBV infection, however, could interfere with HCV replication and suppress antibody response to NS4. The biological significance of selective inhibition of humoral immune response to NS4 in HBV‐HCV coinfection should be further studied.     

A comparative review of HLA associations with hepatitis B and C viral infections across global populations

Hepatitis B (HBV) and hepatitis C (HCV) viral infection or co-infection leads to risk of development of chronic infection, cirrhosis and hepatocellular carcinoma (HCC). Immigration and globalization have added to the challenges of public health concerns regarding chronic HBV and HCV infections worldwide. The aim of this study is to review existing global literature across ethnic populations on HBV and HCV related human leukocyte antigen (HLA) associations in relation to susceptibility, viral persistence and treatment. Extensive literature search was conducted to explore the HLA associations in HBV and HCV infections reported across global populations over the past decade to understand the knowledge status, weaknesses and strengths of this information in different ethnic populations. HLA DR13 is consistently associated with HBV clearance globally. HLADRB1*11/*12 alleles and DQB1*0301 are associated with HBV persistence but with HCV clearance worldwide. Consistent association of DRB1*03 and *07 is observed with HCV susceptibility and non-responsiveness to HBV vaccination across the population. HLA DR13 is protective for vertical HBV and HCV transmission in Chinese and Italian neonates, but different alleles are associated with their susceptibility in these populations. HLA class Ⅰmolecule interactions with Killer cell immunoglobulin like receptors (KIR) of natural killer (NK) cells modulate HCV infection outcome via regulating immune regulatory cells and molecules. HLA associations with HBV vaccination, interferon therapy in HBV and HCV, and with extra hepatic manifestations of viral hepatitis are also discussed. Systematic studies in compliance with global regulatory standards are required to identify the HLA specific viral epitope, stage specific T cell populations interacting with different HLA alleles during disease progression and viral clearance of chronic HBV or HCV infections among different ethnic populations. These studies would facilitate stage specific therapeutic strategies for clearance of HBV and HCV infections or co-infections across global populations and aid in identification of HBV-HCV combined vaccine. HLA associations of chronic HBV or HCV development with confounding host factors including alcohol, drug abuse, insulin resistance, age and gender are lacking and warrant detailed investigation across global populations.     

Clinical aspects and outcomes of volunteer blood donors testing positive for hepatitis‐C virus infection in Taiwan: a prospective study

Abstract: Background/Aim: The natural history of hepatitis‐C virus (HCV) infection has been explored in volunteer blood donors, but not yet in hepatitis‐B endemic areas. Whether previous or concurrent hepatitis‐B virus (HBV) infection influences the natural history of HCV infection remains unknown. Thus, we followed the anti‐HCV‐positive blood donors who had past or concurrent HBV infection in Taiwan. Methods: From 1992 to 1993, 1588 anti‐HCV reactive volunteer blood donors were referred to us from the Taipei Blood Center and 879 (55%) repeatedly reactive for anti‐HCV were enrolled. Two hundred and forty‐three donors (HCV RNA seropositive rate 49% by polymerase chain reaction (PCR)) received regular follow‐ups (mean period: 4.9 years) with their liver disease status determined mainly by clinical and biochemical parameters, serum alpha‐fetoprotein level and imaging studies. Hepatitis‐C virus genotype and occult HBV infection were determined by PCR‐based assays. Results: Of the initial 879 subjects, 250 (28%) had chronic hepatitis, nine (1%) had liver cirrhosis (LC) and two (0.2%) had hepatocellular carcinoma (HCC) already. In the 243 regularly followed donors, 30% had repeatedly normal serum alanine aminotransferase (ALT) and 70% had more than once elevated ALT. Cirrhosis developed in four (1.6%; follow‐up period range: 2–6 years) and HCC in two (0.8%; follow‐up period: 3 and 4 years, respectively). Distribution of HCV genotype and hepatitis‐B surface antigen (HBsAg) did not differ between those with and those without elevation of ALT. Of the 15 donors with LC and/or HCC, only 1(7%) was positive for both HBsAg and HBV DNA and the other 14 were negative for both HBsAg and serum HBV DNA. Conclusions: Incidentally detected hepatitis‐C was progressive in a small proportion of anti‐HCV‐positive volunteer blood donors in Taiwan. Occult HBV infection played a minimal role in the development of LC in this donor population.     

MBL2 and MASP2 gene polymorphisms in patients with hepatocellular carcinoma

Summary.  The pathogenesis of hepatocellular carcinoma (HCC) is not fully understood, but the majority of patients with HCC are associated with hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. Mannan-binding lectin (MBL) is a collectin that can act directly as opsonine or activate MBL-associated serine proteases (MASPs) thus initiating the antibody-independent pathway of the complement system. In our study, we analysed two MBL2 and MASP2 functional polymorphisms ( MBL2 allele A/0 and MASP2 D120G) as well as MASP2 polymorphism (Y371D) responsible for an amino acidic change in the protein in 215 HCC patients (HBV-infected, HCV-infected, HBV/HCV co-infected and patients with HCC with no viral infection) and 164 healthy controls to give new insights regarding the role of these two molecules in HCC and viral infection pathogenesis. No significant association was found between MBL2 or MASP2 alleles or genotypes, neither comparing the total patients with HCC and healthy controls nor between the different groups of HCC subjects divided for type of viral infection. Also, dividing the total HCC patients group into low MBL producer (A0 and 00 genotypes) and normal producer (AA genotype) and comparing MASP2 polymorphisms in these two groups, no significant differences were found. Our data do not seem to suggest a role for MBL2 and MASP2 polymorphisms in HCC susceptibility either for HBV–HCV infection-dependent HCC or for HCC raised as a consequence of exposure to different risk factors.     

Hepatitis B and hepatitis C viruses: a review of viral genomes,viral induced host immune responses,genotypic distributions and worldwide epidemiology

Hepatitis B and hepatitis C viruses (HCV) are frequently propagating blood borne pathogens in global community. Viral hepatitis is primarily associated with severe health complications, such as liver cirrhosis, hepatocellular carcinoma, hepatic fibrosis and steatosis. A literature review was conducted on hepatitis B virus (HBV), HBV genome, genotypic distribution and global epidemiology of HBV, HCV, HCV genome, HCV and host immune responses, HCV genotypic distribution and global epidemiology. The valued information was subjected for review. HBV has strict tissue tropism to liver. The virus infecting hepatocytes produces large amount of hepatitis B surface antigen particles which lack the DNA. It has capability to integrate into host genome. It has been found that genotype C is most emerging genotype associated with more severe liver diseases (cirrhosis). The approximate prevalence rate of genotype C is 27.7% which represents a major threat to future generations. Approximately 8% of population is chronic carrier of HBV in developing countries. The chronic carrier rate of HBV is 2%-7% in Middle East, Eastern and Southern Europe, South America and Japan. Among HCV infected individuals, 15% usually have natural tendency to overcome acute viral infection, where as 85% of individuals were unable to control HCV infection. The internal ribosomal entry site contains highly conserved structures important for binding and appropriate positioning of viral genome inside the host cell. HCV infects only in 1%-10% of hepatocytes, but production of tumor necrosis factor alpha (from CD8+ cells) and interferon-gamma cause destruction of both infected cells and non-infected surrounding cells. Almost 11 genotypes and above 100 subtypes of HCV exists worldwide with different geographical distribution. Many efforts are still needed to minimize global burden of these infections. For the complete eradication of HBV (just like small pox and polio) via vaccination strategies, sincere efforts would be required from government and nongovernmental organizations.     

Prevalence of hepatitis C antibody in patients with chronic liver disease and hepatocellular carcinoma in Korea

Summary. To investigate the contribution of hepatitis C virus (HCV) to chronic liver disease and hepatocellular carcinoma (HCC) in Korea, antibodies to HCV (anti-HCV) were tested by enzyme immunoassay in 1759 patients with chronic liver disease and HCC, and in 808 healthy adults. The prevalence of anti-HCV was 1.6% in 808 controls. Anti-HCV was present in 32 (7.7%) of 418 hepatitis B surface antigen (HBsAg)-positive and 128 (53.1%) of 241 HBsAg-negative patients with chronic hepatitis, 16 (6.0%) of 265 HBsAg-positive and 90 (30.5%) of 295 HBsAg-negative patients with liver cirrhosis, and 16 (4.8%) of 330 HBsAg-positive and 61 (29.0%) of 210 HBsAg-negative patients with HCC. Antibodies to hepatitis B core antigen (anti-HBc) were present in 80–88% of patients who were seropositive for anti-HCV and seronegative for HBsAg. Among the sera from 114 patients with HBsAg-negative and anti-HCV-positive chronic liver diseases, HBV DNA and HCV RNA were detected by polymerase chain reaction (PCR) in 54 (47.4%) and 61 (53.3%), respectively. Both HBV DNA and HCV RNA were detected in 4 (4.4%) samples. The mean age of the patients with both HBsAg and anti-HCV was not different from that of patients who were seropositive for HBsAg alone. These findings indicate that current and/or past HBV infection is still the main cause of chronic liver disease in Korea. Although multivariate analysis showed that anti-HCV is a risk factor for chronic hepatitis, cirrhosis of the liver and HCC, PCR data for HBV DNA and HCV RNA indicate that HCV infection plays only a minor role in HBsAg-positive as well as in HBsAg-negative liver disease and does not accelerate the development of HCC in HBV carriers.