Serum concentration of sFas and sFasL in healthy HBsAg carriers,chronic viral hepatitis B and C patients

AIM:To estimate the amount of apoptosis among healthy HBsAg carriers,patients with chronic HBV infection treated wibh lamivudine and patients with chronic HCV infection treated with interferon alpha and ribavirin.Activity of apoptosis was evaluated by serum sFas/sFasL concentration measurement. Moreover dependence between apoptosis and HBV-DNA or HCV-RNA levels was studied. METHODS:Eighty-six persons were included into study:34 healthy HBsAg carders,33 patients with chronic HBV infecl^on and 19 patients with chronic HCV infection.Serum levels of sFas/sFasL were measured by ELISA assay.HBV-DNA and HCV-RNA were measured by RT-PCR assay.Levels of sFas/sFasL were determined before and 2 and 12 wk after therapy in patients with chronic hepatitis B and C infection. HBV-DNA or HCV-RNA was detected before treatment and 6 mo after treatment. RESULTS:Twenty-four (71%) healthy HBsAg carders showed HBV-DNA over 10~5/mL,which was comparable to the patients with chronic hepatitis B.independently from HBV-DNA levels, the concentration of sFas among healthy HBsAg carders was comparable to healthy persons.Among patients with chronic hepatitis B and C,the concentration of sFas was significantly higher in comparison to healthy HBsAg carriers and healthy persons.In chronic hepatitis B patients the concentration of sFas was decreased during lamivudine treatment.Among chronic hepatitis C patients the concentration of sFas was increased during IFN alpha and ribavirin treatment,sFasL was not detected in control group.Furbhermore sFasL occurred more frequently in chronic hepatitis C patients in comparison to chronic hepatitis B patients. CONCLUSION:There are no correlations between apoptosis and HBV-DNA levels.However ther is an association between apoptosis and activity of inflammation in patients with chronic HBV infection.Apoptosis can be increased in patients with chronic hepatitis C by effective treatment which may be a result of apoptosis stimulation by IFN-α.

Host and viral factors contributing to CD8+ T cell failure in hepatitis C virus infection

Virus-specific CD8+ T cells are thought to be the major anti-viral effector cells in hepatitis C virus (HCV) infection. Indeed, viral clearance is associated with vigorous CD8+ T cell responses targeting multiple epitopes. In the chronic phase of infection, HCV-specific CD8+ T cell responses are usually weak, narrowly focused and display often functional defects regarding cytotoxicity, cytokine production, and proliferative capacity. In the last few years, different mechanisms which might contribute to the failure of HCV-specific CD8+ T cells in chronic infection have been identified, including insufficient CD4+ help, deficient CD8+ T cell differentiation, viral escape mutations, suppression by viral factors, inhibitory cytokines, inhibitory ligands, and regulatory T cells. In addition, host genetic factors such as the host’s human leukocyte antigen (HLA) background may play an important role in the efficiency of the HCV- specific CD8+ T cell response and thus outcome of infection. The growing understanding of the mechanisms contributing to T cell failure and persistence of HCV infection will contribute to the development of successful immunotherapeutical and -prophylactical strategies.

Expression and significance of HBV genes and their antigens in human primary intrahepatic cholangiocarcinoma

AIM To explore the etiology and pathogenesis of human primary intrahepatic cholangiocarcinoma, the expression of HBV genes and HBV-antigens was detected in the cancerous tissue and its surrounding hepatic tissues.METHODS HBV-antigens were detected by immunohistochemical technique and HBV genes were examined with in situ hybridization.RESULTS In 20 cases of cholangiocarcinoma, the positive detection rate of HBxAg, pre-S1, pre-S2, HBsAg and HBcAg was 75%, 40%, 40%, 10% and 0%, respectively, and in the surrounding hepatic tissues of 19 cases the positive rates were 84.2%, 47.9%, 47.9%, 31.6% and 31.6%. Among 40 cases of cholangiocarcinoma, the positive rate of HBV-DNA, x gene, pre-s gene, s gene and s gene fell on 77.5%, 70.0%, 47.5%, 40% and 42.5%, respectively, and of the surrounding hepatic tissues in 33 cases, 87.9%, 84.8%, 63.6%, 69.7% and 66.7%.CONCLUSION The development of human primary intrahepatic cholangiocarcinoma bears a close relationship with chronic persistent HBV infection. Particularly, the x gene of HBV and its protein (HBxAg) might play an important role in pathogenesis of hepatic carcinoma.A large number of studies indicate a close relationship between human primary hepatocellular carcinoma and hepatitis B virus (HBV) infection, which is considered generally as an important factor in the development of hepatic carcinoma[1,2]. In human primary hepatic carcinoma, hepatocellular carcinoma is more frequently encountered, while intrahepatic cholangiocarcinoma (ChC), including hepatocholangiocarcinoma (HChC), is relatively less, being 8%-10%[3]. For a long time, the etiology and pathogenesis of intrahepatic cholangiocarcinoma have been unclear. A few reports considered it to be related to infestation with clonorchiasis sinensis[4,5], but never involved with HBV infection. We used immunohistochemical technique and in situ hybridization methods to detect HBV genes and their -related antigens in the tissues of intrahepatic cholangiocarcinoma and its surrounding hepatic tissues for the purpose of exploring the etiology and pathogenesis of intrahepatic cholangiocarcinoma.

Preparation and application of monoclonal antibodies against hepatitis C virus nonstructural proteins

AIM To prepare hybridoma cell lines which secrete anti HCV recombinant NS3 and NS5 proteins′ monoclonal antibodies, and to evaluate their usage in the study of the distribution of HCV NS3 and NS5 antigen in liver tissues. METHODS The hybridoma cell lines were raised using the spleen cells of BALB/C mouse immunized with recombinant NS3 and NS5 proteins according to the conventional protocols. The antibody secreting cells were screened using solid phase ELISA and cloned by limited dilution method. In order to determine the specificity of these hybridoma cell lines, the culture supernatant of these cells was western blot assayed with expression and nonexpresion E. coli and ELISA with other antigens, including HCV core and NS3 and HBsAg. Immunohistochemistry of 51 cases paraffin embedded liver tissues was performed to determine the distribution of HCV NS5 antigen as well as NS3 antigen in liver tissues. RESULTS Eight hybridoma cell lines secreting monoclonal antibodies against HCV NS3 and NS5 proteins were raised. They are named 2B6, 2F3, 3D8, 3D9, 8B2, 6F11, 4C6 and 7D9. Among them only 2B6 against NS3 protein can react with the polypipetides of C7 that is another recombinant polypipetides of NS3 gene. Others have no reaction with HCV core and HBsAg of HBV, and there is no cross reaction between NS3Ag and anti NS5Ag McAb and between NS5Ag and anti NS3 McAb. The immunohistochemistry results indicate that no HCV antigen was detected in the specimens of HBV infection in 20 cases. In 31 HCV infected specimens the positive rate of NS3Ag and NS5Ag are 51 6% (16/31) and 54 9% (17/31), respectively. There were six pure HCV infected specimens in these 31 specimens and half of them were HCV NS3Ag and NS5Ag positive. In the co infection of HBV and HCV group the positive rate of NS3Ag and NS5Ag were 52% (13/25) and 56% (14/25), respectively, almost the same with that of pure HCV infected group. The positive rates of HCV antigens were 70 6% (12/17) and 76 5% (13/17) in CAC patients. CONCLUSION The monoclonal antibodies we prepared are specific to the recombinant HCV NS3 and NS5 proteins and can be used in the clinical immunohistochemistry diagnosis.

Hepatitis C virus infection of human hepatoma cell line 7721 in vitro

AIM: To establish a cell culture system with long-term replication of hepatitis C virus in vitro. METHODS: Human hepatoma cell line 7721 was tested for its susceptibility to HCV by incubating with a serum from a patient with chronic hepatitis C. Cells and supernatant were harvested at various phases during the culturing periods. The presence of HCV RNA, the expression of HCV antigens in cells and/or supernatant were examined by RTPCR, in situ hybridization and immunohistochemistry respectively. RESULTS: The intracellular HCV RNA was first detected on d2 after infection and then could be intermittently detected in both cells and supernatant over a period of at least three months. The expression of HCV NS3,CP10 antigens could be observed in cells. The fresh cells could be infected by supernatant from cultured infected cells and the transmission of viral genome from HCV-infected 7721 cells to PBMCs was also observed. CONCLUSION: The hepatoma line 7721 is not only susceptible to HCV but also supports its long-term replication in vitro.

Hepatitis C virus may infect extrahepatic tissues in patients with hepatitis C

AIM To explore the status of extrahepatichepatitis C virus(HCV)infection and replicationin hepatitis C patients,and its potentialimplication in HCV infection and pathogenicity.METHODS By reverse-transcriptase poly-merase chain reaction(RT-PCR),in situhybridization(ISH)and immunohistochemistry,HCV RNA,HCV replicative intermediate(minus-strand of HCV RNA),and HCV antigens weredetected in 38 autopsy extrahepatic tissuespecimens(including 9 kidneys,9 hearts,9pancreas,5 intestines,2 adrenal glands,2spleens,1 lymph node,and 1 gallbladder)from 9hepatitis C patients,respectively;and thestatus of HCV replication in extrahepatic tissueswas studied.RESULTS By RT-PCR,all 9 patients werepositive for HCV RNA in kidney,heart,pancreas,and intestine,but only 6(66.7%)patients were positive for HCV replicativeintermediate.HCV RNA and HCV antigens weredetected in kidney,heart,pancreas,intestine,adrenal gland,lymph node,and gallbladder in 5(55.6%)and 6(66.7%)patients by ISH andimmunohistochemistry,respectively.HCV RNA and HCV antigens were not detected in theseextrahepatic organs in 3(33.3%)patients,although their livers were positive for HCV.HCVreplicative intermediate detected by RT-PCR wasconsistent with HCV RNA and HCV antigensdetected by ISH and immunohistochemistry(Kappa=0.42-0.75).HCV RNA and HCVantigens were detected in myocardial cells,epithelial cells of intestinal gladular,interstitialcells of kidney,epithelial cells of tubules andglomerulus,pancreas acinar cells and epithelialcells of pancreatic duct,epithelial cells ofmucous membrane sinus of gallbladder,cortexand medulla cells in adrenal gland,andmononuclear cells in lymph node.HCV RNA wasalso detected in bile duct epithelial cells,sinusoidal cells,and mononuclear cells in livertissues by ISH.CONCLUSION HCV can infect extrahepatictissues,and many various tissue cells maysupport HCV replication;extrahepatic HCVinfection and replication may be of'concomitantstate'in most of patients with hepatitis C.Theinfected extrahepatic tissues might act as areservoir for HCV,and play a role in both HCVpersistence and reactivation of infection.HCVas an etiologic agent replicating and expressingviral proteins in extrahepatic tissues itselfcontributes to extrahepatic syndromeassociated.HCV infection in a few patients withchronic HCV infection.

TT virus and hepatitis G virus infections in Korean blood donors and patients with chronic liver disease

AIM:To determine the prevalences of TTV and HGV infections among blood donors and patients with chronic liver disease in Korea,to investigate the association of TTV and HGV infections with blood transfusion,and to assess the correlation between TTV and HGV viremia and hepatic damage. METHODS:A total of 391 serum samples were examined in this study.Samples were obtained from healthy blood donors(n=110),hepatitis B surface antigen(HBsAg)-positive donors(n=112),anti-hepatitis C virus(anti-HCV)-positive donors(n=69),patients with type B chronic liver disease (n=81),and patients with type C chronic liver disease(n=19). Trv DNA was detected using the hemi-nested PCR.HGV RNA was tested using RT-PCR.A history of blood transfusion and serum levels of alanine aminotransferase(ALT)and aspartate aminotransferase(AST)were also determined. RESULTS:TTV DNA was detected in 8.2%of healthy blood donors,16.1%of HBsAg-positive donors,20.3%of anti- HCV-positive donors,21.0%of patients with type B chronic liver disease,and 21.1%of patients with type C chronic liver disease.HGV RNA was detected in 1.8%of healthy blood donors,1.8%of HBsAg-positive donors,17.4%of anti-HCV-positive donors,13.6%of patients with type B chronic liver disease,and 10.5%of patients with type C chronic liver disease.The prevalence of TTV and HGV infections in HBV- or HCV-positive donors and patients was significantly higher than in healthy blood donors(P<0.05), except for the detection rate of HGV in HBsAg-positive donors which was the same as for healthy donors.There was a history of transfusion in 66.7%of TTV DNA-positive patients and 76.9%of HGV RNA-positive patients(P<0.05).No significant increase in serum ALT and AST was detected in the TTV or HGV-positive donors and patients. CONCLUSION:TTV and HGV infections are more frequently found in donors and patients infected with HBV or HCV than in healthy blood donors.However,there is no significant association between TTV or HGV infections and liver injury.

Significance of hepatitis B virus surface antigen, hepatitis C virus expression in hepatocellular carcinoma and pericarcinomatous tissues

AIM： To investigate the correlation between hepatitis B virus surface antigen （HBsAg）, hepatitis C virus （HCV） expression in hepatocellular carcinoma （HCC）, the HAI score of the noncancerous region of the liver and the serum Alpha fetoprotein （AFP） level. METHODS： The patterns of HBsAg and HCV in 100 cases of HCC and their surrounding liver tissues were studied on paraffin-embedded sections with immunohistochemistry, the histological status was determined by one pathologist and one surgeon simultaneously using the hepatitis activity index （HAIl score, and AFP was detected by radioimmunity. The study included 100 consecutive patients who underwent curative resection for HCC. Based on HBsAg and HCV expression, the patients were classified into 4 groups： patients positive for HBsAg （HBsAg group）, patients positive for HCV （HCV group）, patients negative for both HCV and HBsAg （NBNC group） and patients positive for both HBsAg and HCV （BC group）. RESULTS： The BC group had significantly higher HAI scores than the other three groups. （BC 〉 HCV 〉 HBsAg 〉 NBNC）. HBV and HCV virus infection was positively correlated with HAI （rs = 0.39, P = 0.00011. The positive rate of AFP （85.7%） and the value of AFP （541.2 ng/mL） in the group with HBV and HCV co-infection were the highest among the four groups. The positive rate （53.3%） of AFP and the value of AFP （ 53.3 ng/mL） in the group with none-infection of HBV and HCV were the lowest. HBV and HCV virus infection was positively correlated with AFP（rs = 0.38, P = 0.0001）. CONCLUSION： The AFP increase in patients with liver cancer was positively correlated with the infection of HBV and HCV. The-serum AFP elevation by the infection of HBV and HCV is one of mechanisms which lead to hepatocarcinogenesis, and the antivirus intervening treatment of hepatitis is significant for the prognosis of liver cancer. From our Spearman＇s rank correlation analysis, we can conclude that the severity of virally induced inflammation is correlated with HBsAg and HCV expression in HCC tissues and noncancerous tissues. Prior co-infection of HBV in HCV patients may be an adverse risk factor for intrahepatic inflammation.

Distribution and significance of hepatitis C virus C33c antigen, core antigen and HBxAg in human primary intrahepato-cholangiocarcinoma tissues

To study the distribution and significance of hepatitis C virus (HCV) C33c antigen, and core antigen in human primary intrahepato-cholangiocarcinoma tissues (PIC). Methods: Immunohistochemistry was used to detect HCV antigen and HBxAg. Results: HCV C33c antigen was present in the cytoplasm of cancer cells and hepatic cells and HCV core antigen was present mainly in the nuclei of cancerous tissues and in the cytoplasm of pericancerous liver tissues. In cancerous tissues and pericancerous tissues the positive rates of HCV C33c antigen were 60% (21/35) and 100% (21/21 ) respectively; the positive rates of HCV core antigen were 87. 8% (29/ 33 ) and 61. 9% (13/21) respectively; the positive rates of HBxAg were 74. 3% (26/35) and 76. 2% (16/21) respectively; the simultaneously positive rates of C33c and HBxAg were 48. 6% (17/35) and 76. 2% (16/21). Conclusion: Besides hepatitis B virus (HBV) infection, HCV infection may play an important role in the carcinogenesis of PIC.

丙型肝炎肝组织中HCV RNA和HCV NS5抗原表达及意义

目的研究丙型肝炎肝组织中ＨＣＶＲＮＡ与ＨＣＶＮＳ５抗原分布及其与肝组织损伤的关系．方法应用原位杂交和免疫组化方法检测３４例丙型肝炎病毒（ＨＣＶ）感染者肝组织中ＨＣＶＲＮＡ和ＨＣＶＮＳ５抗原表达状况，采用Ｋｎｏｄｅｌ方法评价肝组织病理损伤程度．结果分别有２１例（６１８％）和２４例（７０６％）患者肝组织中检出ＨＣＶＲＮＡ和ＨＣＶＮＳ５抗原．ＨＣＶＲＮＡ阳性信号主要位于肝细胞浆中，在胆管上皮细胞和炎性浸润细胞中也可检出，其分布与肝组织炎症坏死无固定解剖学关系．ＨＣＶＲＮＡ与肝组织中ＨＣＶＮＳ５抗原表达正相关，但二者在肝组织中的分布存在一定差异．多因素分析显示ＨＣＶＮＳ５抗原的表达与肝组织损伤相关．结论丙型肝炎肝组织中ＨＣＶＲＮＡ和ＨＣＶＮＳ５抗原表达相关。

HDV/HBV感染树鼩肝组织中Bcl_2/Bax表达和肝细胞凋亡

目的 探讨ＨＤＶ感染树Ｑｕ肝组织中Ｂｃ１２／Ｂａｘ表达与ＨＤＶ感染之间的关系，以及Ｂｃ１２／Ｂａｘ在丁型肝炎肝细胞凋亡中的作用。方法 采用免疫组化技术对４５份ＨＤＶ感染树Ｑｕ肝组织中ＨＤＡｇ，Ｂｃ１２／Ｐａｘ的表达进行了检测；应用原位末端标记技术对肝细胞凋亡进行检测；并应用免疫组化双重染色对ＨＤＡｇ，对肝细胞凋亡进行检测；并应用免疫组化双重染色对ＨＤＡｇ。

HCV核心基因cDNA真核表达载体的构建及其表达

丙型肝炎病毒(HCV)感染具有明显的慢性化倾向。与肝细胞癌(HCC)发生关系密切,是肝癌的病因之一.近年来HCV 核心蛋白的作用受到重视,被认为具有基因调节功能.我们采用基因重组技术构建 HCV 核心基因 cDNA真核表达质粒,导入 HepG2细胞株,以期获得永久性表达 HCV核心蛋白的细胞,为进一步探讨 HCV

肝癌组织、癌旁组织中HBsAg、HCV抗原表达与T细胞亚群及NK活性的相关性研究

研究肝癌组织、癌旁组织中HBsAg、HCV抗原表达与T细胞亚群及NK活性的相关性。采用免疫组织化学方法(SP法)对肝癌组织及癌旁组织中的HBsAg、HCV抗原表达进行了标记和分析,同时对外周血T细胞亚群及 NK活性进行检测。肝癌患者中,CD4+细胞减少,CD8+细胞升高,CD4+／CD8+比值及NK细胞的活性均比正常对照组明显降低,且HBsAg阳性、HCV抗原阳性者比阴性者下降更显著。肝癌组织、癌旁组织中HBsAg、HCV抗原表达与外周血T细胞亚群及NK活性Spearman相关性分析,与NK细胞、CD4+细胞、CD8+细胞、CD4+／CD8+相关系数分别为-0．67,-0．28,0．35,-0．50(P<0．001)。肝癌患者出现免疫紊乱与乙肝、丙肝病毒感染有关,且混合感染者免疫功能紊乱较显著,提示抗病毒治疗可能改善肝癌患者的免疫功能。

抗HCV-HRP结合物的制备及其在检测肝组织HCAg中的应用

采用ELISA筛选抗HCV阳性血清,以改良过碘酸盐法制备抗HCV-HRP结合物,用作第一抗体,与兔抗HRP及兔PAP—道建立了改良单桥PAP法。将其试用于检测肝组织中HCAg,并与直接酶标法进行比较。由于本法能消除以同源性抗体作一抗时内源性IgG及其类似物干扰,克服PAP应用中种系限制,其敏感性,显色强度及阳性细胞数目均明显优于直接EHA,在免疫组化研究中具有较高应用价值。

HCV分片段抗原EIA与重组免疫印迹法分析检测HCV抗体的比较研究

【目的】探讨国产丙型肝炎病毒(HCV)分片段抗体试剂的敏感性和特异性,为丙型肝炎的早期诊断和替代昂贵的进口重组免疫印迹法确认试剂(HCV RIBA3.0)提供实验依据。【方法】用HCV分片段抗体试剂检测经确认的标本中HCV-C、NS3、NS4、NS5抗体并与HCV RIBA3.0比较。【结果】82份样品中80份判定为阳性,阳性率为97.56%,2份判定为可疑,为2.4%,40份阴性样品中有2份判定可疑,为5.00%。【结论】国产分片段抗体检测试剂检测HCV抗体,与美国第三代RIBA3.0试剂的检测符合率基本一致,有低价高效的临床实用价值。

HGV/GBV-C与HCV混合感染者肝组织中相关病毒抗原表达

庚型肝炎病毒(HGV/GBV-C)的致病性是目前研究焦点之一,多数研究表明大多数HGV/GBV-C感染者体内常有两种或两种以上的肝炎病毒混合感染,并认为HGV/GBV-C感染对原有乙型肝炎病毒(HBV)或丙型肝炎病毒(HCV)感染的基础病变似无明显影响,但仅从血清学、临床表现及常规病理角度试图说明HGV/GBV-C对机体有无损害的研究工作是很困难,我们应用免疫组织化学技术对HGV/GBV-C与HCV混合感染者肝组织中HGV/GBV-C。HCV相关抗原表达进行研究,试图从免疫病理学角度探讨HGV/GBV-C对机体肝脏的致病性。 1

HGV/GBV-C与HCV混合感染者肝组织中相关病毒表达的免疫组化研究

目的 了解HGV/GBV-C与HCV混合感染者肝组织HGV/GBV-C相关抗原的分布状况,探讨HGV/GBV-C对肝脏的损害机制。方法 以抗HGV/GBV-C NS5单克隆抗体或抗HCV NS3单克隆抗体为试剂,采用免疫组织化学方法检测肝炎病人肝组织中HGV/GBV-C、HCV相关抗原表达。结果 56例肝炎病肝组织中HGV/GBV-C相关抗原表达阳性率为26.79％(15/56);HCV NS3抗原表达阳性率为39.29％(22/56)。HGV/GBV-C NS5抗原表达阳性信号主要位于肝细胞胞浆中,染色阳性细胞周围可见淋巴细胞浸润。结论 肝细胞中存在HGV/GBV-C相关抗原表达,其编码产物可能作为一种靶抗原,诱发免疫病理反应,免疫损伤可能是其发病机制之一。

人原发性肝细胞肝癌中丙型肝炎病毒C_（33c）抗原及HBxAg的分布及意义

作者应用抗ＨＣＶＮＳ３区Ｃ３３ｃ抗原２Ｂ６株单克隆抗体和抗ＨＢｘＡｇ多克隆抗体，采用ＡＢＣ法对１０２例人原发性肝细胞肝癌（ＰＨＣ）组织进行了ＨＣＶ及ＨＢＶ抗原定位研究。ＨＣＶＣ３。抗原及ＨＢｘＡｇ在ＰＨＣ中的阳性检出率分别是８１．４％及７４．５％，Ｃ３３ｃ抗原或ＨＢｘＡｇ阳性占所检病例９４．１％，相同病例二者同时阳性为６１．８％。１０２例ＰＨＣ中５０例有癌旁肝组织，其Ｃ３３ｃ抗原和ＨＢｘＡｇ的阳性检出率分别是６２％和９２％。ＨＣＶＣ３３ｃ抗原定位于肝癌细胞的胞浆内，胞核未见阳性信号。Ｃ３３ｃ抗原阳性细胞在ＰＨＣ中呈散在、局灶分布为主，在癌旁肝组织呈弥漫分布为主。本文结果提示ＨＣＶ感染在ＰＨＣ的发生中可能起重要作用。

肝外和肝组织内HCV抗原表达的特点及其意义

目的:探讨丙型肝炎患者肝外组织内丙型肝炎病毒（HCV）感染状况及其意义。方法:采用免疫组化法检测9例丙型肝炎患者肾、心、胰和肠等肝外组织内HCV抗原，并与肝组织内抗原表达进行对比研究。结果:9例患者肝组织和其中6例（66.7％）的4种肝外组织检出了HCV抗原。抗原定位于组织细胞浆内。肝外组织中抗原表达阳性细胞种类多，但未见明显病变。肝组织中仅肝细胞内抗原表达阳性，病变严重。结论:肝外组织存在HCV感染。与肝组织比较，肝外组织感染可能属一种伴随状态，肝脏是感染的中心器官。肝外组织被感染可能是丙型肝炎易慢性化的重要原因之一。

慢性丙型肝炎患者肝组织中HCV-RNA和HCV、NS_3抗原的研究

为了研究丙型肝炎的发病机理应用原位杂交和免疫级化方法检测了38例慢性肝炎患者肝内HCV－RNA和HCV、NS3。11例丙型肝炎患者肝细胞中8例HCV－RNA阳性，6例HCV、NS3阳性；17例乙、丙肝重叠感染者7例阳性；10例慢性乙肝患者中求发现阳性结果。肝内HCV－RNA和HCV、NS3阳性与否同肝组织学病理改变的严重性无关。结果表明HCV可能无直接致病作用。