慢性肝病患者肝组织HGV抗原的表达及意义

目的 探讨慢性肝病患者组织中庚型肝炎病毒（ＨＢＶ）表达与意义。方法 应用免疫组织化学方法以鼠抗ＨＧＶＮＳ５单克隆抗体检测１４２例慢性肝病患者肝组织中ＨＧＶ抗原，部分患者采用ＲＴ－ＰＣＲ方法检测春血清中ＨＧＶＲＮＡ。结果 １４２例肝病患者中，２９例组织中检出ＨＧＶ抗原，肝硬化组较慢性肝炎和肝癌组检出率高。阳性信号位于胞浆中，阳性细胞可成散在、簇状或弥漫性分布。阳性细胞周围可有炎性坏死；肝癌患者抗原阳     

地高辛素探针原位杂交检测非甲—非戊型肝炎肝组织中HGV RNA

目的观测ＨＧＶＲＮＡ在非甲－非戊型急慢性病毒性肝炎肝组织中的表达，对ＨＧＶ感染与急慢性病毒性肝炎发病的关系进行探讨。方法以地高辛素标记ＨＧＶｃＤＮＡ探针，对３６例血清非甲－非戊型急性和慢性病毒性肝炎患者石蜡包埋肝穿肝组织进行原位杂交，并对急性ＨＧＶ感染病例进行了随访观察。结果３６例肝病患者中，１１例（３０６％）肝组织中检出ＨＧＶＲＮＡ。其中急性重症肝炎１例（１／３），亚急性重症肝炎３例（３／６），急性轻型肝炎５例（５／１６）慢性肝炎２例（２／１１）。阳性信号表达于肝细胞胞浆及／或核内，在急性轻型肝炎，阳性信号多弥漫散在分布。而在慢性肝炎，则多呈片灶状靠近汇管区周围。在检出率和阳性细胞分布方面，原位杂交与免疫组化检测结果（３６１％，１３／３６）基本一致。８－３８个月后的急性轻型肝炎随访二次肝穿检测显示了肝组织中ＨＧＶＲＮＡ持持续存在。结论在急慢性非甲－非戊型病毒性肝炎肝组织中，ＨＧＶ感染较为常见，ＨＧＶ感染可能与急性病毒性肝炎的发病及慢性化有关。     

原发性肝癌患者血清和肝组织中庚型肝炎病毒基因的PCR检测

用逆转录－聚合酶链反应法（ＲＴ－ＰＣＲ）检测了原发性肝癌（ＰＬＣ）患者血清及肝癌和癌旁肝组织中的庚型肝炎病毒（ＨＧＶ）ＲＮＡ，以ＰＣＲ－双脱氧末端终止法测定了ＰＣＲ产物的核苷酸序列。结果显示，血清和肝组织中ＨＧＶＲＮＡ的检出率分别为１９．４％（１３／６７）和２５．７％（９／３５），且ＨＧＶＲＮＡ在肝癌组织呼吕旁肝组织中同时存在，血清和肝组织中ＨＧＶ ＲＮＡ检测结果的符合率为８５％；５′非编码区（５     

庚型肝炎患者肝组织中HGV表达的免疫组化研究

目的探讨庚型肝炎病毒（ＨＧＶ）在庚型肝炎肝组织中的表达状况与临床意义．方法应用免疫组织化学ＰＡＰ方法以鼠抗ＨＧＶＮＳ５单克隆抗体对庚型肝炎患者２０例（急性肝炎２例，慢性肝炎８例，肝硬变１０例，血清ＨＧＶＲＮＡ皆阳性）肝组织中ＨＧＶ抗原进行检测．结果庚型肝炎患者２０例中，８例（４０％）肝组织中检出ＨＧＶ抗原；不同病期检出率分别为：急性肝炎０／２（０％），慢性肝炎２／８（２５％），肝硬变６／１０（６０％），各组间差异无显著意义；阳性信号位于肝细胞胞质；阳性细胞可位于炎症坏死灶周围；抗原阳性与阴性组间肝组织炎症活动度及血清谷丙转氨酶水平无明显差别，但阳性组纤维化指数较高．结论ＨＧＶ感染及其在肝组织中表达可能与肝组织纤维化有一定关系     

血清抗-HBs阳性慢性肝病患者的病因研究

目的部分抗－ＨＢｓ阳性者仍有活动性肝病存在，其病因还不十分清楚．本研究旨在探讨血清抗ＨＢｓ阳性慢性肝病患者的病因．方法应用套式聚合酶链反应检测血清抗ＨＢｓ阳性慢性肝病患者血清中ＨＢＶＤＮＡ和ＨＣＶＲＮＡ．患者３２例，男２５例，女７例，平均年龄４１７岁（２１岁～６３岁），其中慢性肝炎１８例，肝硬变１４例．９例慢性肝炎和５例肝硬变经肝活检证实，其余为临床诊断．结果血清中ＨＢＶＤＮＡ和ＨＣＶＲＮＡ的检出率分别为６２５％（２０／３２）和２８１％（９／３２）；ＨＢＶＤＮＡ和（或）ＨＣＶＲＮＡ总检出率为８１３％（２６／３２）．结论血清抗ＨＢｓ阳性慢性肝病患者的病因多数与ＨＢＶ和（或）ＨＣＶ感染有关．     

庚型肝炎病毒在慢性肝炎肝硬化中致病性及病理特征

探讨ＨＢＶ在慢性肝炎肼硬化当中感染率、临床脑病理特征,应用ＥＬＩＳＡ法检测血清抗－ＨＧＶ,用ＨＧＶＮＳ５抗原制备ＭＣＡｂ,检测５４例慢笥肝炎硬化患者肝组织中ＨＧＶ抗原,同时应用ＳＰ法分别对肝组织进行ＨＢｓＡｇ、ＨＢｃＡｇ、ＨＣＶ ＮＳ３Ａｇ肝脏免疫组化检测。结果提示５４例肝病患者肝组织检出２７．７８％ＨＧＶ抗原阳性。其中２４例慢性肝炎轻度中５例;１６例慢性肝炎中度中５２称;１５例肝硬中５例。ＨＧＶ     

24例非甲—戊型肝炎患者血清庚肝病毒RNA检测结果分析

采用逆转录－套式聚合酶链反应（ＲＴ－ｎＰＣＲ）技术对２４例非甲－戊（Ａ－Ｅ）型肝炎患者进行庚肝病毒ＲＮＡ（ＨＧＶ－ＲＮＡ）检测。结果：ＨＧＶ－ＲＮＡ阳性６例（２５．０％），其中急性肝炎１例（１／９）、慢性肝炎２例（２／９）、肝为肝硬变３例（３／４）；１例有输血史，余５例均无输血或血浆史。提示庚肝病毒可能为非Ａ－Ｅ型肝炎的病原体之一，且存在输血外传播途径。     

庚型肝炎病毒RNA、NS5抗原在肝组织中表达的研究

研究ＨＧＶ ＲＮＡ及ＨＧＶ抗原在肝组织中的表达。方法 对１７例ＨＧＶ血清标志阳性患者进行了肝组织ＨＧＶ ＲＮＡ的原位杂交及免疫组织化学的研究。结果 原位杂交ＨＧＶ ＲＮＡ阳性８例，阳性率４７．０５％，阳性信号均存在于肝细胞的胞浆中；免疫组化３例ＨＧＶ ＮＳ５抗原阳性，阳性率１７．６４％，均为胞浆型。     

庚型肝炎肝脏免疫组化研究

目的探讨庚型肝炎病毒（ＨＧＶ）抗原在肝组织中定位，进一步研究ＨＧＶ引起肝脏损害的机制。方法采用ＨＧＶＮＳ５区抗原制备单克隆抗体（ＭｃＡｂ），对４例经临床和病理确诊的血清ＨＧＶＲＮＡ阳性的慢性庚型肝炎患者肝活检标本，进行免疫组化观察。结果１例呈阳性染色，光镜观察显示：特异染色大部分定位于肝细胞胞浆中，部分有核着色和膜型染色，呈黄色或棕黄色颗粒状，阳性细胞数量少，大多散在分布，部分呈灶性分布；阳性细胞周围可见较多淋巴细胞浸润。结论ＨＧＶ抗原可在肝细胞中定位，大多呈胞浆型，部分呈核型和膜型，ＨＧＶ属嗜肝病毒；免疫损伤可能参与了庚型肝炎的肝脏损伤机制     

血液病患者中庚型肝炎病毒检测及感染情况研究

目的：了解武汉地区血液病患者中庚型肝炎病毒（ＨＧＶ）的感染情况,探讨ＨＧＶ的传播途径。方法：采用酶联免疫吸附试验（ＥＬＩＳＡ）及逆转 录聚合酶链反应（ＲＴ－ＰＣＲ）方法测定各型血液病患者血清中的抗ＨＧＶ和ＨＧＶＲＮＡ。结果：５１例血液病患者中血清抗ＨＧＶ阳性６例,占１１．８％（５／６１）,ＨＧＶＲＮＡ均阴性。６例抗ＧＨＶ阳性患者中急粒２例,占２５％（２／８）,慢粒１例,占５０％（１／２）,再障２例     

HGV/GBV-C感染在肝细胞损伤中的作用探讨

目的 研究单一HGV/GBV-C感染者肝组织中该病毒核酸定位及相关抗原表达,探讨HGV/GBV-C感染在肝细胞损伤中的作用。方法 12例单一HGV/GBV-C感染者经肝穿获取的肝组织常规病理诊断,采用地高辛标记探针原位杂交法检测病毒RNA,并用免疫组织化学法检测病毒相关抗原表达。结果 病理诊断急性肝炎8例,慢性肝炎4例。HGV/GBV-C NS5抗原检出阳性率为66.67％(8/12),阳性信号主要位于肝细胞胞浆中;HGV/GBV-C RNA检出阳性率为58.33％(7/12),阳性信号位于胞浆,分布无一定规律,阳性细胞与肝细胞变性、淤胆、炎性细胞浸润、细胞坏死程度等并无相关关系。单一HGV/GBV-C感染者临床表现轻,不易被发现。结论 HGV/GBV-C RNA并不直接损害肝细胞;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。     

不同临床型肝病患者中庚型肝炎病毒感染的研究

目的:了解不同临床型肝病患者的庚型肝炎病毒(HGV)感染状况。方法:应用酶联免疫法(ELISA)检测不同临床型肝病患者血清中抗-HGV,并对抗-HGV阳性血清应用逆转录套式聚合酶链反应法(RT-nPCR)检测HGV RNA。结果:肝硬变,慢性乙型和丙型肝炎病人及HBsAg携带者的抗-HGV阳性率(分别为36.36％、26.2％、12.5％和12.0％),均显著高于急性肝炎(4.17％)。急性和慢性非甲-戊型肝炎病人的抗-HGV阳性率也较高,分别为33.3％(1/3)和16.67％(1/6)。各临床型肝病患者中,抗-HGV阳性和阴性组血清天门冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)水平无明显差异。结论:HGV与乙型和丙型肝炎病毒(HBV和HCV)具有较高的共同感染率,部分非甲-戊型肝炎为HGV感染;重叠感染HGV似并不加重肝损害程度。     

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。     

Analysis of hepatitis G virus infection markers in blood donors and patients with hepatitis

The incidence and clinical significance of hepatitis G virus (HGV) is still not fully known. The aim of our study was to assess the frequency of HGV RNA and antibody to HGV E2 protein (anti-E2) in Polish blood donors and patients with hepatitis, and to compare the sequence of HGV clones with those reported by others. Two-hundred and nineteen blood donors and 83 patients with hepatitis were studied. HGV was detected in 3.2% and anti-E2 in 24.2% of blood donors and in 26.5% and 8.4% of patients with hepatitis, respectively. HGV was detected as a co-infection with HCV in four of 18 patients with chronic hepatitis, in four of 16 patients with acute hepatitis and in one of six patients with fulminant liver failure (FLF), and as a co-infection with HBV in one of six patients with FLF and in three of 10 patients with chronic hepatitis. In non-A–C hepatitis, eight of 23 patients with acute hepatitis and one of four patients with FLF were positive for HGV but all 10 patients with chronic cryptogenic hepatitis were negative. In the follow-up studies of patients with HGV alone, a correlation with viraemia and clinical symptoms was observed in two patients, but in three others HGV RNA was detected in spite of clinical resolution. Two HGV clones were sequenced, and the sequence of the HGV helicase region of the HGV isolates from donor and patient were homologous to those described by others. Hence, the frequency of HGV RNA in blood donors is similar to that obtained in other countries but the anti-E2 (marker of a past infection) frequency is higher. The incidence of HGV RNA and anti-E2 in hepatitis patients suggests that HGV plays a role in liver pathology, but careful analysis of individual cases does not confirm this.     

HGV/GBV-C infection in patients with acute hepatitis of different etiology and in patients with chronic hepatitis C

To investigate the prevalence of hepatitis G virus (HGV/GBV-C) in patients with liver disease and to confirm its hypothesized ability to cause liver damage, we studied 130 subjects; 61 had chronic hepatitis C virus infection and 69 had acute hepatitis of either defined etiology (n = 57) or of unknown origin (n = 12). Positivity for HGV/GBV-C RNA was detected in 10 of the 61 subjects with chronic hepatitis C (16.3%) and in 11 of the 57 subjects with acute hepatitis of defined etiology (19%), whereas we failed to detect HGV/GBV-C viremia in subjects with hepatitis of non-established etiology. Patients exhibiting positivity for HGV/GBV-C RNA were found to be comparable to those exhibiting negativity for HGV/GBV-C RNA in terms of both liver function tests and Knodell's score (in liver biopsies); the affect of HGV/GBV-C infection on the biohumoral and histological activity in patients with chronic hepatitis C therefore appears to be minimal or absent. Similar clinical features were observed in patients with acute hepatitis of known etiology whether they were positive or negative for HGV/GBV-C RNA. However, long-term clinical studies are still required to clarify the actual impact of HGV/GBV-C co-infection. In our geographic, i.e., a region or north-east Italy, HGV/GBV-C infection appears to be strictly related to intravenous drug use, and this agent does not seem to be responsible for acute hepatitis of unknown etiology; other etiological agents are probably involved. Received Feb. 17, 1997; accepted June 27, 1997