庚型肝炎——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的庚型肝炎病毒（HGV）感染状况。方法：应用酶联免疫法（ELIS）检测不同临床肝病患血清中抗-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HGVRNA。结果：肝硬变，慢性乙型和丙型肝炎病人及HBsAg携带的抗-HGV阳性率（分别为36．36％、26．2％、12．5％和12．0％）均显高于急性肝炎（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）。各临床型肝病患中，抗-HGV阳性和阴性组血清天门冬氨酸转氨酶（AST）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似乎并不加重肝损害程度。     

哲盟地区不同民族、不同年龄人群庚型肝炎病毒感染的研究

目的：研究哲盟地区不同民族,不同年龄人群良型肝炎病毒感染喜笑颜开同情况,方法：采用ELISA方法对298例健康人群的111例肝炎患者进行抗－HGV检测,对3例HGV阳性血清进行了核苷酸序列测定,结果：健康人群HGV感染率为2．5％,汉族为1．69％,在肝炎患者中蒙古族HGV感染率38．7％,汉族18．75％,健康人群HGV感染。92．07％,肝炎患者为24．32％,单纯HGV感染以急性肝炎为主,重叠感染以慢性肝炎肝硬化为主。在单纯HGV感染者ALT,TBiL明显高于重叠感染组,与国外HGV部分核苷酸序列同源性平均91．0％,与国内同源性为97．08％,结论：（1）蒙古族HGV感染明显高于汉族人群。（2）肝炎患者HGV感染明显高于健康人群,HGV感染大多与HBV,HCV重叠感染,说明HGV与HBV,HCV有共同传染途径,（3）HGV有较强致病性,（4）重叠感染不加重病情。（5）老年HGV感染单纯HGV感染病情重。（6）HGV部分核苷酸序列与国外株有一定差异,与国内株同源性较高,说明HGV具有准种的特性。     

原位杂交法检测非甲─非庚型肝炎患者肝组积中新型肝炎病毒DNA

目的证实在非甲-非庚型病毒性肝炎患者肝组织中一种新型肝炎病毒（transfusion－transmittedvirus，TTV）的存在．方法采用地高辛素标记TTVDNA探针以原位杂交技术对51例血清学病毒标记非甲-非戊型、免疫组化检测肝组织中HGVNSS阴性的病毒性肝炎患者石蜡包埋肝组织进行了检测．结果各型病毒性肝炎肝组织中TTV基因的总检出率为27．5％，其中急性轻型肝炎的检出率为30．8％（4／13），急性重型肝炎（1／8，12．5％），亚急性重型肝炎（3／7，42．9％），慢性肝炎（2／6，33．3％），活动性肝硬变（2／9，22．2％），慢性重型肝炎（1／4，25％），原发性肝癌（1／4，25％）TTVDNA表达于肝细胞核或胞浆内，以核型多见．在急性肝炎，TTV阳性细胞弥漫分布于肝小叶内，慢性肝炎于汇管区附近较为密集，而在肝硬变病例，阳性细胞在假小叶内多呈片簇状不规则分布结论在不明原因病毒性肝炎患者血清及肝组织中TTVDNA的检出表明TTV为一种新型的肝炎病毒，TTV为一种嗜肝性病毒，在我国存在着TTV感染     

庚型肝炎病毒感染的初步调查

采用酶联免疫法(ELISA)检测94例病毒性肝炎患者血清中抗庚型肝炎病毒抗体(抗-HGV),阳性率为23.4％。其中急性肝炎、慢性肝炎、重型肝炎抗-HGV阳性率分别为21.4％、21.1％、30.4％,在22例抗-HGV阳性病人中,HBV与HGV重叠感染率为36.3％。39例非甲-戊型肝炎抗HGV的阳性率(35.5％)明显高于55例乙型肝炎的阳性率(14.5％、P<0.05),说明HGV感染主要存在于非甲-戊型肝炎病人中。23例重型肝炎中有16例死亡,抗HGV(+)7例全部死亡,而单纯HBV感染的死亡率为56.25％。结果显示:HGV感染系非甲-戊型肝炎的主要原因,HGV可以与HBV重叠感染,且可能影响重型肝炎的愈后。     

17例庚型肝炎临床病理分析

对17例经逆转录聚合酶链反应(RT-PCR)法检测HGV RNA阳性的庚型肝炎患者进行临床和/或肝脏组织分析。结果发现经输血感染者8例(47.1％),散发性病例9例(52.9％)。单纯HGV感染者8例(47.1％),HGV和HBV或HCV二重、三重感染者9例(52.9％)。临床病理分型发现急性肝炎2例,慢性肝炎12例,重型肝炎2例和肝硬变1例。单纯HGV感染多呈隐匿发病,症状轻,,无黄疸,ALT轻度升高,但慢性化程度高。本文结果提示HGV感染易致病程慢性化,病理损伤轻,HGV与HBV重叠感染时,HGV有可能干扰HBV的复制。     

病毒性肝炎患者血清AFP与临床、病理的关系

目的：探讨肝炎患者AFP水平与临床,病理的关系。方法：临床诊断为病毒性肝炎并经肝穿刺活检的310例患者,常规检测血清TB－ALT,AST,A／G,AFP及肝炎病毒标志,观察异常AFP水平与临床类型,病理类型,有无家族史和病因等的关系。结果：310例肝炎患者中发现AFP异常115例,阳性率为37．1％,急性肝炎,慢性肝炎,慢性重型肝炎患者中均见有AFP异常者,根据病理,急性肝炎患者AFP阳性率最低,慢性肝炎,慢性肝炎肝硬化患者较高,慢性重型肝炎患者阳性率最高,分别为11．7％．34．2％,57．5％和66．7％,按临床表现诊断,阳性率以慢性重型肝炎最高,慢性肝炎最低,而急性肝炎居中,在肝炎病因分类中单纯HBV感染或HBV基础上又有HAV／HEV感染者AFP阳性率较高,为35．3％和62．8％,HBV与HCV双重感染者为27．3％,单一HCV感染者6例中1例AFP阳性,单纯HAV或HEV阳性者未见AFP异常,此外,有肝癌家族史的肝炎患者AFP阳性率为57．9％,高于无肝癌家族史者。结论：肝炎患者AFP异常颇为常见,一旦发现肝炎患者AFP异常时,应考虑患者有HBV感染的背景,或为单纯HBV感染的慢性乙型肝炎,或HBV基础上有HAV或HEV重叠感染者。     

重型肝炎中HEV感染的临床意义

为探讨重型戊肝的临床表现及转归，对75例重型肝炎中的13例戊肝病毒（HEV）感染者进行临床分析。以单纯乙肝病毒（HBV）感染20例为对照组，比较其与单纯HEV，HEV合并HBV感染的重型肝炎在临床表现，实验室检查，预后等方面的差异。结果显示，重型肝炎的HEV感染率为17．3％（13／75），HEV与HBV重叠感染率为8．0％（6／75），在临床表现方面各组差异无显著性意义（P＞0．05）。HEV合并HBV感染组SB，PT及死亡率明显高于单纯HEV组及单纯HBV组，差异有显著性差异（P＜0．05）。肝炎病毒重叠感染是影响戊型重型肝炎预后的重要因素。     

急慢性乙型肝炎肝硬变失代偿血清乙肝病毒感染标志的比较

目的比较乙型肝炎（简称乙肝）中急、慢性乙肝及肝硬变失代偿期乙型肝炎病毒（HBV）复制情况．方法对100例三种类型肝炎检查肝功、血清乙型肝炎病毒感染标志（二对半）、抗－HAV、抗－HCV，及年龄性别分组结果代表HBV复制的模式77例．三种肝炎复制模式经统计学处理无显著性差异．男：女为3：1．急性肝炎多见于40岁以下．肝硬变失代偿多见于40岁以上．急性乙肝与甲、丙型肝炎病毒重叠感染率均为6．25％，慢性乙肝重叠甲型肝炎为11．1％．结论急慢性乙型肝炎及其肝硬变与乙肝病毒复制有关，应抗病毒治疗．     

各型肝炎病毒单纯及重叠感染的研究

目的 探讨病毒性肝炎患者甲～戊，庚型肝炎病毒(HAV-HEV，HGV)单纯感染及重叠感染情况。方法 采用EIA法检测病毒性肝炎患者血清抗-HAV IgM，HBV标志物、抗-HCV IgM、抗-HDV IgM、抗-HEV IgM、抗-HGV IgM。结果 共检测210例病毒性肝炎患者HAV-HEV、HGV血清标志物，20例未检出(9．5％)，190例患者检出标志物阳性(90．5％)。HBV感染率89，5％(188／210，其中有34例为既往感染，占16．2％，现症感染154例，占73．3％)；HAV感染率29．0％(61／210)，HCV、HDV感染率均为8．1％(17／210)、HEV、HGV感染率依次为10．0％(21／210)、7．1％(15／210)。各临床类型中单纯感染占61．4％(129／210)，二重感染占32．4％(68／210)，以HAV HBV、HBV HDV、HBV HEV感染模式最常见，三重感染占6．2％(13／210)，以HAV HBV HDV感染模式最常见；临床上以肝炎肝硬化、重型肝炎重叠感染常见，急性肝炎最少见。结论 病毒性肝炎中HBV感染最常见，其次为HAV感染；单纯感染、二重感染多见，三重感染少见；重叠感染发生率随病情加重而增加。     

戊型肝炎病毒与甲乙丙型肝炎病毒重叠感染的研究

本文对419例病毒性肝炎患者进行抗-HEV-IgM/IgG及其它病毒标志物检测。结果:HEV感染者112例(26.2％);其中单纯HEV感染者30例,两种以上肝炎病毒重叠感染占73.2％;43.75％为HBV和HEV重叠感染,HAV和HEV合并感染占急性肝炎的40.58％。在重型肝炎中HEV感染率占57.89％,均为HBV和HEV重叠感染,病死率达72.73％。16.67％的单纯HEV感染者为慢性肝炎和肝硬变。结果表明,本地区戊型肝炎以散发为主,重叠感染多见。HBV与HEV重叠感染和HAV与HEV重叠感染是较常见的感染模式。在HBV感染的基础上重叠HEV感染是肝炎重症化的重要原因。HEV感染有导致慢性化的可能性。     

GBV-C/HGV在血清学非甲～戊型急性肝炎发生中的作用

探讨GBV-C/HGV在血清学非甲～戊型急性肝炎发生中的作用及临床意义.采用免疫组化方法对56例血清学非甲～戊型急性肝炎患者肝组织标本进行GBV-C/HGV NS5抗原的检测,结合临床资料进行分析.血清学非甲～戊型急性肝炎肝组织中GBV-C/HGV NS5抗原检出率为53.6%,主要是以和HBV/HCV重叠感染的形式存在,重叠感染组的ALT升高和HBV/HCV感染组差异无显著意义.单纯GBV-C/HGV感染占16.1%,所引起的血清ALT升高明显低于HBV/HCV感染,而与病原不明病例差异无显著意义.GBV-C/HGV可能没有致病性或者有弱致病性,不是血清学非甲～戊型急性肝炎的主要致病因子.     

TTV阳性肝病患者的临床与病理学特征初步观察

目的 观察ＴＴＶ阳性肝病患者的临床和病理特征。方法 用巢式ＰＣＲ法检测ＴＴＶ－ＤＮＡ,同时观察血清生化指标,肝组织活检观察其病理变化。结果 ＴＴＶ感染者的血清学模式以重叠ＨＢＶ、ＨＣＶ、ＨＡＶ、ＨＥＶ、ＨＧＶ二重感染为主占５７．９％（２２／３８）,以乏力、纳差、腹胀为临床特征,ＴＢｉＬ、ＡＬＴ变化不明显,ＴＴＶ单独感染者为４２．１％（１６／３８）,急性发病者临床特征多与“急性黄疸性肝炎”相似,病理改变与各型病毒性肝炎的病理变化基本相似,但主要以肝门脉区炎症,小叶间胆管损伤,灶状坏死为多见。结论 ＴＴＶ可与各型已知肝炎病毒重叠感染也可单独感染。     

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     

Two patients with acute hepatitis B with suspected sexual transmission of hepatitis G virus

Two patients with acute hepatitis B with suggested sexual transmission of hepatitis G virus (HGV) are reported. A total of 18 patients with community acquired acute hepatitis B were analyzed in this study. Two of the 18 patients (patients 1 and 2) were positive for serum HGV RNA at the initial consultation. Both patients had had sexual contact with prostitutes several weeks before the onset of acute hepatitis, and hepatitis B virus (HBV) was suggested to be infected through the sexual contacts. These patients showed no other history of exposure to possible transmission routes for blood-borne hepatitis viruses. Patient 1 was diagnosed as with acute HGV infection because the antibody to HGV envelope-2 protein seroconverted to positive during the course of acute hepatitis. HGV RNA was negative in a serum sample collected from patient 2 before the onset of acute hepatitis, also suggesting acute HGV infection. These results indicate that in patients 1 and 2 HGV was infected along with HBV through sexual contact. The clinical manifestations of acute hepatitis in the two patients with HGV co-infection did not differ from those in the 16 patients with HBV infection alone. (Received Aug. 6, 1997; accepted Oct. 30, 1997)     

Coinfections with hepatitis g and/or c virus in hepatitis B-related chronic liver disease

Concurrent infections with HGV and/or HCV (HGV/HCV) were investigated in 196 patients with HBV-related chronic liver disease (115 chronic hepatitis, 31 liver cirrhosis, 50 hepatocellular carcinoma), and in 100 HBsAg carriers. Coinfections were detected in 18 (9.2%) patients with HGV (10) or HCV (5) or both agents (3), but in none of the HBsAg carriers. Patients with coinfection were more frequently exposed to blood transfusions (55.6% vs 5.6%) and also were more commonly anti-HBe positive. Serum levels of HBV-DNA were lower in patients with HCV coinfection than in those coinfected with HGV. Interferon was administered to 39 patients with chronic active hepatitis including 7 patients with HGV/HCV coinfection. Sustained clearance of HBV-DNA was observed in 10 (25.6%) patients who were solely infected with HBV. These patients were significantly younger and had much lower histological scores than non-responders. Patients with HCV coinfection had significantly higher pre-treatment histological scores than those without HCV. After interferon treatment, a significant reduction in histological scores was observed in all patients except those coinfected with HGV/HCV. None of the 7 patients with coinfection had sustained clearance of HBV-DNA or HCV-RNA, and only one had cleared HGV-RNA. These results suggest that parenteral exposure is a risk factor for HGV/HCV coinfection in chronic HBV infection. HGV infection shows no significant impact on chronic HBV infection. HCV coinfection appears to inhibit HBV replication, but causes more severe chronic hepatitis and increases resistance to interferon therapy.     

Hepatitis G virus infection in Japanese haemophiliacs

The recently identified hepatitis G virus (HGV) (also known as GB virus-C) has been considered as a blood-transmissible agent. As many haemophiliacs have risk factors for infectious agents, to clarify the frequency of HGV infection is important. HGV-RNA was investigated in 77 Japanese haemophiliacs who had been treated with nonvirus-inactivated concentrates derived from pooled plasma. Detection of HGV-RNA was performed with a nested RT-PCR that recognizes the 5'-NCR of the HGV genome. HGV-RNA was detected in 19 (24.7%), including four (21.0%) infected with HGV alone, 12 (63.2%) co-infected with HCV and three (15.8%) who were HBV carriers. The patients infected with HGV alone showed a normal ALT level of 18.7 ± 4.1 IU L⁻¹. Most (36/37, 97.3%) of the patients with abnormal ALT levels had HCV-RNA. Patients infected with HCV alone or co-infected with HCV and HGV showed higher ALT levels of 108.8 ± 90.2 IU L⁻¹ ( n = 39) and 67.6 ± 62.6 IU L⁻¹ ( n = 11), respectively. However, there was no significant difference ( P = 0.16) in ALT levels between HCV infection alone and HCV/HGV co-infection. On the other hand, four of the patients who could be followed over 10 years showed HGV-RNA persistently. In two who underwent liver biopsy, the histological evidence showed no definitive fibrotic and necro-inflammatory changes. These results indicate that HGV infection has frequently occurred in haemophiliacs. It is possible that HGV infection does not cause aggressive hepatitis with elevated ALT levels, and that co-infection with HGV may not aggravate hepatitis caused by HCV.