各型病毒性肝炎患者庚型肝炎病毒感染状况

目的:了解武汉地区各型病毒性肝炎患者中庚型肝炎病毒(HGV)感染的情况。方法:用酶联免疫吸附试验(ELISA)及逆转录聚合酶链反应(RT-PCR)方法测定各型病毒性肝炎患者的抗HGV和HGV RNA,并对庚肝病毒感染者进行临床分析。结果:351例各型病毒性肝炎患者中抗HGV阳性者56例,占15.05％;此56例中HGV RNA阳性者21例,占37.50％。各型病毒性肝炎患者中抗HGV阳性率及庚肝抗体阳性者中HGV RNA阳性率分别为:甲肝14.29％(5/35)及20.00％(1/5);乙肝17.29％(37/214)及35.14％(13/37);丙肝14.52％(9/62)及55.56％(5/9);戊肝4.00％(1/25),0.00％(0/1);非甲～戊肝26.67％(4/15),50.00％(2/4)。56例抗HGV阳性者中43例有输血、使用血制品或静脉药癌史,占76.79％。HGV感染在肝炎各临床类型分布为急性、慢性和重型肝炎患者无明显差异,且无性别和年龄分布的差异。HBV重叠感染HGV患者的SALT及TBil水平明显高于单纯HBV感染者(P<0.05),而HGV和其它肝炎病毒((HAV、HCV、HEV)重叠感染患者与单纯其它肝炎病毒感染者的SALT及TBiL水平无明显差异(P>0.05)。结论:武汉地区各型病毒性肝炎患者均可存在HGV感染。HGV可单独感染或与其它病毒混合感染。血液传播是HGV感染的主要途径。乙型肝炎患者合并庚肝病毒重叠感染可加重病情,而甲、丙、戊型肝     

病毒性肝炎患者1055例中巨细胞病毒活动性感染的研究

对1992年4～11月入院的急性病毒性肝炎散发病例,用ELISA捕捉法测定急性期抗CMV-IgM与IgG。结果:患者1055例中抗CMV-1gM(+)37例,占3.51％,次于甲肝48.62％,乙肝44.26％,高于戊肝3.13％、丁肝3.02％、丙肝1.14％。排列病毒性肝炎病原谱第三位。在肝炎各类型分布中,重肝18.18％,慢活肝13.33％,慢迁肝3.86％,急肝1.34％,肝硬化未检出。37例患者中,原发感染1例,再发感染36例。随机抽查125例不同年龄肝炎患者,其抗CMV-IgG(+)109例,阳性率87.2％,抗体GMT372。由于感染普遍,对于成人患者CMV感染多为再发而极少原发。本文37例CMV感染者均为合并感染。合并感染有5种模式,即乙、巨二重12例,乙、丁、巨三重15例,甲、乙、巨三重3例,甲、乙、丁、巨四重4例,乙、丙、丁、巨四重3例。5种模式均有HBV存在,机体免疫功能下降是乙肝病人临床多发主要原因,反过来CMV感染进一步加重机体免疫功能抑制,这就构成恶性循环。在有丁肝合并感染22例患者中(占59.46％),慢活肝(63.64％)与重肝(9.09％)比例较大,合并感染无疑会加重病情变化。     

慢性病毒性肝炎的多重感染

了解慢性病毒性肝炎多重感染,有助于临床诊断及治疗。采用ELISA和连续监测法对43例慢性病毒性肝炎多重感染及76例乙型肝炎单纯感染患者血清进行HBVM以及肝功能指标检测。慢性病毒性肝炎多重感染的检出率为2.1%,与其他病毒性肝炎相比,差异有显著性(x2=5.0,P<0.05),说明慢性病毒性肝炎患者多重感染者较多。多重感染与单纯感染相比,患者年龄高(t=3.119,P<0.01),住院时间长(t=3.780,P<0.01),临床症状和肝功能损害重,疗效差(x2=12.98,P<0.01),说明慢性病毒性肝炎多重感染会加重病情。     

肝功能异常患者中自身抗体及自身免疫性肝病的检测

目的 自身免疫性肝病临床流行病学调查,观察在肝功能异常患者中自身抗体检测的阳性率、自身免疫性肝病检出率及临床意义。方法 连续收集就诊病例中肝功能异常患者丙氨酸氨基转移酶(ALT)大于40 U/L血清511份,分别进行相关自身抗体(ANA)检测,并查阅临床资料。结果 511份血清检测出ANA阳性率为14.09％,抗平滑肌抗体(SMA)阳性率0,59％,抗线粒体抗体(AMA)阳性率2.94％,抗线粒体抗体亚型-丙酮酸脱氢酶复合物(AMA-M2)阳性率0.98％;ANA谱中的SS-A阳性率0.59％、SS-B阳性率0.20％、JO-1阳性率0.20％,dsDNA阳性率0.78％;未检出抗肝肾微粒体抗体(LKM-1)、可溶性肝抗原/肝胰抗原(SLA/LP)、抗肝细胞溶质抗原1型抗体(LC-1)及ANA谱中其他抗体。从ALT升高的患者中收集到的511份血清,可查到完整临床资料者共469例。原发性胆汁性肝硬化(PBC)及自身免疫性肝炎(AIH)患者检出率分别为1.06％及0.43％,未检出原发性硬化性胆管炎患者。自身抗体阳性患者77.78％诊断为病毒性肝炎及相关疾病。病毒性肝炎及相关疾病中自身抗体阳性率为18.29％。结论 高滴度(>1:320)自身抗体对自身免疫性肝病诊断有意义。PBC及AIH患者检出率近似丙型及戊型肝炎检出率,临床不能忽视,病毒性肝炎及相关疾病中可检测出自身抗体。     

重型及慢性活动性乙肝75例血清抗—HD抗体检测分析

本文应用抗—HD(EIA)试剂检测75例HBsAg阳性重型肝炎及慢性活动性肝炎血清标本:同时测定HBV标志及肝功能。其中47%病例有肝组织学病理诊断及肝内HBsAg、HBcAg检测。所选病例系Rizzetto认为的抗—HD高检出人群。结果显示,75例血清抗—HD全部阴性。     

病毒性肝炎合并甲状腺功能亢进症11例临床分析

目的分析病毒性肝炎合并甲亢时的病情，探讨有效治疗方案。方法选择病毒性肝炎合并甲状腺功能亢进症11例，仅予护肝支持对症治疗9例，护肝和^131碘治疗2例。结果病毒性肝炎合并甲亢大多肝功损害明显，病情较重，其中重型肝炎5例，慢性肝炎重度4例，慢性肝炎中度2例。9例不抗甲亢治疗效果差，2例^131碘治疗病情好转。结论病毒性肝炎合并甲亢易造成肝损害及甲亢加重，不抗甲亢治疗预后差。     

抗可溶性肝抗原/肝胰抗原抗体阳性的肝病患者临床与实验室特征

目的研究肝功能异常伴抗可溶性肝抗原／肝咦抗原（SLA／LP）抗体阳性患者临床与实验室特点。方法收集肝功能异常患者血清5500例，分别完成相关自身抗体的检测。结果8例（0．15％）患者检测出sLA／LP抗体阳性，女性6例，以中老年女性为主，男性2例，年龄分别为27岁和33岁，8例中6例无甲、乙、丙、丁、戊型等病毒性肝炎现症感染证据，2例分别伴乙、丙型肝炎病毒标志物，无现症感染证据。8例中7例已发展至肝硬化，除sLA／LP抗体阳性外，抗核抗体均为阳性，部分患者伴抗平滑肌抗体，抗线粒体抗体，抗线粒体抗体亚型-丙酮酸脱氢酶复合物阳性。结论sLA／LP抗体在所检测患者中阳性率较低，以女性患者为主，多数临床与实验室特点符合自身免疫性肝炎特征，女性患者慢性肝病原因未名者应检测此抗体。     

原发性干燥综合征的肝脏损害

目的　研究原发性干燥综合征 (pSS)合并肝脏损害的临床特点 ,探讨其病理本质。方法　分析 5 6例 pSS病例中合并肝脏损害及不伴肝脏损害的临床资料。 结果　 5 6例 pSS病例中 13例合并肝脏损害 ,发生率为 2 3 2 % ,其性别、年龄、从发病到确诊时间以及ANA、抗SSA、抗SSB、类风湿因子、IgG、γ 球蛋白阳性率方面与不伴肝脏损害之间的差异均无显著性 (P >0 0 5 )。 13例中 6例AKP、γ GT同时升高 ,4例AKP、γ GT、TBIL、DBIL同时升高。查抗平滑肌抗体 (抗SMA)、抗线粒体抗体 (AMA)的 8例中 ,5例AMA阳性。 6例进行肝穿刺活组织检查 ,病理诊断为慢性活动性肝炎 3例 ,其中 2例合并肝硬化 ;慢性迁延性肝炎 1例 ,小胆管炎 2例。 6例中 5例均有不同程度的汇管区单个核细胞浸润。结论　pSS合并肝脏损害并不少见 ,可能与原发性胆汁性肝硬化相关。患者对激素治疗敏感 ,预后较好。     

重症病毒性肝炎的病原学研究

对79例亚急性及慢性重型病毒性肝炎(重肝)进行了肝炎病毒标志的研究,结果发现:甲型肝炎病毒抗体(抗HAV)IgM阳性8例(10.12%);HBsAg和(或)抗HBcIgM阳性76例(96.20%);丙型肝炎病毒抗体(抗HCV)阳性41例(51.89%),其中35例合并乙型肝炎病毒(HBV)感染,5例与HAV和(或)HBV     

肝病患者抗LKM-1和抗SLA／LP的检测及其自身抗体特征分析

目的回顾性研究在肝功能异常患者中肝。肾微粒体抗体和可溶性肝抗原／肝胰抗体检测的意义和免疫特征。方法收集肝功能异常患者丙氨酸氨基转移酶（ALT）〉40u／L的患者血浆5500例，分别检测肝肾微粒体抗体、可溶性肝抗原／肝胰抗体和相关自身抗体，查阅临床资料。结果5500例血浆中检测出SLA／LP阳性8例，占1．45‰，LKM阳性者4例，占0．73‰。12例阳性病例中，有乙型和丙型病毒性肝炎现症感染证据的分别有1例和2例。大多数患者同时还伴有ANA、AMA、SMA和（或）LSP等抗体阳性。结论抗LKM-1和抗SLA／LP在我国肝病患者中出现的比例较低，抗LKM-1和抗SLA／LP是自身免疫性肝病的特征性抗体，检测此抗体对自身免疫性肝炎诊断具有重要的意义。     

两种新发现的脑炎病毒

1994年爆发了两次能感染马和人类的一种新的病毒性疾病 ,引起昆士兰和澳大利亚 2 3匹马和 3人感染 ,其中一人死于爆发的呼吸道疾病 ,另一人死于脑炎 ,第三位患者出现流感样症状并完全康复 ,引起该病的病毒最初称为马麻疹病毒 (ｅｑｕｉｎｅｍｏｒｂｉｌｌｉｖｉｒｕｓ ,ＥＭＶ) ,后命名为Ｈｅｎｄｒａ病毒。 1998年 9月下旬至1999年 6月中旬在马来西亚爆发的一种病毒性脑炎 ,发病例数高达 2 65例 ,其中 10 5例死亡。绝大多数患者是养猪场或屠宰场工人。 1999年 3月 10日～ 19日在新加坡 1个屠宰场的 11名工人出现脑炎或不典型肺炎的临床表现…     

GB virus C/hepatitis G virus

GB virus C (GBV-C), or hepatitis G virus (HGV), is a recently discovered enveloped RNA virus belonging to the Flaviviridae family. GBV-C/HGV is transmitted by contaminated blood and/or blood products, intravenous drug use, from mother to child, sexually, and possibly through close social contacts. Several reports indicate a high prevalence of GBV-C/HGV viremia (1-4%) within healthy populations in Europe and North America, and an even higher prevalence (10-33%) among residents in South America and Africa. GBV-C/HGV has been suggested to be a causative agent for non-A-non-E hepatitis. However, several contradictory observations suggest that its ability to cause hepatitis is questionable. Taken together most data suggest that GBV-C/HGV is not a major cause of liver disease despite recent data indicating that it may infect and replicate in hepatocytes.     

Hepatitis B virus infection: co-infection with hepatitis C virus, hepatitis D virus, and human immunodeficiency virus

Hepatitis B virus (HBV) shares routes of transmission, namely exchange of infected body fluids, sharing of contaminated needles, and blood transfusion, with other hepatotropic viruses, such as hepatitis C virus (HCV) and hepatitis D virus (HDV) and with systemic retroviral infections, such as the human immunodeficiency virus (HIV). Thus, many HBV infected patients are co-infected with other viral pathogens. Co-infection appears to increase the risk of progression of liver disease and may have important ramifications on choice of antiviral medication and treatment regimen. This article reviews the current knowledge of co-infection of HBV with HCV, HDV, and HIV.     

Immunological memory after exposure to variola virus, monkeypox virus, and vaccinia virus

We compared cellular and humoral immunity to vaccinia virus (VV) in individuals exposed to 3 different orthopoxviruses: 154 individuals previously vaccinated with VV, 7 individuals with a history of monkeypox virus infection, and 8 individuals with a history of variola virus infection. Among individuals vaccinated >20 years prior, 9 (14%) of 66 individuals demonstrated VV-specific interferon (IFN)- gamma enzyme-linked immunospot (ELISPOT) assay responses; 21 (50%) of 42 had lymphoproliferative (LP) responses, and 29 (97%) of 30 had VV-specific neutralizing antibodies. One year after monkeypox virus infection, 6 of 7 individuals had IFN- gamma ELISPOT responses, all had VV-specific LP responses, and 3 of 7 had VV-specific neutralizing antibodies. Of 8 individuals with a history of variola virus infection, 1 had a VV-specific IFN- gamma ELISPOT response, 4 had LP responses against whole VV, 7 had LP responses against heat-denatured vaccinia antigen, and 7 had VV-specific neutralizing antibodies. Survivors of variola virus infection demonstrated VV-specific CD4 memory cell responses and neutralizing antibodies >40 years after infection.     

Epstein-Barr virus and virus human protein interaction maps

A comprehensive mapping of interactions among Epstein-Barr virus (EBV) proteins and interactions of EBV proteins with human proteins should provide specific hypotheses and a broad perspective on EBV strategies for replication and persistence. Interactions of EBV proteins with each other and with human proteins were assessed by using a stringent high-throughput yeast two-hybrid system. Overall, 43 interactions between EBV proteins and 173 interactions between EBV and human proteins were identified. EBV-EBV and EBV-human protein interaction, or "interactome" maps provided a framework for hypotheses of protein function. For example, LF2, an EBV protein of unknown function interacted with the EBV immediate early R transactivator (Rta) and was found to inhibit Rta transactivation. From a broader perspective, EBV genes can be divided into two evolutionary classes, "core" genes, which are conserved across all herpesviruses and subfamily specific, or "noncore" genes. Our EBV-EBV interactome map is enriched for interactions among proteins in the same evolutionary class. Furthermore, human proteins targeted by EBV proteins were enriched for highly connected or "hub" proteins and for proteins with relatively short paths to all other proteins in the human interactome network. Targeting of hubs might be an efficient mechanism for EBV reorganization of cellular processes.