慢性肝炎中乙型和丙型病毒混合感染的重症化研究

在慢性肝炎中,乙、丙型病毒性肝炎混合感染相当多见,可使肝炎慢性化、重症化,肝组织损伤加重,肝硬化(LC)和肝癌(HCC)发生率增加[1]。本文应用血清学和分子生物学方法对196例肝病患者的血清进行检测,初步探讨了乙型肝炎病毒(Hepatitis B virus,HBV)、丙型肝类病毒(Hepatitis C virus,HCV)的复制状况以及两者间的相互作用与预后的关系。1材料和方法1.1病例受检的196例病例均为2004年1月至2005年7月我院住院及门诊病人,男149例,女47例,年龄15~82岁,其中慢性肝炎(CH)患者139例,肝硬化(LC)患者42例,肝癌(HCC)患者15例。所有病例诊断符合…     

河北省丙型肝炎病毒基因分型研究

丙型肝炎病毒 (Hepatitis C virus, HCV)感染是输血后肝炎的主要原因[1],主要通过输血或使用污染的血制品传播[2],且与肝硬化和肝细胞癌的发生有密切关系.     

戊型肝炎病毒衣壳蛋白结合CYP 2A6并降低其底物催化能力

肝炎病毒的感染常常导致人体肝脏代谢能力变化,研究表明甲型肝炎病毒(Hepatitis A Virus,HAV)、乙型肝炎病毒(Hepatitis B Virus,HBV)和丙型肝炎病毒(Hepatitis C Virus,HCV)的感染都会影响肝细胞对药物的代谢能力。在本研究中,通过酵母双杂交系统在人肝cDNA文库中筛选与戊型肝炎病毒重组衣壳蛋白E2结合的蛋白,发现了与细胞色素P450 2A6(CYP2A6)部分片段高度同源的蛋白序列。通过pull-down、免疫共沉淀以及特异性底物催化反应评价等方法进一步证实了CYP2A6与重组衣壳蛋白E2、p239间的相互作用,并发现与p239结合可以降低CYP2A6对其特异性底物香豆素的催化能力。上述结果提示CYP2A6可能在戊肝病毒入侵细胞后的细胞病变过程中起作用。     

HCV感染过程中的相关免疫反应

丙型肝炎病毒(Hepatitis C Virus,HCV)是慢性丙型病毒性肝炎的主要病因,也是引发肝硬化和肝癌的主要诱因。在HCV感染过程中,伴随着干扰素信号通路的激活和干扰素刺激基因(IFN-stimulated gene,ISG)的持续表达,且有HCV独特的免疫逃逸和免疫细胞的功能损伤。现就HCV感染过程中机体的固有免疫反应和适应性免疫反应的研究进展作一综述。     

丁型肝炎病毒的分子生物学研究进展

丁型肝炎病毒(Hepatitis delta virus,HDV)是一种缺陷病毒,必须在嗜肝DNA病毒的辅助下才能复制并组装成有感染的病毒颗粒[1].     

丙肝病毒非灵长类同源病毒的研究进展北大核心CSCD

丙型肝炎病毒(Hepatitis C virus,HCV)是一种危害人类健康的病原体,感染人体后极易导致慢性肝炎,并能引起肝纤维化或脂肪肝,可能进一步发展成为肝硬化、肝癌等终末期肝病。尽管已被发现20多年,丙肝病毒的来源以及进化途径一直没有确定。与此同时,缺乏合适的动物模型严重阻碍HCV致病机理的研究。从2011年起,随着新型测序技术的应用,多种丙肝非灵长类同源病毒相继被发现,这些研究成果将在研究丙肝病毒来源、进化途径以及相关动物模型建立中起重要作用。     

丙肝病毒非灵长类同源病毒的研究进展

丙型肝炎病毒(Hepatitis C virus,HCV)是一种危害人类健康的病原体,感染人体后极易导致慢性肝炎,并能引起肝纤维化或脂肪肝,可能进一步发展成为肝硬化、肝癌等终末期肝病。尽管已被发现20多年,丙肝病毒的来源以及进化途径一直没有确定。与此同时,缺乏合适的动物模型严重阻碍HCV致病机理的研究。从2011年起,随着新型测序技术的应用,多种丙肝非灵长类同源病毒相继被发现,这些研究成果将在研究丙肝病毒来源、进化途径以及相关动物模型建立中起重要作用。     

脂滴在丙肝病毒生命周期中的作用

脂滴是细胞内中性脂的主要储存细胞器。最近许多研究都发现脂滴与丙型肝炎病毒(Hepatitis C virus,HCV)有着密切的关系。脂滴对HCV的生命周期发挥着重要作用,影响HCV的感染、复制、组装和分泌一系列生命过程。本文就脂滴在病毒生命周期中的作用的最新进展进行综述。     

丙型肝炎病毒囊膜蛋白基因DNA疫苗的构建及动物免疫试验

丙型肝炎病毒(Hepatitis C virus,HCV)主要通过输血传播,可以导致多种临床型的肝炎及其它肝脏疾病,包括肝硬化及肝细胞癌[1,2].目前尚无一种有效的抗HCV的措施,这使人们把眼光放到该病的预防上,DNA疫苗的产生为研制丙型肝炎(丙肝)的预防及治疗性疫苗提供了新的思路.     

丙型肝炎病毒蛋白的分子生物学研究进展

丙型肝炎病毒(Hepatitis C viruS,HCV)是造成慢性肝炎,肝硬化及肝癌的重要原因之一.目前全球发现约有1亿7千万人口感染HCV.HCV的急性感染通常是没有症状的,但50%～80%的病人会转变成为慢性感染患者,而且大约20%的患者会在20年内转变成为肝硬化.     

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。     

Enhanced host immune responses in presence of HCV facilitate HBV clearance in coinfection

Hepatitis B virus (HBV)/Hepatitis C virus (HCV) coinfection is frequently observed because of the common infection routine. Despite the reciprocal inhibition exerted by HBV and HCV genomes, the coinfection of HBV and HCV is associated with more severe forms of liver diseases. However, the complexity of viral interference and underlying pathological mechanism is still unclarified. With the demonstration of absence of direct viral interplay, some in vitro studies suggest the indirect effects of viral-host interaction on viral dominance outcome. Here, we comprehensively investigated the viral replication and host immune responses which might mediate the interference between viruses in HBV/HCV coinfected Huh7-NTCP cells and immunocompetent HCV human receptors transgenic ICR mice. We found that presence of HCV significantly inhibited HBV replication in vitro and in vivo irrespective of the coinfection order, while HBV did not affect HCV replication. Pathological alteration was coincidently reproduced in coinfected mice. In addition to the participation of innate immune response, an involvement of HCV in up-regulating HBV-specific immune responses was described to facilitate HBV clearance. Our systems partially recapitulate HBV/HCV coinfection and unveil the uncharacterized adaptive anti-viral immune responses during coinfection, which renews the knowledge on the nature of indirect viral interaction during HBV/HCV coinfection.     

吉林省延边地区丙型肝炎病毒基因型分布

为了解延边地区不同丙型肝炎病毒(HCV)基因型的分布特点,应用逆转录-聚合酶链反应(RT-PCR)技术,检测了48例本地区抗HCV阳性血清,结果有29例出现HCVRNA阳性.再利用限制性片段长度多态性(RFLP)技术,对29例RT-PCR阳性标本进行HCV基因分型.结果延边地区主要流行HCVⅡ型,其次是HCVⅢ型,也存在HCVⅡ/Ⅲ混合型,且HCVⅢ型的感染率较高.     

HCV/HBV复合抗原基因的克隆、表达及免疫应答研究

为探讨ＨＣＶ／ＨＢＶ 复合疫苗的可行性,将合成的丙型肝炎病毒（ＨＣＶ）复合多表位抗原基因ＰＣＸ与ＨＢｓＡｇ 基因连接成ＰＣＸＳ基因,与β－半乳糖苷酶（ＧＺ）基因融合后在大肠杆菌及减毒鼠伤寒沙门氏菌中获得表达．目的蛋白ＧＺ－ＰＣＸＳ可被抗－ＨＢｓ 及抗－ＨＣＶ 抗体所特异识别．ＧＺ－ＰＣＸＳ抗原皮下注射免疫ＩＣＲ小鼠后,诱发了较高水平的抗－ＧＺ－ＰＣＸＳＩｇＧ反应．构建的重组减毒鼠伤寒沙门氏菌ＳＬ３２６１（ｐＷＲ／ＰＣＸＳ）口服免疫小鼠后,诱发了高水平的ＣＤ８＋ Ｔ细胞增殖反应及抗ＧＺ－ＰＣＸＳＩｇＧ反应．所有免疫小鼠均未见明显的毒副作用．该研究揭示,ＨＣＶ／ＨＢＶ 复合抗原可诱发特异性体液免疫及细胞免疫应答,而活菌苗口服可能是理想的免疫途径,为ＨＣＶ／ＨＢＶ 双价疫苗研究提供了一定的理论及实验依据．     

Microarray multiplex assay for the simultaneous detection and discrimination of hepatitis B, hepatitis C, and human immunodeficiency type-1 viruses in human blood samples

Hepatitis B virus (HBV), hepatitis C virus (HCV), and human immunodeficiency virus type-1 (HIV-1) are transfusion-transmitted human pathogens that have a major impact on blood safety and public health worldwide. We developed a microarray multiplex assay for the simultaneous detection and discrimination of these three viruses. The microarray consists of 16 oligonucleotide probes, immobilized on a silylated glass slide. Amplicons from multiplex PCR were labeled with Cy-5 and hybridized to the microarray. The assay detected 1 International Unit (IU), 10 IU, 20 IU of HBV, HCV, and HIV-1, respectively, in a single multiplex reaction. The assay also detected and discriminated the presence of two or three of these viruses in a single sample. Our data represent a proof-of-concept for the possible use of highly sensitive multiplex microarray assay to screen and confirm the presence of these viruses in blood donors and patients.     

乙肝病毒X蛋白结合蛋白最新研究进展

乙肝病毒X蛋白结合蛋白(HBXIP)是肝细胞癌变过程的一个关键因素,它能在动物肌肉组织和恶性肿瘤组织中过表达。近年来研究显示:HBXIP能与人体内多种蛋白结合。本文综述了HBXIP蛋白参与细胞凋亡与增殖、细胞周期进程、中心体复制、肿瘤细胞迁移等过程,以期为以HBXIP蛋白为靶标的新的抗乙肝病毒等药物设计提供基础。     

HIV and HCV: from Co-infection to epidemiology, transmission, pathogenesis, and treatment

Human immunodeficiency virus (HIV) is the infectious agent causing acquired immunodeficiency syndrome (AIDS), a deadliest scourge of human society. Hepatitis C virus (HCV) is a major causative agent of chronic liver disease and infects an estimated 170 million people worldwide, resulting in a serious public health burden. Due to shared routes of transmission, co-infection with HIV and HCV has become common among individuals who had high risks of blood exposures. Among hemophiliacs the co-infection rate accounts for 85%; while among injection drug users (IDU) the rate can be as high as 90%. HIV can accelerate the progression of HCV-related liver disease, particularly when immunodeficiency has developed. Although the effect of HCV on HIV infection is controversial, most studies showed an increase in mortality due to liver disease. HCV may act as a direct cofactor to fasten the progression of AIDS and decrease the tolerance of highly active antiretroviral therapy (HARRT). Conversely, HAART-related hepatotoxicity may enhance the progression of liver fibrosis. Due to above complications, co-infection with HCV and HIV-1 has imposed a critical challenge in the management of these patients. In this review, we focus on the epidemiology and transmission of HIV and HCV, the impact of the two viruses on each other, and their treatment.