中国不同地区商品猪中戊型肝炎病毒感染情况调查

戊型肝炎病毒(HEV)是戊型肝炎(戊肝,HE)的病原体,其基因组结构及病毒形态与杯状病毒科有一定相似之处,但仍有较大差别,因此目前其分类地位尚不明确。戊型肝炎在我国及许多发展中国家均是一种危害严重的急性传染性疾病。其临床表现与甲型肝炎类似,但病死率更高一些,尤其在孕妇中病死率可达20％。HEV主要通过粪口传播,经     

慢性戊型肝炎的研究进展

戊型肝炎病毒(hepatitis E virus,HEV)引起的戊型肝炎一直被认为是一种急性自限性感染过程,然而最近发现,器官移植、人类免疫缺陷病毒(human immunodeficiency virus,HIV)感染者等免疫力低下的患者感染HEV能够发展为慢性戊型肝炎.有些慢性戊型肝炎病例肝脏快速纤维化而出现肝硬化,并最终导致肝脏衰竭.患者免疫抑制作用减弱,免疫功能恢复有助于体内持续存在的HEV清除.研究发现干扰素和利巴韦林对治疗慢性戊型肝炎有效.     

误诊为药物性肝炎的艾滋病合并慢性戊型肝炎2例报道并文献复习

正戊型病毒性肝炎是由戊型肝炎病毒(HEV)引起的急性病毒性肝炎[1],教科书中关于戊型病毒性肝炎的讲述其为急性自限性肝炎,长期以来一直被认为是一种急性发病过程,不形成慢性感染[2]。但近些年多个研究报道在器官移植[3～5]、人类免疫缺陷病毒(HIV)感染者[6～8]等免疫力低下的患者感染戊型肝炎病毒能够发展为慢性戊型肝炎。此类患者在临床上很容易误诊为药物型肝炎而迁延不愈,现将我科收集到的2例因服用     

HAV、HEV混合感染与散发性HA、HE的临床研究

1 资料与方法 1.1 临床资料 本组全部病例均为我院传染病科住院治疗者,其中甲型肝炎病毒(HAV)、戊型肝炎病毒(HEV)感染35例,散发性甲型肝炎(HA)45例,散发性戊型肝炎(HE)61例。年龄与性别构成见表1。     

戊型肝炎病毒感染的免疫发病机制

戊型肝炎大多是急性自限性的，但免疫功能低下患者(如实体器官移植受者、HIV感染和血液疾病)会出现慢性感染。免疫反应是决定戊型肝炎病毒(HEV)感染结局的关键因素，其中包括天然免疫和适应性免疫。通过细胞培养、动物模型和临床试验等多种研究，对HEV免疫发病机制的认识更加深入，这些为HEV新的抗病毒治疗和有效疫苗的开发提供了思路。本综述讨论了近年来有关HEV的免疫发病机制，并提出了对该疾病预防及治疗的展望。     

重组抗原检测戊型肝炎病毒IgM抗体及其意义

用戊型肝炎病毒(HEV)重组抗原建立酶联免疫吸附试验(ELISA)，检测肝炎患者和健康供血人群血清中抗戊型肝炎病毒IgM类抗体(抗-HEV IgM)，并评价其检测意义。在与合成肽抗原比较检测的77份急性戊型肝炎患者血清中，有54份(70.1%)由重组抗原捡测抗-HEV IgM阳性。其阳性率明显高于台成酞抗原(21/77,27．3％)。15例戊型肝炎患者双份血清用重组抗原ELISA检铡，急性期血清有11份抗-HEV IgM阳性，恢复期血清仅1份阳性。抗-HEV IgG阳性的健康供血者(8人)和甲、乙、丙型肝炎患者(11例)无1例IgM抗体阳性。结果表明，抗-HEV IgM可以作为戊型肝炎病毒新近感染的标志。HEV重组抗原检铡抗-HEV IgM敏感性高，特异性强，有助于戊型肝炎病毒感染的早期诊断。     

免疫抑制人群中的慢性戊型肝炎病毒感染

戊型肝炎是戊型肝炎病毒（hepatitis Evirus,HEV）引起的传染病,在全球均有分布。既往认为,HEV感染呈急性自限性经过。最近,人们开始关注并认识到,存免疫抑制人群中存在着慢性HEV感染,并可进展为肝硬化,其感染可能通过输血或者动物源性传播。目前尚无慢性HEV感染的预防指南和治疗规范,但减少免疫抑制剂用量以恢复免疫抑制患者的细胞免疫可能有助于HEV的清除,HEV疫苗的接种也可能成为预防免疫抑制患者HEV感染的有效方法。     

锌指抗病毒蛋白协同IFNβ抑制戊型肝炎病毒的复制

正【据Journal of Viral Hepatitis 2021年8月报道】题:锌指抗病毒蛋白通过协同IFNβ抑制戊型肝炎病毒复制(作者:Yu WH等)戊型肝炎病毒(HEV)感染是导致全球急性病毒性肝炎的主要原因。然而,HEV与宿主相互作用的机制尚不清楚。锌指抗病毒蛋白(ZAP)是一种新型的IFN刺激基因,可与IFNβ协同作用抑制多种病毒的复制。本研究旨在探讨ZAP与HEV复制之间的相互作用。     

免疫抑制受体接受戊型肝炎病毒阳性供体血制品捐献的相关风险

正【据《J Hepatol》2018年3月报道】题:免疫抑制受体接受戊型肝炎病毒阳性供体血制品捐献的相关风险(作者Dirk W等)英国和荷兰最近对血制品进行了常规戊型肝炎病毒(HEV)测定。在欧洲,输血和HEV感染间的相关性仍具有争议。作者对2016年10月-2017年5月汉堡-埃彭多夫大学医学中心的所有献血者使用混合标本检测PCR法进行前瞻性的HEV RNA测定。反应性样本单独重新测定。此外,对先前阳性献血者的储存样本进行测定以确定HEV病毒血症的持续时间。HEV RNA阳性的献血者和对照组均被要求填写一份问卷调查。18 737名献血者中有23例HEV RNA阳性(0.12%)。只有2例阳性捐献者     

戊型肝炎已成为全球和我国严重的公共卫生问题之一

正戊型肝炎是由戊型肝炎病毒(HEV)感染引起的急性病毒性肝炎,多为自限性,极少数免疫功能低下者如器官移植患者、HIV感染者等也可慢性化~([1-2])。HEV分为4个基因型,Ⅰ型和Ⅱ型仅感染人类,主要分布在卫生条件相对较差的亚洲、非洲、中美洲等发展中国家和地区,污染饮用水源后可引起大规模的暴发和流行。基因Ⅲ型和Ⅳ型为人畜共患,在发达国家和地区多以散发为主。成年人尤其是中老年人群感染HEV多表现     

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.     

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.     

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.     

GB virus type C/Hepatitis G virus

After hepatitis G virus (HGV) and GB virus type C (GBV-C) were independently discovered, it was determined that they were two isolates of the same virus. The HGV/GBV-C genome sequence and organization are closely related to hepatitis C virus. Although HGV/GBV-C infection is common and frequently persists in humans, infection has not been found to be associated with any known disease state. Because this virus is not associated with acute or chronic hepatitis, most people refer to it as GBV-C. GBV-C appears to grow in lymphocytes and not in hepatocytes, and presumably this is why the virus does not cause liver disease. Recent studies suggest that GBV-C infection in HIV-positive people is associated with prolonged survival. In vitro coinfection of human lymphocytes with GBV-C and HIV lead to decreased HIV replication. Further understanding of the mechanism(s) responsible for this interaction with HIV may provide novel approaches for treating HIV and AIDS.