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。     

戊型肝炎合并甲乙丙丁肝炎病毒感染病例的分析

本文对３５４例各型肝炎病人检测了甲，乙，丙，丁，戊各型肝炎病毒的标志物，发现戊型肝炎（抗－ＨＥＢ阳性）６６例，占１８．６４％，戊型肝炎临床主要表现为急性黄疸型（６３．６４％）另还有急性无黄疸型，胆汁瘀积型及重症型，戊型肝为具有典型肝炎症状者多见（９３．９４％），黄疸多见（８３．３３％），ＡＬＴ均有升高，ＨＥＶ可与ＨＡＶ，ＨＢＶ，ＨＣＶ混合感染，总的混合感染率为３４．８５％，以乙＋戊为最多（１６．６     

重叠感染的戊型肝炎103例临床分析

１９９５年１月至１９９６年１２月住院的重叠感染戊型肝炎（戊肝）１０３例,我们以单纯戊肝４６例作对照,进行比较,现报告如下。临床资料一、一般资料１９９５年１月～１９９６年１２月我院共收治戊肝患者１８０例,男１４２例,女３８例;平均年龄３９．７岁（１４～８１岁）。５９例有肝炎或肝病史,占３２．８％,既往肝炎（病）史距本次发病平均１５．４年。本组病例中重叠感染戊肝１０３例,占５７．２％。按１９９５年（北京）全国传染病与寄生虫病学术会议修订的病毒性肝炎诊断标准,重叠感染戊肝病例可分为乙＋戊组７０例,丙＋…     

慢性乙型肝炎重叠戊型肝炎病毒感染1例

我国是乙肝大国，在临床上慢性乙肝重叠戊型肝炎的患者不在少数，发病后患者往往有向重症肝炎发展的倾向，应及时治疗，否则会危及生命。现将临床上乙型肝炎重叠戊型病毒肝炎1例报告如下。     

肝炎患者906例戊型与甲,乙,丙各型肝炎病毒重叠感染血清学分析

肝炎患者９０６例戊型与甲、乙、丙各型肝炎病毒重叠感染血清学分析沙安莉，曹立森为了解无锡地区戊型肝炎感染的情况，本文作者对９０６例肝炎患者作了戊型肝炎病毒抗体（抗－ＨＥＶ）的调查，并将其中１１６例抗－ＨＥＶ阳性者与甲、乙、丙型肝炎病毒合并感染的血清学结...     

慢性乙型肝炎重叠戊型肝炎病毒感染的研究

目的了解慢性乙型肝炎重叠戊型肝炎病毒(HEV)感染的临床特点、乙型肝炎病毒(HBV)复制指标、肝功能损伤程度及预后。方法收集慢性乙型肝炎患者和慢性乙型肝炎重叠HEV感染(重叠感染组)各115例,两组病情(轻、中、重度)和HBV DNA定量相同,对两组患者进行临床分析,慢性乙型肝炎组中74例和重叠感染组中的51例患者,在B超引导下做肝活组织检查；应用酶联免疫吸附试验和聚合酶链反应分别检测两组患者HBV标志物,HBV DNA及抗HEV lgM。结果重叠感染组重型肝炎57例,发生率49．6%,死亡29例,病死率25．2%；慢性乙型肝炎组重型肝炎5例,发生率4．4%,死亡2例,病死率1．7%,两组比较,x~2值分别为58．80和27．01,P值均＜0．01,差异有统计学意义。血清HBV DNA≥10~4患者：重叠感染组占83．7%(36/43),单纯慢性乙型肝炎组占97．1%(67/69),x~2=4．73,P＜0．05；重叠感染组总胆红素平均(495．0±217．0)μmol/L、丙氨酸氨基转移酶平均(967．0±395．0) U/L,单纯慢性乙型肝炎组总胆红素平均(216．0±195．0)μmol/L和丙氨酸氨基转移酶平均(373．0±212．0)U/L,两组比较,t值分别为10．20和14．52,P值均＜0．01,差异有统计学意义；肝组织炎症G3和G4重叠感染组33例,占64．7%,单纯慢性乙型肝炎组25例,占33．8%,x~2=12．46,P＜0．01,差异有统计学意义。结论重叠感染组肝功能损害严重,肝组织炎症程度高,HBV DNA水平低,病死率高,预后差。     

慢性乙型肝炎患者重叠戊型肝炎病毒感染的临床与病理学研究

目的：观察重叠戊型肝炎病毒（HEV）感染对慢性乙型肝炎（CHB）肝脏损害及HBV复制的影响。方法：应用ELISA法对122例CHB患者血清进行了抗－HEV IgkM,IgG检测,同时应用肝穿刺活检、荧光定量PCR及免疫组化等技术对重叠与未重叠HEV感染者分别进行了ALT、总胆红素（TBil)、凝血酶原活动度（PTA）、白蛋白／球蛋白（A／G）、电泳γ球蛋白（γ－EP）水平、肝脏病理学、血清HBeAg及肝组织HBcAg阳性率、血清及肝组织中HBV DNA含量对比。具有可比性的重叠（7例）与未重叠HEV感染者（14例）1年后做第2次肝穿活检并做病理学比较;HBeAg阴性重叠HEV感染者8例做HEV感染急性期、恢复期血清HBeAg定性、HBV DNA含量对比。结果：重叠HEV感染者21例（17．2％）。重叠HEV感染者较未重叠感染者ALT、TBil增高,PTA降低（P＜0．05）,但A／G、γ－EP水平未见显著差别（P＞0．05）;血清HBeAg及肝组织HBcAg阳性率、血清及肝组织HBV DNA含量低（P＜0．05）;肝组织炎症活动度重（P＜0．05）,但纤维化程度未见明显差别（P＞0．05）。两组患者1年前肝组织炎症活动度及纤维化程度无显著差别,1年后仍无显著差别（P＞0．05）。HEV感染恢复期血清HBeAg阳性率、HBV DNA含量高于急性期（P＜0．05）。结论：重叠HEV感染可加重CHB肝组织炎症活动度;对HBV复制具有短暂抑制作用。     

老年慢性乙型肝炎重叠感染戊型肝炎的临床特点

戊型病毒性肝炎是老年急性病毒性肝炎的主要病因，同时我国有大量老年慢性乙型肝炎患者，为探索老年慢性乙型肝炎患者重叠感染急性戊型肝炎的临床特点，作者对本院2002年6月至2005年1月收治的老年乙、戊型肝炎重叠感染患者20例进行分析如下。     

Overview of hepatitis E virus

Hepatitis E virus (HEV) is an enterically transmitted virus usually presenting as an acute self-limiting disease. However, mortality increases dramatically from around 1% to 20% in pregnant women. HEV has been the cause of very large outbreaks of hepatitis in developing countries and is also responsible for a significant number of sporadic cases. It is clear that cases occur outside the endemic areas, and new isolates have been identified. HEV-like viruses have also been found in various animal groups, and it is likely that HEV can be regarded as a zoonotic infection. Preventative measures at the moment depend mainly on the provision of clean water supplies, although a vaccine is now undergoing clinical trials.     

人工肝治疗戊型肝炎合并高胆红素血症

目的观察人工肝（ALSS）治疗戊型肝炎合并高胆红素血症的临床疗效。方法在内科综合治疗的基础上,采用人工肝治疗52例戊型肝炎合并高胆红素血症患者,并随机选择43例戊型肝炎合并高胆红素血症患者作为对照组,评价临床疗效并观察治疗前后TBil、AST、ALT、ALB、BUN、Cr及PTA等指标。结果经人工肝治疗后84.62%患者原有的乏力、恶心呕吐、食欲等症状明显改善;治疗后治疗组血清中ALT较对照组显著下降（P〈0.05）,PTA、ALB明显上升（P〈0.05）,BUN、Cr无明显差异。治疗组戊型肝炎合并高胆红素血症治愈好转率为84.62%（44/52）;对照组治愈好转率为55.81%（24/43）,两组比较有统计学差异（P〈0.05）。结论在内科综合治疗基础上,及时采用人工肝辅助治疗,能提高戊型肝炎合并高胆红素血症患者治愈好转率。还可以通过TBil反弹的现象来判断患者的预后。     

Thermal stability of hepatitis E virus

The thermal stability of virulent hepatitis E virus (HEV) and hepatitis A virus (HAV) was compared. Fecal suspensions of virus were heated to temperatures between 45 degrees C and 70 degrees C, and residual infectivity was determined in a cell culture system that was permissive for both viruses. Although HEV was less stable than was HAV, some HEV would most likely survive the internal temperatures of rare-cooked meat.     

Culture systems for hepatitis E virus

The lack of an efficient cell culture system for hepatitis E virus (HEV) has greatly hampered detailed analyses of this virus. The first efficient cell culture systems for HEV that were developed were capable of secreting infectious HEV progenies in high titers into culture media, using PLC/PRF/5 cells derived from human hepatocellular carcinoma and A549 cells derived from human lung cancer as host cells. The success achieved with the original genotype 3 JE03-1760F strain has now been extended to various HEV strains in fecal and serum samples obtained from hepatitis E patients and to HEV strains in fecal and serum samples and liver tissues obtained from pigs and wild boar across species barriers. In addition, infectious HEV cDNA clones of the wild-type JE03-1760F strain and its variants have been engineered. Cell culture-generated HEV particles and those in circulating blood were found to be associated with lipids and open reading frame 3 (ORF3) protein, thereby likely contributing to the assembly and release of HEV from infected cells both in vivo and in vitro. The ORF3 protein interacts with the tumor susceptibility gene 101, a critical cellular protein required for the budding of enveloped viruses, through the Pro, Ser, Ala, and Pro (PSAP) motif in infected cells; ORF3 is co-localized with multivesicular bodies (MVBs) in the cytoplasm of infected cells, thus suggesting that HEV requires the MVB pathway for the egress of virus particles. This article reviews the development of efficient cell culture systems for a wide variety of infectious HEV strains obtained from humans, pigs, and wild boar, and also provides details of a new model for virion egress.     

Extrahepatic manifestations of hepatitis E virus

Hepatitis E virus can cause acute, fulminant and chronic hepatitis and has been associated with a range of extrahepatic manifestations. Guillain–Barré syndrome, neuralgic amyotrophy and encephalitis are the main neurological manifestations associated with acute and chronic hepatitis E virus infection. Renal injuries have been also reported, including membranoproliferative glomerulonephritis with or without cryoglobulinemia and membranous glomerulonephritis. Acute pancreatitis, haematological disorders and other autoimmune extrahepatic manifestations of hepatitis E virus, such as myocarditis and thyroiditis, have been also reported. In this comprehensive article, we review all published reports describing hepatitis E virus–associated extrahepatic manifestations.     

Epidemiology of hepatitis E virus infection

Hepatitis E is an acute, icteric, self-limiting disease, which is spread widely in many tropical and subtropical countries where it occurs both in the form of epidemics of variable magnitude or sporadically. Hepatitis E affects young adults, rather than children, and causes a high mortality rate, particularly in pregnant women. In industrialized countries this disease occurs occasionally as imported sporadic cases. The aetiological cause of hepatitis E is a virus, hepatitis E virus (HEV), which is temporally classified as a member of the Calicivirus family, although its genomic composition is unique. There are experimental data as well as epidemiological observations allowing us to assume that hepatitis E may be a zoonosis as HEV is pathogenic for some domestic and wild animals. Recently, serological assays based on the use of recombinant or synthetic antigens were developed and applied to determine the prevalence of antibody to HEV (anti-HEV) in various epidemic and non-epidemic settings. In suspected hepatitis E cases, anti-HEV seropositivity was detected at an elevated rate but the overall seroprevalence of anti-HEV in normal human populations of endemic areas appeared to be unexpectedly low. A low but constant presence of anti-HEV seropositivity was observed also in non-endemic industrialized countries. In some of these countries, anti-HEV seropositivity was accumulated in groups of patients with various liver and non-liver pathologies and certain groups at risk for blood-borne infections.