部分病毒性肝炎和肝炎高危人群中抗-HGV血清流行病学调查

为了解庚型肝炎病毒(HGV)在本地区部分人群中的感染状况,应用ELISA法对355例各型肝病患者及120例肝炎高危人群进行了抗-HGV检测,急性肝炎、慢性肝炎、重型肝炎、肝硬变和原发性肝癌患者抗-HGV检出率分别为22.0％(12/54)、23.7％(46/194)、25.7％(9/35)、26.2％(11/42)和23.3％(7/30)。在HAV、HBV、HCV、HEV、MBV+HAV、HBV+HCV、HBV+HDV、HBV+HEV及HCV+HEV感染的肝病患者中抗-HGV检出率分别为11.5％(3/26)、28.1％(51/181)、22.6％(7/31)、8.3％(1/12)、20.0％(4/20)、22.2％(5/18)、15.8％(3/19)、15.4％(2/13)和16.7％(1/6);非甲-戊肝炎患者中抗-HGV阳性率28.3％(8/29);健康献血员、血液透析者及静脉吸毒者中抗-HGV检出率分别为15.6％(6/40)、7.5％(3/40)和10.0％(4/40)。以上结果组间均无显著性差异(P<0.05)。研究发现本地区各种肝病患者及肝炎高危人群中存在HCV感染。各种肝病患者重叠感染HGV组与未重叠组ALT、AST及总胆红素(TB)水平无显著性差异(P>0.05),表明重叠感染者病情不加重。对21例单纯抗-HCV阳性者连续20个月动态检测血消ALT、AST、TB及白蛋白,其中仅14.6％(3/12)的患者表现为急性肝炎,ALT、AST轻度升高,1个月恢复正常,血清TB和白蛋白无异常;另85.4％(18/21)血清ALT、AST、TB及白蛋白始终正     

临床肝病患者中庚型肝炎病毒(GBV-C/HGV)的感染

本文应用抗-HGV酶联免疫法(EIA)和逆转录套式聚合酶链反应法(RT-PCR)检测150份乙型、120份丙型、15份戊型和49份非甲-戊型肝炎患者血清。结果显示:乙肝、丙肝、戊肝和非甲-戊型肝炎患者中抗-HGV抗体的阳性率分别为22.0％(33/150)、25.0％(30/120)、33.3％(5/15)和40.1％(20/49)。其中乙型、丙型、戊型和非甲-戊型肝炎的抗-HGV抗体阳性者中,HGV RNA的阳性率分别为58.3％(7/12)、60.0％(6/10)、40.0％(2/5)和45.5％(9/12)。说明GBV-C/HGV可与HBV、HCV或HEV合并感染,该病毒可能引起临床型肝炎。     

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.     

中国的庚型肝炎病毒感染

庚型肝炎病毒是最近从非甲→非戊型肝炎病人中分离到的,并为独立的两组,分别命名为GBV 病毒(GBV-C)和庚型肝炎病毒(HGV)。比较这两种病毒的序列显示高度的同源性,揭示它们是一个病毒的两个基因型。故病毒暂命名为GBV-C/HGV.中国HGV感染分布较广     

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。     

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者的庚型肝炎病毒(HGV)感染状况。方法:应用酶联免疫法(ELISA)检测不同临床型肝病患者血清中抗-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HGV RNA。结果:肝硬变,慢性乙型和丙型肝炎病人及HBsAg携带者的抗-HGV阳性率(分别为36.36％、26.2％、12.5％和12.0％),均显著高于急性肝炎(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)。各临床型肝病患者中,抗-HGV阳性和阴性组血清天门冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)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似并不加重肝损害程度。     

乌鲁木齐地区部分高危人群庚型肝炎病毒感染状况的研究

目的 了解新疆乌鲁木齐地区部分高危人群中庚型肝炎病毒的感染状况。方法 首先运用酶标法(ELISA)检测不同人群中庚型肝炎病毒抗体(抗-HGV),然后对抗-HGV阳性血清运用逆转录聚合酶链反应(RT-PCR)检测HGV RNA。结果 在各类高危人群中,抗-HGV阳性率分别是:手术受血者为35.59％(21/59),静脉吸毒者为38％(19/50),非甲～戊型肝炎病人为18％(9/50);均显著高于对照人群(2％,1/50,P<0.05);职业供血员抗-HGV阳性率也较高(13.79％,8/58),但与对照人群无显著性差异(P>0.05);58份抗-HGV阳性血清有18份血清HGV RNA阳性,其中手术受血者血清1份,静脉吸毒者血清12份,职业供血员血清2份,非甲～戊型肝炎病人血清3份。结论 (1)本研究首次在乌鲁木齐地区部分高危人群中证实有较高的庚型肝炎病毒感染率;(2)再次证实该病毒主要通过注射、输血途径传播。     

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。     

HGV/GBV-C与HCV混合感染者肝组织中相关病毒抗原表达

庚型肝炎病毒(HGV/GBV-C)的致病性是目前研究焦点之一,多数研究表明大多数HGV/GBV-C感染者体内常有两种或两种以上的肝炎病毒混合感染,并认为HGV/GBV-C感染对原有乙型肝炎病毒(HBV)或丙型肝炎病毒(HCV)感染的基础病变似无明显影响[1-3].但仅从血清学、临床表现及常规病理角度试图说明HGV/GBV-C对机体有无损害的研究工作是很困难,我们应用免疫组织化学技术对HGV/GBV-C与HCV混合感染者肝组织中HGV/GBV-C.HCV相关抗原表达进行研究,试图从免疫病理学角度探讨HGV/GBV-C对机体肝脏的致病性.     

乙型肝炎患者丁、戊、庚型肝炎病毒混合感染

乙型肝炎发病率高,严重危害劳动人民的身心健康,其发病机制目前仍未彻底阐明.近年来美国学者Linen et al[1],Simons et al[2 ]通过分子生物学方法在病毒性肝炎患者血清中发现了新型肝炎病毒-庚型肝炎病毒(HGV/GBV-C).先前我们的研究发现川北地区存在HGV感染,HGV感染病例肝损伤轻,预后好[3].在重型肝炎组中HGV感染病例病死率较低,预后好[4].国内一些学者[5-8]对乙肝患者感染HCV,HDV及HGV分别进行了研究,但缺乏系统性.乙肝患者中丁、戊、庚型肝炎病毒混合感染情况如何,它们的感染对乙肝患者病情有何影响,目前国内尚未见有关方面的报道.检测乙肝患者血清中丁、戊、庚型肝炎病毒感染情况,对患者的病原学诊断、判断病情、估计预后有较为重要的临床参考价值.为此,我们对乙肝患者血清进行了丁、戊、庚肝抗体检测,旨在探讨其混合感染情况以及混合感染对发病的影响,现将结果报告如下.     

HGV/GBV-C infection in patients with acute hepatitis of different etiology and in patients with chronic hepatitis C

To investigate the prevalence of hepatitis G virus (HGV/GBV-C) in patients with liver disease and to confirm its hypothesized ability to cause liver damage, we studied 130 subjects; 61 had chronic hepatitis C virus infection and 69 had acute hepatitis of either defined etiology (n = 57) or of unknown origin (n = 12). Positivity for HGV/GBV-C RNA was detected in 10 of the 61 subjects with chronic hepatitis C (16.3%) and in 11 of the 57 subjects with acute hepatitis of defined etiology (19%), whereas we failed to detect HGV/GBV-C viremia in subjects with hepatitis of non-established etiology. Patients exhibiting positivity for HGV/GBV-C RNA were found to be comparable to those exhibiting negativity for HGV/GBV-C RNA in terms of both liver function tests and Knodell's score (in liver biopsies); the affect of HGV/GBV-C infection on the biohumoral and histological activity in patients with chronic hepatitis C therefore appears to be minimal or absent. Similar clinical features were observed in patients with acute hepatitis of known etiology whether they were positive or negative for HGV/GBV-C RNA. However, long-term clinical studies are still required to clarify the actual impact of HGV/GBV-C co-infection. In our geographic, i.e., a region or north-east Italy, HGV/GBV-C infection appears to be strictly related to intravenous drug use, and this agent does not seem to be responsible for acute hepatitis of unknown etiology; other etiological agents are probably involved. Received Feb. 17, 1997; accepted June 27, 1997     

A case-control study of transmission routes for GB virus C/hepatitis G virus in Swedish blood donors lacking markers for hepatitis C virus infection.

BACKGROUND AND OBJECTIVES: The transmission routes for GB virus-C (GBV-C)/hepatitis G virus (HGV) in blood donors unexposed to hepatitis C virus (HCV) are unknown. We performed a case-control study of risk factors for GBV-C/HGV exposure in blood donors. MATERIALS AND METHODS: After testing stored sera from 458 HCV-negative blood donors for GBV-C/HGV RNA and GBV-C/HGV E2 antibodies, 66 donors with GBV-C/HGV markers and 125 age- and gender-matched controls were interviewed regarding risk factors for viral transmission. RESULTS: Exposure to GBV-C/HGV was strongly associated with previous treatment for a sexually transmitted disease (odds ratio [OR] 4.6; 95% confidence interval [CI] 2.2-9.8), with multiple sexual partners (OR 2.9; 95% CI 1.4-5.7) and with a past history of endoscopy (OR 7.0; 95% CI 3.0-16.4). CONCLUSIONS: In blood donors with GBV-C/HGV markers, sexual contacts and medical procedures appear to be the main transmission routes.     

GB virus C/hepatitis G virus infection in patients investigated for chronic liver disease and in the general population in southern Sweden

Serum samples from patients referred for liver biopsy for investigation of suspected chronic liver disease (n = 286) and from healthy middle-aged volunteers (n = 445) were analyzed for markers of exposure to GB virus C/hepatitis G virus (GBV-C/HGV), hepatitis B virus and hepatitis C virus. GBV-C/HGV analyses included GBV-C/HGV PCR for detection of viremia and GBV-C/HGV enzyme-linked immunosorbent assay for anti-GBV-C/HGV E2 antibodies. Liver biopsies were re-evaluated by a hepatopathologist. GBV-C/HGV markers were detected in 97/286 (34%) patients (GBV-C/HGV RNA = 26; anti-GBV-C/HGV E2 antibodies = 74) compared to 86/445 (19%; p < 0.0001) controls (GBV-C/HGV RNA = 7, anti-GBB-C/HGV E2 antibodies = 79). A significantly higher proportion of GBV-C/HGV-exposed subjects in the patient group were viremic compared to controls (27% vs. 8.1%; p = 0.0015). GBV-C/HGV markers were more commonly found in patients with chronic hepatitis B and C. In patients with GBV-C/HGV viremia, a higher occurrence of bile duct degeneration was detected than in non-viremic patients. Markers of GBV-C/HGV infection were over-represented among patients investigated for chronic liver disease, and ongoing GBV-C/HGV viremia was more common in this group than in controls. Apart from a higher prevalence of bile duct degeneration in viremic patients, infection with GBV-C/HGV did not confer any specific histological characteristics.     

GB Virus C/Hepatitis G Virus Infections in Traumatologic Outpatients, Chronic Non-A-E Hepatitis and Extrahepatic Malignancies

Summary GB virus C/hepatitis G virus (GBV-C/HGV) is a recently discovered flavivirus of still unknown pathogenic relevance. We examined traumatologic outpatients to determine GBV-C/HGV viremia for further epidemiological studies, as blood donors hitherto used as controls represent healthy individuals without risk factors. Anti-GBV-C/HGV antibodies were detectable in 13.2% (95% confidence interval [CI] 9.3–18.2) and GBV-C/HGV RNA was detectable in 4.5% (95% CI 2.4–8.2) of the outpatients. In chronic non-A-E hepatitis patients GBV-C/HGV viremia was detectable at a significantly higher level of 16.1% (95% CI 6.1–:34.5), while the prevalence of anti-GBV-C/HGV antibodies was 12.9% (95% CI 4.2–30.8). The rate of GBV-C/HGV viremia in patients with malignant diseases (different types of tumors, blood recipients were excluded) was 12.5% (95% CI 8.4– 18.1), a significant elevation compared to traumatologic outpatients. The seroprevalence in the tumor group was 22.1% (95% CI 16.7–28.6), also significantly elevated. Thus, there are two messages. Firstly, testing for GBV-C/HGV may be a useful extension of the diagnostic procedure of viral hepatitis. Secondly, common risk factors or etiologic relations of GBV-C/HGV and extrahepatic malignancies should be discussed. Received: March 29, 1999 · Revision accepted: November 22, 1999     

Prevalence of hepatitis G virus RNA in a monocentric population of French haemophiliacs

Hepatitis G virus (HGV) and hepatitis GB virus (GBV-C) have been reported as possible causes of non-A–E transfusional hepatitis. To assess the prevalence of hepatitis G virus infection in haemophiliacs we retrospectively investigated the presence of viral RNA in 92 patients with and without HCV infection. HGV/GBV-C RNA was reverse transcribed and amplified with primers from the 5' non-coding region of the genome. RNA was detected in 16/92 patients (17.4%). Restriction enzyme analysis revealed that the 16 patients belonged to the HGV-like genotype. Serology with E2-specific antibodies demonstrated that HGV viraemia underestimates previous infection by HGV. 33 patients were positive for HGV; all but two have cleared HGV RNA. 47/92 patients had a marker of prior infection by HGV.
No difference between HGV RNA positive and negative patients was observed concerning age, diagnosis, HIV and HCV status. Previous HBV infection correlated with the frequency of HGV infection. There was no difference in alanine aminotransferase levels between HGV positive and negative patients. All 18 patients exposed to only virally inactivated plasma-derived concentrates were negative for both HGV RNA and anti E2 antibodies.
Prior exposure to untreated concentrates correlated with HGV viraemia ( P =0.03), HGV seropositivity ( P =0.0002), and markers of HGV infection ( P <0.0001).
In haemophiliacs with a past exposure to non-inactivated concentrates, persistence of HCV RNA (53/74 patients) was more frequent than HGV RNA persistence (16/74 patients) although HGV viraemia is more frequent than HCV viraemia in blood donors. This may be related to a greater ability of individuals to clear HGV infection and suggests that hepatitis G virus infection in multi-transfused patients has a better outcome than infection with other blood-borne viruses.     

Minimal role of GB virus-C/hepatitis G virus in fulminant and subfulminant hepatitis in Taiwan

BACKGROUND: The role of GB virus-C/hepatitis G virus (GBV-C/HGV) in fulminant hepatitis (FH) and subfulminant hepatitis (SFH) remains unclear. METHODS: Thirty-two FH or SFH patients, with adequate clinical information and serum specimens, were studied. Serum samples were tested for hepatitis markers and genomes of hepatitis A-E viruses, as well as GBV-C/HGV. RESULTS: Of the cases of FH/SFH studied, one (3%) was caused by anti-tuberculosis agents, 26 (81%) had hepatotropic virus infection, and five (16%) had no identifiable cause. Of the 26 patients with hepatotropic virus infection, five had acute hepatitis B infection (one with acute hepatitis D virus (HDV) co-infection), one had acute hepatitis C infection, 16 were hepatitis B surface antigen carriers with reactivation or superimposed by unidentified agent(s) (two had triple virus infections), three were hepatitis B carriers with HDV superinfection, and one had GBV-C/HGV infection in addition to exposure to halothane. GBV-C/HGV-RNA was detected in only three of 32 patients (9%) and all had a history of blood transfusion or co-existing causative factors. Of the 26 patients with hepatotropic virus infection, 18 were tested for antibodies against GBV-C/HGV envelope protein and seven were reactive, suggesting past infection. CONCLUSIONS: The role of GBV-C/HGV in causing FH and SFH is minimal in Taiwan and HBV infection remains the major aetiology. These findings also suggest the existence of as yet unrecognized agents, responsible for such catastrophic illnesses.