Feucht H H, Zöllner B, Polywka S, Knödler B, Schröter M, Nolte H, Laufs R
Institute of Medical Microbiology and Immunology, Universitätskrankenhaus Eppendorf, Hamburg, Germany.
Hepatology. 1997 Aug;26(2):491-4. doi: 10.1002/hep.510260234.
A new virus named hepatitis G virus (HGV) has been detected recently. Until now, no assays for the detection of antibodies against different HGV proteins have been commercially available. Therefore, a strip immunoblot assay has been established to investigate seroreactivity against recombinant structural (core) and nonstructural proteins (NS3 and NS4) of HGV produced in Escherichia coli. Seropositivity for HGV was evaluated and concordanced with HGV polymerase chain reaction (PCR) results in 709 subjects. These individuals were classified into a nonrisk or a risk group, on the basis of infection with human immunodeficiency virus (HIV) or hepatitis C virus (HCV) or frequent parenteral exposure, including hemophilia, intravenous drug addiction, receipt of blood transfusion, or hemodialysis. The nonrisk group consisted of 257 healthy blood donors with normal alanine transaminase (ALT) levels (ALT < 30 U/L) and 154 patients with suspected non-A-E hepatitis (ALT > 45 U/L). In the group of healthy blood donors, 1.9% (5 of 257) had detectable HGV viremia and 15.9% (41 of 257) showed antibody response to HGV. In the collective of patients with suspected non-A-E hepatitis, results from 1.9% of patients (3 of 154) were positive by HGV PCR, and 15.6% of patients (24 of 154) showed seropositivity against the recombinant HGV proteins. In six groups of patients (n = 298) with different risk factors, the prevalence of both HGV viremia (V) and serological reactivity (SR) was higher compared with that of the nonrisk group: V, 6.80%-35.2%; serological reactivity (SR), 25.4%-52.9%. The following conclusions can be derived from our data. HGV infection is widespread in the general population. The prevalence of antibodies against HGV or detectable HGV viremia is higher in patients with risk factors for parenteral viral transmission than in those without risk factors. The majority of HGV infections (70.2%) is self-limiting and not persistent in our collective of patients. We found no correlation between HGV viremia and clinical or biochemical signs of hepatitis in individuals without risk factors for acquiring parenterally transmitted agents.
最近发现了一种名为庚型肝炎病毒（HGV）的新型病毒。到目前为止，尚无用于检测针对不同HGV蛋白抗体的检测方法可供商业使用。因此，已建立了一种条带免疫印迹法，以研究针对在大肠杆菌中产生的HGV重组结构（核心）蛋白和非结构蛋白（NS3和NS4）的血清反应性。在709名受试者中评估了HGV血清阳性，并将其与HGV聚合酶链反应（PCR）结果进行比对。根据是否感染人类免疫缺陷病毒（HIV）或丙型肝炎病毒（HCV）或频繁接受非肠道暴露，包括血友病、静脉吸毒、输血或血液透析，将这些个体分为无风险组或风险组。无风险组包括257名丙氨酸转氨酶（ALT）水平正常（ALT<30 U/L）的健康献血者和154名疑似非甲-戊型肝炎患者（ALT>45 U/L）。在健康献血者组中，1.9%（257名中的5名）可检测到HGV病毒血症，15.9%（257名中的41名）显示对HGV有抗体反应。在疑似非甲-戊型肝炎患者群体中，1.9%的患者（154名中的3名）HGV PCR结果为阳性，15.6%的患者（154名中的24名）显示对重组HGV蛋白血清阳性。在六组具有不同风险因素的患者（n=298）中，HGV病毒血症（V）和血清学反应性（SR）的患病率均高于无风险组：V为6.80%-35.2%；血清学反应性（SR）为25.4%-52.9%。从我们的数据中可以得出以下结论。HGV感染在普通人群中广泛存在。有非肠道病毒传播风险因素的患者中，抗HGV抗体或可检测到的HGV病毒血症的患病率高于无风险因素的患者。在我们的患者群体中，大多数HGV感染（70.2%）是自限性的，并非持续性感染。我们发现，在没有获得非肠道传播病原体风险因素的个体中，HGV病毒血症与肝炎的临床或生化体征之间没有相关性。
