CLINICAL ASPECTS OF HEPATITIS G VIRUS INFECTION

庚型肝炎病毒（HGV）是一种新发现的成员， 黄病毒科家族，与 丙型肝炎病毒（HCV）。其临床意义尚不清楚。我们 HGV及其与输血风险的关系。HGV是 在大约1.5%的捐赠者中发现， 显示为HGV急性出现时输血传播 输血后的RNA，HGV阳性供体与 受感染者，输血受试者的发病率较高 与未输血的对照组相比。HGV被证明持续存在于 大多数受感染的受试者，但几乎40%的人似乎 随着时间的推移清除病毒虽然13例患者中有3例（23%） 甲、非乙、非丙型输血相关性肝炎有急性HGV 感染，HGV在这些病例中的因果作用尚不清楚， HGV RNA与HGV DNA之间没有明确的时间关系， 水平和丙氨酸氨基转移酶（ALT）升高，因为 病例对ALT异常有其他解释。总的来说， 在35例观察到的HGV感染和84例预测的HGV感染中， 发生在肝炎患者中（描述的三例病例 上述），7%发生在那些与HCV共存的患者中， ALT升高被证明与HCV相关，16%的患者与HCV相关。 接受者ALT轻微升高， 被归类为肝炎，73%发生在 接受者没有肝炎的生化或临床证据。 因此，绝大多数HGV感染患者没有证据表明 肝脏疾病和少数人做，因果关系无法证明。 同样，我们研究了肾透析患者中的HGV， 血友病患者、静脉吸毒者和急性和 慢性非甲、非乙、非丙、非丁、非戊型肝炎。虽然 在胃肠外暴露人群中，HGV的流行率非常高， 个体（10-20%），与肝脏疾病无关， 这些HGV感染的人群。在HGV和HCV合并感染者中 结果表明，HGV并没有使患者的病程恶化， 同时存在HCV感染。

The hepatitis G virus (HGV) is a newly discovered member of the flaviviridae family that has approximately 25 percent homology with hepatitis C virus (HCV). Its clinical significance is unknown. We have studied HGV and its relation to blood transfusion risk. HGV was found in approximately 1.5 percent of the donor population and was shown to be transfusion transmitted by the acute appearance of HGV RNA following transfusion, linkage between HGV positive donors and infected recipients, and a higher incidence in transfused subjects as compared with nontransfused controls. HGV was shown to persist in the majority of infected subjects, but almost 40 percent appear to clear the virus over time. Although 3 of 13 patients (23%) with non- A, non-B, non-C transfusion-associated hepatitis had acute HGV infection, the causal role of HGV in these case is not clear because there was no definite temporal relationship between the HGV RNA level and alanine aminotransferase (ALT) elevations and because one case had alternate explanations for the ALT abnormalities. Overall, of 35 observed and 84 projected HGV infections, only 4 percent occurred in patients with hepatitis (the three cases described above), 7 percent occurred in those with coexisting HCV where the ALT elevations were shown to be HCV related, 16 percent were in recipients who had such minor ALT elevations that they were not classified as having hepatitis, and 73 percent occurred in recipients with no biochemical or clinical evidence of hepatitis. Hence, the vast majority of HGV-infected patients have no evidence of liver disease and in the few who do, causality cannot be proved. Similarly, we have studied HGV in renal dialysis patients, patients with hemophilia, intravenous drug users, and patients with acute and chronic non-A, non-B, non-C, non-D, and non-E hepatitis. Although the prevalence of HGV is very high among parenterally exposed individuals (10-20%), there is no association with liver disease in these HGV-infected populations. Among HGV and HCV coinfected patients, it was shown that HGV did not worsen the course of the coexistent HCV infection.