CLINICAL ASPECTS OF HEPATITIS G VIRUS INFECTION

庚型肝炎病毒(HGV)是新发现的 与黄病毒科有大约25%同源性的黄毒科 丙型肝炎病毒(HCV)。其临床意义尚不清楚。我们 研究了HGV及其与输血风险的关系。HGV是 在大约1.5%的捐赠者群体中发现了这种病毒 显示是通过HGV的急性出现而传播的输血 输血后的RNA，HGV阳性献血者和 感染受者，输血受试者发病率较高 与未输血的对照组比较。HGV被证明持续存在于 大多数感染者，但近40%的人似乎 随着时间的推移清除病毒。尽管13名患者中有3名(23%)没有 甲型、非乙型、非丙型输血相关性肝炎有急性HGV HGV在这些病例中的因果作用尚不清楚，因为 HGV RNA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 1例对ALT异常有不同的解释。总的来说， 在35例观察到的和84例预测的HGV感染中，只有4% 发生在肝炎患者中(描述的三个病例 上图)，7%发生在与丙型肝炎共存的患者中，其中 ALT升高与丙型肝炎病毒有关，16%的人在 ALT轻度升高的受者他们没有 被归类为肝炎，73%发生在 无生化或临床肝炎证据的受者。 因此，绝大多数感染HGV的患者没有证据 在少数肝病患者中，因果关系无法得到证明。 同样，我们也研究了肾透析患者中的HGV 血友病患者，静脉注射吸毒者，以及急性和慢性疾病患者 慢性非甲非乙非丙非丁非戊型肝炎。虽然 在非肠道接触者中，HGV的流行率很高 个人(10%-20%)，与肝病无关 这些感染庚型肝炎病毒的人群。庚型肝炎病毒与丙型肝炎病毒混合感染的研究 患者的研究表明，HGV并没有恶化患者的病程。 同时存在丙型肝炎病毒感染。

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.