McHutchison J G, Nainan O V, Alter M J, Sedghi-Vaziri A, Detmer J, Collins M, Kolberg J
Division of Gastroenterology/Hepatology, Scripps Clinic and Research Foundation, La Jolla, CA 92037, USA.
Hepatology. 1997 Nov;26(5):1322-7. doi: 10.1002/hep.510260534.
Hepatitis G virus (HGV), a positive sense RNA virus, is distantly related to hepatitis C virus (HCV): its genetic organization and identity are consistent with the Flaviviridae family. Coinfection with HGV occurs in 10% to 20% of HCV-infected subjects. These similarities raise two theoretical questions. First, could HGV coinfection play any role in the response of HCV to antiviral therapy and second, would this coinfected population have changes in serum HGV-RNA induced by interferon. To address these questions, 98 patients with documented chronic HCV underwent interferon therapy (3 million units three times a week) for 6 months. Response to therapy was categorized using standard biochemical criteria. Changes in HGV-RNA levels were evaluated before, during, and after interferon therapy by a quantitative branched DNA amplification research-based assay. Eleven of 98 (11%) patients with HCV infection had detectable serum HGV-RNA. There was no difference between the groups (HGV+ vs. HGV-) when baseline alanine aminotransferase (ALT) values, HCV-RNA levels, HCV genotype, histological severity, or other demographic features were analyzed. Interferon response was similar in both groups and HGV was not associated with outcome following therapy. Antiviral therapy appeared to induce a reduction in HGV-RNA load in five of nine patients coinfected with HCV serially tested. In two patients, the fall in serum HGV-RNA correlated with biochemical response, independent of changes in HCV-RNA. These observations indicate that a larger study of an HGV population is required to more clearly define the relationship between HCV and HGV coinfection and their response to antiviral therapy.
庚型肝炎病毒（HGV）是一种正义RNA病毒，与丙型肝炎病毒（HCV）亲缘关系较远：其基因结构和特征与黄病毒科一致。10%至20%的丙型肝炎病毒感染患者同时感染HGV。这些相似之处引发了两个理论问题。第一，HGV合并感染是否会在丙型肝炎病毒对抗病毒治疗的反应中发挥任何作用；第二，这一合并感染人群的血清HGV-RNA是否会因干扰素而发生变化。为了解决这些问题，98例确诊为慢性丙型肝炎病毒感染的患者接受了为期6个月的干扰素治疗（每周3次，每次300万单位）。根据标准生化标准对治疗反应进行分类。通过基于定量分支DNA扩增研究的检测方法，评估干扰素治疗前、治疗期间和治疗后的HGV-RNA水平变化。98例丙型肝炎病毒感染患者中有11例（11%）血清HGV-RNA可检测到。分析基线丙氨酸转氨酶（ALT）值、丙型肝炎病毒RNA水平、丙型肝炎病毒基因型、组织学严重程度或其他人口统计学特征时，两组（HGV阳性组与HGV阴性组）之间没有差异。两组的干扰素反应相似，HGV与治疗后的结果无关。在连续检测的9例丙型肝炎病毒合并感染患者中，有5例抗病毒治疗似乎导致HGV-RNA载量降低。在2例患者中，血清HGV-RNA的下降与生化反应相关，与丙型肝炎病毒RNA的变化无关。这些观察结果表明，需要对更大规模的HGV人群进行研究，以更清楚地界定丙型肝炎病毒与HGV合并感染之间的关系及其对抗病毒治疗的反应。
