Brandhagen D J, Gross J B, Poterucha J J, Charlton M R, Detmer J, Kolberg J, Gossard A A, Batts K P, Kim W R, Germer J J, Wiesner R H, Persing D H
Division of Gastroenterology and Hepatology, Mayo Clinic and Foundation, Rochester, Minnesota, USA.
Am J Gastroenterol. 1999 Apr;94(4):1000-5. doi: 10.1111/j.1572-0241.1999.01003.x.
Hepatitis G virus (HGV) is a recently discovered member of the flavivirus family that has been associated with acute and chronic hepatitis. HGV infection has been reported to coexist in 10-20% of patients with chronic hepatitis C. The significance of simultaneous infection with HGV and hepatitis C virus (HCV) remains to be clarified, as do the effects on HGV of therapeutic interventions such as interferon treatment or liver transplantation.
Pre-treatment sera were available in 65 patients with chronic hepatitis C treated with interferon; pretransplant sera were available in 49 patients transplanted for end stage liver disease associated with chronic hepatitis C. Information collected included age, sex, risk factors for hepatitis, concurrent liver disease, patient and allograft survival, biochemical response to interferon, histological activity index, and degree of fibrosis/cirrhosis. HCV genotyping was performed by sequencing the NS-5 region. HGV quantitation was performed using a research-based branched DNA (bDNA) assay with a set of probes directed at the 5' untranslated region.
HGV was detected in 10 of 49 patients (20%) before transplant and in 13 of 65 patients (20%) treated with interferon. There was a female predominance among HGV-positive compared with HGV-negative transplant patients (80% vs 20%; p < 0.01), but such a difference was not observed in the interferon-treated group. Hepatic iron concentration was lower in hepatic explants from patients who were HGV-positive than in those who were HGV-negative (318 +/- 145 microg/g dry weight vs 1497 +/- 2202 microg/g dry weight; p = 0.02). HCV exposure after 1980 was more common in the HGV-positive patients than in those who were HGV-negative for the entire study population (10 of 20 [50%] vs 16 of 66 [24%]; p = 0.03), as well as for the nontransplant subgroup (8 of 12 [67%] vs 12 of 39 [31%]; p = 0.03). HGV RNA levels declined at 1 yr after transplant in seven of eight patients. Among nine patients tested during or after interferon treatment, HGV RNA levels declined from pretreatment levels in all and disappeared in three.
Among patients with chronic hepatitis C treated with either interferon or liver transplantation, the frequency of coinfection with HGV is about 20%. HGV may be a more recent virus in the US than HCV. Coinfection with HGV does not appear to affect the likelihood of response to interferon in patients with hepatitis C. Finally, HGV RNA levels appear to decline after both liver transplantation and interferon therapy, suggesting possible suppression by increased HCV replication in the former case, and a possible drug treatment effect in the latter.
庚型肝炎病毒（HGV）是黄病毒科最近发现的成员，与急慢性肝炎相关。据报道，10%至20%的慢性丙型肝炎患者同时感染HGV。HGV与丙型肝炎病毒（HCV）同时感染的意义以及诸如干扰素治疗或肝移植等治疗干预对HGV的影响仍有待阐明。
1）检测肝移植和丙型肝炎干扰素治疗患者中HGV感染的频率；2）比较肝移植或干扰素治疗前后的HGV RNA水平。
65例接受干扰素治疗的慢性丙型肝炎患者有治疗前血清样本；49例因与慢性丙型肝炎相关的终末期肝病接受移植的患者有移植前血清样本。收集的信息包括年龄、性别、肝炎危险因素、并发肝病、患者和移植物存活情况、对干扰素的生化反应、组织学活性指数以及纤维化/肝硬化程度。通过对NS-5区域进行测序进行HCV基因分型。使用基于研究的分支DNA（bDNA）检测法和一组针对5'非翻译区的探针进行HGV定量。
49例移植前患者中有10例（20%）检测到HGV，65例接受干扰素治疗的患者中有13例（20%）检测到HGV。与HGV阴性的移植患者相比，HGV阳性患者中女性占优势（80%对20%；p<0.01），但在干扰素治疗组中未观察到这种差异。HGV阳性患者肝外植体中的肝铁浓度低于HGV阴性患者（318±145μg/g干重对1497±2202μg/g干重；p = 0.02）。对于整个研究人群，1980年后HCV暴露在HGV阳性患者中比在HGV阴性患者中更常见（20例中的10例[50%]对66例中的16例[24%]；p = 0.03），非移植亚组也是如此（12例中的8例[67%]对39例中的12例[31%]；p = 0.03）。8例患者中有7例在移植后1年HGV RNA水平下降。在干扰素治疗期间或治疗后检测的9例患者中，所有患者的HGV RNA水平均从治疗前水平下降，3例患者的HGV RNA水平消失。
在接受干扰素治疗或肝移植的慢性丙型肝炎患者中，HGV合并感染的频率约为20%。在美国，HGV可能比HCV出现得更晚。HGV合并感染似乎不影响丙型肝炎患者对干扰素的反应可能性。最后，肝移植和干扰素治疗后HGV RNA水平似乎均下降，提示在前一种情况下可能被增加的HCV复制所抑制，在后一种情况下可能是药物治疗的效果。
