首页> 外文期刊>Journal of viral hepatitis. >Prevalence and clinical significance of GB virus type C/hepatitis G virus coinfection in patients with chronic hepatitis C undergoing antiviral therapy.
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Prevalence and clinical significance of GB virus type C/hepatitis G virus coinfection in patients with chronic hepatitis C undergoing antiviral therapy.

机译:在接受抗病毒治疗的慢性丙型肝炎患者中,GB C型/ G型肝炎病毒合并感染的发生率和临床意义。

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Summary. Coinfection with GBV-C/HGV in patients with chronic hepatitis C (CHC) may influence clinical course and response rates of antiviral therapy. Aim of the study was to investigate the prevalence of GBV-C/HGV/HCV coinfection and its influence on outcome of interferon/ribavirin combination therapy. Three hundred and four patients with CHC [m/f = 211/93, age: 42 (18-65)] were investigated. HGV RNA detection was performed by polymerase chain reaction prior to and 6 months after the end of antiviral therapy. HGV/HCV coinfection could be identified in 37/304 (12.2%) patients with intravenous drug abuse as the most common source of infection (N = 21, (56.8%)). The predominant HCV genotype in coinfected individuals was HCV-3a (HCV-3a: 51.4%, HCV-1: 37.8%, HCV-4: 10.8%). HGV coinfection was more prevalent in patients infected with HCV-3 compared to HCV-1 or HCV-4 [19/45 (42.2%) vs 14/185 (7.6%) vs 4/52 (7.7%), P < 0.01]. Patients with HGV/HCV coinfection were younger [35 (18-56) vs 43 (19-65), years; P < 0.01], and advanced fibrosis (F3-F4) was less frequent (22.2%vs 42.9%, P < 0.05). A sustained virological response was achieved more frequently in HGV/HCV coinfected patients [26/37 (70.3%)] than in monoinfected patients [120/267 (44.9%), P < 0.01]. HGV RNA was undetectable in 65.7% of the coinfected patients at the end of follow-up. Intravenous drug abuse seems to be a major risk factor for HGV coinfection in patients with chronic hepatitis C. Coinfection with HGV does not worsen the clinical course of chronic hepatitis C or diminish response of HCV to antiviral therapy. Interferon/ribavirin combination therapy also clears HGV infection in a high proportion of cases.
机译:概要。慢性丙型肝炎(CHC)患者与GBV-C / HGV合并感染可能会影响抗病毒治疗的临床过程和反应率。这项研究的目的是调查GBV-C / HGV / HCV合并感染的发生率及其对干扰素/利巴韦林联合治疗结局的影响。调查了304例CHC患者[m / f = 211/93,年龄:42(18-65)]。 HGV RNA检测在抗病毒治疗结束之前和结束后6个月通过聚合酶链反应进行。 HGV / HCV合并感染可以在37/304(12.2%)静脉吸毒的患者中被确定为最常见的感染源(N = 21,(56.8%))。在合并感染的个体中,主要的HCV基因型为HCV-3a(HCV-3a:51.4%,HCV-1:37.8%,HCV-4:10.8%)。与HCV-1或HCV-4相比,HGV合并感染在HCV-3感染的患者中更为普遍[19/45(42.2%)对14/185(7.6%)对4/52(7.7%),P <0.01] 。患有HGV / HCV合并感染的患者年龄较小[35(18-56)岁,而43(19-65)岁。 P <0.01],晚期纤维化(F3-F4)的发生率较低(22.2%vs 42.9%,P <0.05)。 HGV / HCV合并感染的患者[26/37(70.3%)]比单一感染的患者[120/267(44.9%)更能实现持续的病毒学应答(P <0.01)。在随访结束时,在65.7%的合并感染患者中未检测到HGV RNA。静脉药物滥用似乎是慢性丙型肝炎患者发生HGV合并感染的主要危险因素。HGV合并感染不会使慢性丙型肝炎的临床进程恶化或降低HCV对抗病毒治疗的反应。干扰素/利巴韦林的联合疗法还可以在很大比例的病例中清除HGV感染。

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