Background and Aim: Coinfection with GBV-C/HGV in patients with chronic hepatitis C (CHC) may influence clinical course and response rates of antiviral therapy with interferon/ribavirin. Aim of the study was to investigate prevalence of GBV-C/HGV/HCV coinfection and outcome of antiviral combination therapy in coinfected patients.
Patients and methods: Three hundred and four patients with chronic hepatitis C (f/m=93/211, age: 42 [18–65], median[range]) were investigated. HGV RNA detection was done by polymerase chain reaction prior to initiation of interferon/ribavirin combination therapy with standard (N=111) or pegylated Interferon (N=193) and after a six month follow up period. A pre-treatment liver biopsy was done and stage of fibrosis was determined according to the Metavir scoring system.
Results: A HGV/HCV co-infection could be identified in 37 (12.2%) out of 304 patients. The predominant HCV-genotype in HGV coinfected individuals was HCV-3a (51.4%). The most common source of infection was intravenous drug abuse (N=21). HGV coinfection was more common in patients infected with HCV-3 compared to HCV-1 or HCV-4 (19/52 (36.5%) vs. 14/187 (7.5%) vs. 4/61 (6.5%), p<0.01). As compared to patients with HCV infection alone, patients with HGV/HCV coinfection were younger (35 [18–56] vs. 41 [19–65], years; median [range], p<0.01) and advanced fibrosis (F3-F4) was less frequent (21.6% vs. 33%, p<0.05). With respect to HCV, a sustained virological response was achieved more frequently in HGV/HCV co-infected patients (26/34 [76.5%]; HCV-3a: 14/16 [87.5%]; HCV-1: 9/14 [64.2%]; HCV-4: 3/4 [75%]) than in monoinfected patients (116/222 [52.3%], p<0.01; HCV-3a: 22/26 [84.6%], HCV-1: 63/147 [42.8%], HCV-4: 31/47 [65.9%]). HGV RNA was undetectable in 65.8% of the coinfected patients at the end of follow up. In patients with still detectable HGV RNA (but a sustained virological response of HCV) ALT levels remained within the normal range at the end of follow up.
Conclusion: Intravenous drug abuse is a major risk factor for HGV coinfection in patients with chronic hepatitis C. Coinfection with HGV does not aggravate clinical course of chronic hepatitis C or diminish response of HCV to antiviral therapy. Due to the younger age, less fibrosis and the high frequency of HCV-3a HGV coinfected patients show a favourable response to antiviral combination therapy.
Interferon/ribavirin combination therapy also clears HGV infection in a high proportion of cases.
