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Hepatitis G infection and therapeutic response to interferon in HCV-related chronic liver disease
C Pramoolsinsap1, Y Poovorawan, T Sura
1Department of Medicine, Ramathibodi Hospital, Mahidol University Bangkok, Thailand.
Insights
Hepatitis G virus (HGV) RNA prevalence is low in Hepatitis C virus (HCV)-related liver disease patients and blood donors. HGV coinfection does not impact disease severity or interferon treatment response in HCV patients.
Area of Science:
- Hepatology
- Virology
- Infectious Diseases
Background:
- Hepatitis C virus (HCV) infection is a major cause of chronic liver disease, cirrhosis, and hepatocellular carcinoma (HCC).
- The role of Hepatitis G virus (HGV) co-infection in HCV-related liver disease progression and treatment response remains unclear.
Purpose of the Study:
- To determine the prevalence of circulating HGV-RNA in patients with HCV-related chronic liver disease and healthy blood donors.
- To investigate the impact of HGV co-infection on disease severity and response to interferon therapy in HCV patients.
Main Methods:
- Detection of HGV-RNA in 117 HCV patients (classified as chronic hepatitis, liver cirrhosis, or HCC) and 200 healthy blood donors.
- Analysis of HCV genotypes and serological markers for Hepatitis B virus (HBV) in co-infected patients.
- Evaluation of interferon treatment response and sustained virological response in a subset of chronic active hepatitis patients.
Main Results:
- HGV-RNA was detected in 4.3% of HCV patients and 5% of blood donors, with a higher prevalence in chronic hepatitis cases.
- HGV co-infection was observed in 4 out of 5 patients positive for anti-HBs and anti-HBc, with no jaundice.
- Interferon therapy showed a 55.6% initial response rate, but only 22.2% achieved sustained response. Favorable factors included younger age, low HCV-RNA, and HCV genotype III/2a.
- HGV co-infection did not significantly alter clinical severity, disease progression, or interferon treatment outcomes.
Conclusions:
- The prevalence of HGV infection is low in both HCV patients and the general population.
- HGV co-infection does not appear to influence the clinical course or treatment efficacy of HCV-related liver disease.
- Younger age, low viral load, and specific HCV genotypes (III/2a) are associated with better interferon treatment outcomes.
Abstract:
Circulating HGV-RNA was determined in 117 patients with HCV-related chronic liver disease and in 200 healthy blood donors. The patients, aged 50.8+/-13.8 years, were classified as chronic hepatitis (CH; n = 82), liver cirrhosis (n = 25) and hepatocellular carcinoma (HCC; n = 10). HGV-RNA was detected in 5 (4.3%) patients, all with CH and in 10 (5%) of blood donors. The majority of all groups (52% to 70%) were infected with HCV genotype II/1b, including 4/5 patients with HGV co-infection. Of 5 patients with HGV co-infection, 4 were positive for anti-HBs and anti-HBc and none exhibited jaundice. A 24-week course of interferon treatment with 12-month follow-up was achieved in 27 patients with chronic active hepatitis, including 3 with HGV co-infection. Of these, 55.6% responded to the therapy, but only 6/27 (22.2%) patients were sustained responders. The majority of sustained responders were HCV genotype III/2a (4/6) while genotype II/1b was found in the majority of patients with relapse (7/9) and non-responders (9/12). At the 48- month follow up, 2/6 sustained responders (one with HGV co-infection) became HCV RNA positive. These results show that the prevalence of HGV infection in HCV-related chronic liver disease is low, as in the general population, and is found in younger patients with chronic hepatitis. HGV coinfection does not interfere with clinical severity, disease progression or response to interferon in patients with HCV-related chronic liver disease. The favorable factors ofinterferon treatment for HCV infection are young age, low HCV-RNA levels and HCV genotype III/2a.
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