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Hepatitis G virus infection in chronic hepatitis C: frequency, features and response to interferon therapy
J C Sáiz1, S Ampurdanés, E Olmedo
1Liver Unit, Hospital Clinic, Barcelona, Spain.
Insights
Hepatitis G virus (HGV) co-infection is uncommon in chronic hepatitis C patients and does not alter disease progression or interferon treatment response. HGV shows sensitivity to interferon, especially with lower initial viral loads.
Area of Science:
- Hepatology
- Virology
- Infectious Diseases
Background:
- Investigating the clinical significance of Hepatitis G virus (HGV).
- Assessing the impact of HGV co-infection on Hepatitis C virus (HCV) patients.
- Determining HGV sensitivity to interferon therapy.
Purpose of the Study:
- Determine the prevalence of HGV infection in chronic Hepatitis C patients.
- Evaluate if HGV co-infection influences the clinical course of Hepatitis C.
- Assess the effect of HGV co-infection on response to interferon therapy.
Main Methods:
- Reverse transcription-polymerase chain reaction (RT-PCR) to detect HGV-RNA in serum.
- Analysis of 143 chronic Hepatitis C patients treated with interferon alpha-2b.
- Comparison of clinical features and treatment responses between HGV-infected and non-infected patients.
Main Results:
- HGV-RNA detected in 5.6% of patients.
- No significant differences in baseline characteristics or interferon response between HGV-infected and non-infected groups.
- HGV-RNA clearance observed in all treated patients; sustained inhibition linked to low viral load.
Conclusions:
- HGV infection prevalence is low in this Hepatitis C patient cohort.
- HGV co-infection does not appear to alter the clinical presentation or interferon treatment outcomes in chronic Hepatitis C.
- HGV demonstrates interferon sensitivity, particularly with lower pretreatment viral loads.
Background/Aims:
The pathogenic relevance of the hepatitis G virus (HGV) and its sensitivity to interferon are currently under investigation. This study aimed to investigate the prevalence of HGV infection in patients with chronic hepatitis C and to elucidate if HGV co-infection modifies the clinical course and the response to interferon therapy in this disease.
Methods:
HGV-RNA was investigated by reverse transcription-polymerase chain reaction in serum from 143 consecutive patients who received interferon alpha-2b (3 MU t.i.w.) for 24 weeks. Baseline features and response to therapy in HGV-infected and non-infected patients were compared. To assess the antiviral effect of interferon, serial quantitative measurement of HCV-RNA and HGV-RNA in serum was performed in patients co-infected with HCV and HGV.
Results:
Eight patients (5.6%) presented HGV-RNA sequences in serum. No significant differences were found between HGV-infected and non-infected patients in relation to age, sex, source of infection, liver function tests, liver histology and HCV genotype, nor in the biochemical response to interferon, which was sustained in 12% and 15%, transient in 37% and 30% and absent in 50% and 55% of HGV-infected and non-infected patients, respectively. HGV-RNA became negative in all treated patients, but sustained viral inhibition was observed only in those with low viral load.
Conclusions:
The prevalence of HGV infection in HCV-infected patients is relatively low in our geographical area. HGV co-infection does not appear to modify the clinical presentation nor the response to interferon in chronic hepatitis C. HGV is sensitive to interferon, particularly if pre-treatment viral load is low.