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Clinical implications of GBV-C/HGV infection in patients with "HCV-related" chronic hepatitis
R Francesconi1, F Giostra, G Ballardini
1Servizio di Semeiotica Medica II, Azienda Ospedaliera, Università degli Studi, Bologna, Italy.
Insights
Hepatitis G virus (HGV) coinfection in patients with chronic hepatitis C virus (HCV) liver disease did not worsen outcomes, but was associated with increased liver steatosis and potential for interferon treatment response.
Area of Science:
- Hepatology
- Virology
- Infectious Diseases
Background:
- Chronic liver disease is often caused by Hepatitis C Virus (HCV).
- Hepatitis G Virus (HGV), also known as GB Virus C (GBV-C), is a potential co-infecting agent.
Purpose of the Study:
- To investigate the clinical, biochemical, and histological effects of HGV coinfection in patients with HCV-related chronic liver disease.
Main Methods:
- Eighty-three patients with HCV RNA-positive chronic liver disease were tested for GBV-C/HGV coinfection using heminested PCR.
- Clinical, biochemical, and histological data were analyzed for coinfected versus non-coinfected patients.
Main Results:
- HGV/GBV-C RNA was detected in 26.5% of patients.
- HGV/GBV-C positive patients were younger, had a higher history of drug addiction, and showed a trend towards better interferon response.
- HGV/GBV-C coinfection did not worsen liver disease markers (ALT, histology) or specific HCV aspects but was linked to increased liver steatosis.
Conclusions:
- HGV/GBV-C coinfection does not significantly alter the course of HCV-related chronic liver disease, except for a potential increase in liver steatosis.
- HGV/GBV-C appears sensitive to interferon treatment, though recurrence is more frequent post-treatment withdrawal.
Background/Aims:
To evaluate the clinical, biochemical and histological implications of a concomitant HGV infection in "HCV-related" chronic liver disease.
Methods:
Eighty-three HCV-RNA positive patients with chronic liver disease were tested for GBV-C/HGV coinfection by heminested PCR.
Results:
Twenty-two (26.5%) patients were found to be positive for GBV-C/HGV RNA. GBV-C/HGV+ patients differed significantly from GBV-C/HGV- ones for younger age, higher frequency of history of drug addiction, which in turn might favor coinfection with interferon-sensitive HCV genotypes (3a), and increased probability of long-term response to interferon. GBV-C/HGV infection appears to have no responsibility for specific aspects of HCV infection such as biochemical or histological cholestatic features, lymphoid follicles, symptomatic cryoglobulinemia or presence of serum autoantibodies, including LKM1. It does not worsen the HCV-related disease (ALT levels and histological activity) and does not significantly interfere with HCV infection, as explored by the number of hepatocytes positive for HCV antigens. The amount of steatosis (mean score) was shown to be higher in GBV-C/HGV+ patients. A virological follow up was performed in 17 interferon-treated GBV-C/HGV+ patients On the whole, GBV-C/HGV seems to be as sensitive to IFN treatment as HCV, but recurrence after withdrawal is more frequent. In spite of this, ALT levels often remain normal after treatment withdrawal.
Conclusions:
The present data suggest that GBV-C/HGV infection, apart from more marked liver steatosis, does not modify the overall picture of chronic hepatitis due to HCV infection.