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Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection
Published on: November 7, 2018
Coinfections with hepatitis g and/or c virus in hepatitis B-related chronic liver disease
C Pramoolsinsap1, V Sirikulchayanonta, W Busakorn
1Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Insights
Hepatitis B virus (HBV)-related liver disease patients with concurrent Hepatitis G virus (HGV) or Hepatitis C virus (HCV) infections showed increased resistance to interferon therapy. HCV coinfection worsened liver disease severity and inhibited HBV replication.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Chronic Hepatitis B virus (HBV) infection affects millions globally, with coinfections potentially altering disease progression and treatment outcomes.
- Hepatitis G virus (HGV) and Hepatitis C virus (HCV) are blood-borne viruses that can coinfect individuals with HBV.
- Understanding the impact of HGV/HCV coinfections on HBV-related liver disease is crucial for optimizing patient management.
Purpose of the Study:
- To investigate the prevalence and impact of HGV and/or HCV coinfections in patients with HBV-related chronic liver disease.
- To assess the influence of HGV/HCV coinfection on HBV replication and liver disease severity.
- To evaluate the response to interferon therapy in HBV patients with and without HGV/HCV coinfections.
Main Methods:
- Studied 196 patients with HBV-related chronic liver disease and 100 HBsAg carriers for HGV/HCV coinfections.
- Analyzed patient history for risk factors like blood transfusions and assessed serological markers (anti-HBe).
- Measured serum HBV-DNA levels and evaluated liver histology before and after interferon treatment in a subset of patients.
Main Results:
- Coinfections with HGV (10), HCV (5), or both (3) were found in 9.2% of HBV patients, with no coinfections in HBsAg carriers.
- Coinfected patients had higher rates of blood transfusion exposure and were more frequently anti-HBe positive.
- HCV coinfection was associated with lower HBV-DNA levels, higher pre-treatment histological scores, and significantly increased resistance to interferon therapy, with none achieving sustained HBV-DNA clearance.
Conclusions:
- Parenteral exposure is a significant risk factor for HGV/HCV coinfection in chronic HBV infection.
- HGV coinfection did not significantly impact chronic HBV infection.
- HCV coinfection appears to inhibit HBV replication but exacerbates liver disease severity and hinders interferon treatment efficacy.
Abstract:
Concurrent infections with HGV and/or HCV (HGV/HCV) were investigated in 196 patients with HBV-related chronic liver disease (115 chronic hepatitis, 31 liver cirrhosis, 50 hepatocellular carcinoma), and in 100 HBsAg carriers. Coinfections were detected in 18 (9.2%) patients with HGV (10) or HCV (5) or both agents (3), but in none of the HBsAg carriers. Patients with coinfection were more frequently exposed to blood transfusions (55.6% vs 5.6%) and also were more commonly anti-HBe positive. Serum levels of HBV-DNA were lower in patients with HCV coinfection than in those coinfected with HGV. Interferon was administered to 39 patients with chronic active hepatitis including 7 patients with HGV/HCV coinfection. Sustained clearance of HBV-DNA was observed in 10 (25.6%) patients who were solely infected with HBV. These patients were significantly younger and had much lower histological scores than non-responders. Patients with HCV coinfection had significantly higher pre-treatment histological scores than those without HCV. After interferon treatment, a significant reduction in histological scores was observed in all patients except those coinfected with HGV/HCV. None of the 7 patients with coinfection had sustained clearance of HBV-DNA or HCV-RNA, and only one had cleared HGV-RNA. These results suggest that parenteral exposure is a risk factor for HGV/HCV coinfection in chronic HBV infection. HGV infection shows no significant impact on chronic HBV infection. HCV coinfection appears to inhibit HBV replication, but causes more severe chronic hepatitis and increases resistance to interferon therapy.
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