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Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection
Published on: November 7, 2018
Hepatitis type C virus infection in patients with type B chronic liver disease
1First Department of Internal Medicine, Okayama University Medical School, Japan.
Insights
Coinfection with hepatitis B virus (HBV) and hepatitis C virus (HCV) was studied in 152 patients. HBV may drive active liver inflammation in HBeAg-positive patients, while HCV appears responsible for ongoing inflammation in HBeAg-negative cases.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Chronic liver diseases are often caused by viral infections.
- Coinfection with hepatitis B virus (HBV) and hepatitis C virus (HCV) presents complex clinical challenges.
- Understanding the distinct roles of HBV and HCV in coinfection is crucial for patient management.
Purpose of the Study:
- To investigate the prevalence of HBV and HCV coinfection in patients with chronic liver disease.
- To differentiate the impact of HBV and HCV on liver inflammation based on hepatitis B e antigen (HBeAg) status.
Main Methods:
- Sera from 152 HBs antigen-positive patients were tested for anti-c100-3 antibodies (HCV marker).
- HCV-RNA detection using reverse transcription-polymerase chain reaction (RT-PCR) and HBeAg status were assessed.
- Liver function tests (SGPT) and liver biopsy findings were correlated with viral markers and HBeAg status.
Main Results:
- Eleven patients (7.2%) were positive for anti-c100-3, indicating HCV coinfection.
- HCV-RNA was detected in all 11 anti-c100-3 positive patients.
- HBeAg-positive patients showed elevated SGPT and active HBV replication, correlating with chronic active hepatitis.
- HBeAg-negative patients exhibited fluctuating SGPT without clear HBV replication, but liver biopsy revealed active inflammation in some, suggesting HCV's role.
Conclusions:
- HBV appears to contribute significantly to active liver inflammation in HBeAg-positive patients coinfected with HCV.
- HCV may be the primary driver of persistent liver inflammation in HBeAg-negative patients with HBV/HCV coinfection.
- These findings highlight the differential roles of HBV and HCV in the pathogenesis of chronic liver disease in coinfected individuals.
Abstract:
Anti-c100-3 (Ortho) was determined in the sera of 152 patients with HBs antigen-positive chronic liver diseases to assess coinfection of hepatitis B virus (HBV) and hepatitis C virus (HCV). Eleven patients (7.2%) were positive for anti-c100-3. Anti-CP-9 (Okamoto) and HCV-RNA (RT-PCR) were also examined in these 11 patients. Anti-CP-9 was detected in 7 patients and HCV-RNA was detected in all 11 patients. Four of the 11 anti-c100-3-positive patients were positive for HBe antigen (HBeAg) and others were negative. In 8 of the 11 patients, HCV was suspected to be superinfected by blood transfusion. In HBeAg-positive patients, serum glutamic pyruvic transaminase (SGPT) was elevated in relation to active replication of HBV shown by DNA-polymerase activity. The histological findings showed chronic active hepatitis, with or without cirrhosis. On the other hand, in HBeAg-negative patients, SGPT fluctuated without evidence of active replication of HBV. Active inflammation in the liver was observed in 3 of 5 HBeAg-negative patients by liver biopsy. These findings suggest that HBV might play an important role in chronic active inflammation in HBeAg-positive patients coinfected with HCV, and that HCV might be responsible for continuous inflammation in HBeAg-negative patients coinfected with HCV.
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