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Updated: Sep 20, 2026

Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection
Published on: November 7, 2018
[Incidence of hepatitis B, C and D infection in chronic liver diseases]
1BM Központi Kórház és Intézményei, I. Belgyógyászati Osztály, Budapest.
Insights
This study investigated viral markers in 204 chronic liver disease patients, finding viral causes in 62%. Hepatitis B, C, and D virus co-infections were common and linked to more severe liver disease.
Area of Science:
- Hepatology
- Virology
- Immunology
Context:
- Chronic liver diseases (CLDs) are a significant global health burden.
- Determining the viral etiology of CLDs is crucial for effective management.
- Hepatitis B virus (HBV), Hepatitis C virus (HCV), and Hepatitis D virus (HDV) are major causes of CLD.
Purpose:
- To investigate the prevalence of HBV, HCV, and HDV markers in patients with histologically confirmed chronic liver disease.
- To assess the correlation between viral seropositivity and the severity of liver disease.
- To explore the interplay between different hepatitis virus infections.
Summary:
- Serological tests for HBV, HCV, and HDV markers were performed on 204 CLD patients.
- Viral etiology was identified in 62% of cases, with HBV (52.5%), HCV (33.3%), and HDV (11.2% of HBV-positive cases) being prevalent.
- Co-infections with two or three viruses were observed in 26% and 2% of cases, respectively.
- Viral seropositivity, particularly co-infections, was associated with more severe liver disease, including chronic hepatitis and cirrhosis.
- HCV and HDV infections may suppress HBV replication, and their presence influences disease severity and stage.
Impact:
- Provides insights into the complex viral landscape of chronic liver disease.
- Highlights the increased disease severity associated with viral co-infections.
- Suggests potential mechanisms of viral interaction, such as suppression of HBV replication by HCV and HDV.
- Informs diagnostic and therapeutic strategies for patients with chronic viral hepatitis.
Abstract:
The authors tested hepatitis B (HBsAg, anti-HBs, anti-HBc, IgM anti-HBc, HBe, anti-HBe), C (anti-HCV) and D (anti-HD, IgM anti-HD) virus markers in the sera of 204 patients, who suffered from histologically confirmed chronic liver diseases (age: 18-72, average: 46.8 y) by Sorin Biomedica RIA and Abbott ELISA kits. On the basis of detailed virus serological tests, they obtained data indicating viral etiology in 62% of the cases. 33.3% of the patients were anti-HCV, 52.5% of the patients were HBV marker seropositive and 11.2% of the HBV seropositive cases were anti-HD seropositive. In 2% of the cases seropositivity of all the three viruses was proved. In 26% of the patients seropositivity of two viruses (HBV and HCV, or HBV and HDV) was proved. They observed severe, progressing liver diseases in patients with HBV, HCV and HDV marker seropositivity in a higher ratio than in seronegative patients. In the cases of combined virus marker seropositivity the incidence rate of chronic hepatitis and liver cirrhosis was higher than in only HBV marker seropositive patients, but did not differ significantly from those only anti-HCV seropositive. In the cases of fought-off HBV infection the severity of the liver disease was milder than in the cases of replication and integration stage. Anti-HD seropositivity occurred in all stages of HBV infection, but active HDV infection, in most of the cases, was observed only in cases in the integration stage. Anti-HCV seropositivity was observed mainly in the fought-off HBV infection stage. Their results suggest that HCV infection, like HDV infection, may suppress HBV replication.(ABSTRACT TRUNCATED AT 250 WORDS)
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