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Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection
Published on: November 7, 2018
[Follow-up of chronic hepatitis B carriers. Serological course and risk of reactivation]
L Bujanda1, M García Bengoechea, G Cilla
1Servico de Aparato Digestivo, Hospital Ntra. Sra. de Aránzazu, San Sebastian.
Insights
Hepatitis B carriers with normal GPT levels may not require frequent monitoring. However, those with abnormal GPT levels and negative DNA HBV are at high risk for hepatitis B virus (HBV) reactivation.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Chronic Hepatitis B (HBV) infection affects millions globally.
- Understanding serologic changes and reactivation risk is crucial for patient management.
- Hepatitis B e antigen (HBeAg) seroconversion is a key indicator of disease progression.
Purpose of the Study:
- To investigate serologic changes in chronic Hepatitis B carriers.
- To assess the risk of HBV reactivation in different carrier groups.
- To identify factors associated with HBV reactivation.
Main Methods:
- A cohort of 200 HBsAg-positive patients with >18 months follow-up.
- Patients classified into three groups based on HBeAg/Anti-HBe status.
- Regular monitoring included serology, HBV DNA, liver function tests (GPT), alpha-fetoprotein, and ultrasound.
Main Results:
- HBeAg seroconversion occurred in 10% annually in HBeAg-positive patients.
- Only 0.25% of patients lost HBsAg and developed Anti-HBs annually.
- Reactivation was frequent (17.3%) in Anti-HBe positive, DNA.HBV negative patients with high GPT levels.
Conclusions:
- Hepatitis B virus reactivation is common in HBsAg carriers who are Anti-HBe positive, DNA.HBV negative, and have elevated GPT levels.
- These patients require careful monitoring due to their high risk of reactivation.
- Prophylaxis for HBV infection in contacts should consider increased infectiousness during reactivation phases.
Aim:
To investigate serologic changes and risk of reactivation in hepatitis B chronic carriers.
Patients And Methods:
Two hundred chronic HBs-Ag positive patients were included (follow-up greater than 18 months). According to the HBeAg/Anti-HBe status at the moment of inclusion they were classified in 3 groups: I: 40 patients HBeAg positive, II: 158 anti-HBe positive and III: 2 HBeAg/Anti-HBe negatives. All patients were screened in the follow-up for biochemical test, hepatitis B, C and D virus serology, DNA.HBV by hybridization, alpha fetoprotein and abdominal ultrasound.
Results:
Mean age was 35 +/- 12 years (14-61), and mean follow-up 71 +/- 35.1 months (18-252). In the follow-up 28 patients in group I seroconverted HBeAg/Anti-HBe, 18 spontaneously (annual rate 10%). In group II four patients out off 158 were DNA HBV positive. Only 3 chronic HBV carriers lost HBsAg and developed Anti-HBs (annual rate 0,25%). Reactivation of viral activity was detected in 13 patients Anti-HBe positive, DNA.HBV negative. HBeAg appeared during reactivation in six, both HBeAg/Anti-HBe were negative in one, and six were unchanged. Reactivation was significantly more frequent in chronic carriers with high GPT activity (13 out off 75, 17.3%) than in patients with normal GPT (0 out off 107, 0%) (p < 0.0005).
Conclusions:
Reactivation of HBV activity is frequent in HBsAg chronic carriers Anti-HBe positive, DNA.HBV negative and who are abnormal GPT levels; these patients should be considered at risk of reactivation. The control in the follow-up of HBV chronic carriers with persistently normal GPT, without advanced liver disease, may not be so frequent. The increased infectiousness during reactivation of HBV activity must be taken account for prophylaxis of HBV infection in chronic carriers contacts.
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