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Management Of Patients With Hepatitis B Virus Reactivation Post-DAA Treatment Of Chronic Hepatitis C Virus Infection
Heba Ahmed Osman1, Ali A Ghweil1, Abeer Mm Sabry2
1Tropical Medicine and Gastroenterology Department, Faculty of Medicine, South Valley University, Qena, Egypt.
Insights
Hepatitis C virus (HCV) and Hepatitis B virus (HBV) coinfection requires careful management. In coinfected patients with mild liver disease, direct-acting antiviral therapy for HCV can be safely completed without concurrent HBV antiviral treatment, provided close monitoring is in place.
Area of Science:
- Hepatology
- Virology
- Internal Medicine
Background:
- Hepatitis C virus (HCV)-HBV coinfection presents a significant clinical challenge, often leading to rapid liver disease progression.
- Precise diagnosis and treatment strategies for coinfected patients remain critical for managing liver disease outcomes.
Purpose of the Study:
- To investigate the role and safety of HBV antiviral therapy in patients experiencing HBV reactivation after direct-acting antiviral (DAA) therapy for HCV-HBV coinfection.
- To evaluate the clinical course and outcomes of HCV-HBV coinfected patients undergoing DAA treatment without concomitant HBV antiviral therapy.
Main Methods:
- A prospective randomized study involved 140 patients with chronic HCV and HBV coinfection.
- Patients received sofosbuvir and daklatasvir for 3 months; all had pretreatment HBeAg seroconversion, low HBV DNA, normal liver enzymes, and mild hepatic fibrosis (F0/F1).
- FibroScan, liver function tests, and viral load (HCV PCR, HBsAg, HBeAg) were assessed pretreatment, with follow-up at 1, 3, 6, and 12 months.
Main Results:
- All 140 patients achieved sustained virologic response for HCV, with undetectable HCV PCR by 3 months post-treatment.
- Four patients (2.8%) experienced HBV reactivation, characterized by elevated HBV DNA and liver enzymes.
- These four patients showed significant improvement in liver enzymes, bilirubin, INR, and increased platelet count by 12 months post-treatment, with undetectable HBV PCR.
Conclusions:
- Direct-acting antiviral therapy for HCV can be safely administered to coinfected patients with no/mild hepatic fibrosis, HBeAg seroconversion, and low HBV DNA levels.
- Close monitoring is essential during HCV treatment in coinfected individuals, but concurrent HBV antiviral therapy may not be necessary in this specific patient group.
- The study suggests that HBV reactivation, while occurring in a small subset, is manageable and does not preclude successful HCV treatment completion without preemptive HBV antiviral intervention.
Background And Aim:
Hepatitis C virus (HCV)-HBV coinfection is a significant health problem with rapid progression of liver disease without precise diagnosis and treatment. We aimed in this study to identify if there were any role of HBV antiviral therapy in patients with HBV reactivation after direct-acting antiviral therapy in HCV-HBV coinfected patients.
Methods:
A prospective random study was carried out on 140 patients presenting with chronic HCV and chronic HBV coinfection. All patients had pretreatment HBeAg seroconversion, HBV DNA <2,000 IU/mL, normal liver enzymes, and F0/F1 hepatic fibrosis. They treated with sofosbuvir 400 mg and daklatasvir 60 mg once daily for 3 months. All patients underwent pretreatment hepatic fibrosis assessment using Fibro Scan and laboratory investigations: platelet count, liver-function tests, quantitative HCV PCR, HBsAg, HBc IgG, HBeAg, and HBeAb. All patients were followed up at 1, 3, 6, and 12 months from the start of HCV therapy.
Results:
The study enrolled 140 HCV-HBV coinfected patients: 55% were F0 and the rest F1. All our patients had negative HCV PCR at 1 month posttreatment and had achieved sustained virologic response with negative HCV PCR 3 months after treatment end. Four patients showed HBV reactivation with raised HBV DNA PCR and liver enzymes. Their mean age was 23.7±2.7 years, and three were male. Regarding patients with HBV reactivation, at 12 months posttreatment they showed significant decreases in liver enzymes, bilirubin, and INR, with increased platelet count (P=0.001), each with undetectable HBV PCR (P=0.001).
Conclusion:
HBV-HCV coinfected patients with no/mild hepatic fibrosis, HBeAg seroconversion, and HBV DNA <2,000 IU/mL can complete direct-acting antiviral therapy without HBV antiviral treatment with close monitoring.
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