S5658 An Old Problem With a Re-Purposed Solution: Novel Application of Emtricitabine-Tenofovir to Treat Persistent HBV Viremia

Introduction: As multi-level efforts seek to expand indications for – and access to – nucleos(t)ide analogues (NUC) for chronic hepatitis B (CHB), a corresponding uptick in cases of persistent viremia is expected. Persistent hepatitis B virus (HBV) viremia occurs in nearly 20% of cases and is defined as detectable HBV DNA despite 48 weeks of uninterrupted therapy. Its significance is underlined by 2 interrelated observations: HBV DNA correlates with future risk of liver-related complications, whereas viral suppression with therapy decreases this risk. A defined clinical approach to persistent HBV viremia is needed, as a paucity of literature on this topic limits current guidance. Described here are 4 cases of persistent HBV viremia, who were effectively treated with fixed dose combination medications: emtricitabine-tenofovir disoproxil fumarate (FTC-TDF) or emtricitabine-tenofovir alafenamide (FTC-TAF). Case Description/Methods: Included cases have CHB without HIV and varying degrees of underlying liver fibrosis. Two cases have cirrhosis including one with HCC, which all predated FTC-TDF or FTC-TAF therapy. HBV viremia persisted despite a minimum 1-year course of NUC monotherapy across cases, though baseline HBV DNA levels differed them. Different NUC combinations and sequences were universally unsuccessful. Genetic profiles were obtained, showing variable resistance patterns. Response to antiviral therapies is depicted. FTC-TDF was prescribed in 3 cases, while FTC-TAF was provided in the remaining case. Both led to complete viral suppression within 48 weeks of therapy. Non-invasive tests show stability or regression of underlying fibrosis following therapy. Neither de novo HCC nor virological breakthroughs have been seen after long-term follow-up (range of 1-11 years). Similarly, medication-related adverse events have not occurred with either therapy. Discussion: Persistent HBV viremia is an understudied problem without a defined treatment pathway. As first reported here, FTC-TDF or FTC-TAF can effectively gain virological control in these cases. FTC is a NUC commonly incorporated into HIV prophylactic and treatment regimens, though it also shows antiviral activity against HBV. It is commercially available and readily prescribed in fixed-dose combination tablets. Thus, FTC-TDF and FTC-TAF are attractive options for persistent HBV viremia. Larger scale studies are warranted to validate these findings and inform future treatment algorithms for persistent HBV viremia.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001150092.14617.0c
Primary Topic
Hepatitis B Virus Studies
Type
article
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article

S5658 An Old Problem With a Re-Purposed Solution: Novel Application of Emtricitabine-Tenofovir to Treat Persistent HBV Viremia

Peter D. Block, L. W. Law, Ceena Chandrabos, Viviana Figueroa-Diaz
The American Journal of Gastroenterology
Hepatitis B Virus Studies
article

S5658 An Old Problem With a Re-Purposed Solution: Novel Application of Emtricitabine-Tenofovir to Treat Persistent HBV Viremia

Peter D. Block, L. W. Law, Ceena Chandrabos, Viviana Figueroa-Diaz
article en

Abstract

Introduction: As multi-level efforts seek to expand indications for – and access to – nucleos(t)ide analogues (NUC) for chronic hepatitis B (CHB), a corresponding uptick in cases of persistent viremia is expected. Persistent hepatitis B virus (HBV) viremia occurs in nearly 20% of cases and is defined as detectable HBV DNA despite 48 weeks of uninterrupted therapy. Its significance is underlined by 2 interrelated observations: HBV DNA correlates with future risk of liver-related complications, whereas viral suppression with therapy decreases this risk. A defined clinical approach to persistent HBV viremia is needed, as a paucity of literature on this topic limits current guidance. Described here are 4 cases of persistent HBV viremia, who were effectively treated with fixed dose combination medications: emtricitabine-tenofovir disoproxil fumarate (FTC-TDF) or emtricitabine-tenofovir alafenamide (FTC-TAF). Case Description/Methods: Included cases have CHB without HIV and varying degrees of underlying liver fibrosis. Two cases have cirrhosis including one with HCC, which all predated FTC-TDF or FTC-TAF therapy. HBV viremia persisted despite a minimum 1-year course of NUC monotherapy across cases, though baseline HBV DNA levels differed them. Different NUC combinations and sequences were universally unsuccessful. Genetic profiles were obtained, showing variable resistance patterns. Response to antiviral therapies is depicted. FTC-TDF was prescribed in 3 cases, while FTC-TAF was provided in the remaining case. Both led to complete viral suppression within 48 weeks of therapy. Non-invasive tests show stability or regression of underlying fibrosis following therapy. Neither de novo HCC nor virological breakthroughs have been seen after long-term follow-up (range of 1-11 years). Similarly, medication-related adverse events have not occurred with either therapy. Discussion: Persistent HBV viremia is an understudied problem without a defined treatment pathway. As first reported here, FTC-TDF or FTC-TAF can effectively gain virological control in these cases. FTC is a NUC commonly incorporated into HIV prophylactic and treatment regimens, though it also shows antiviral activity against HBV. It is commercially available and readily prescribed in fixed-dose combination tablets. Thus, FTC-TDF and FTC-TAF are attractive options for persistent HBV viremia. Larger scale studies are warranted to validate these findings and inform future treatment algorithms for persistent HBV viremia.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 49%
Hepatitis B Virus Studies
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