ArticleScientific reports2026
True reactivation versus transient viremia: a retrospective analysis of HBV reactivation in resolved infection.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Safety of Immune Checkpoint Inhibitors in Hepatitis B Virus-Positive Cancer Patients: A Multicenter Retrospective Cohort Study.Current oncology (Toronto, Ont.) · 2026Article
- Case Report: Long-term survival of refractory high-grade B-cell lymphoma with MYC, BCL2, and BCL6 rearrangements through glofitamab monotherapy consolidated by ASCT.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) reactivation is a major complication of immunosuppressive therapy or chemotherapy in patients with resolved HBV infection, yet the clinical significance of low-level HBV DNA reappearance remains unclear. We retrospectively analyzed 69 patients with resolved HBV infection who developed HBV DNA reappearance under immunosuppression. Among them, 38 patients were initially managed without immediate nucleos(t)ide analogue therapy, allowing assessment of HBV DNA kinetics. True reactivation was defined as HBV DNA ≥ 3.3 log IU/mL after initial detection. Of the 38 monitored patients, 7 (18%) progressed to true reactivation, 18 (47%) achieved spontaneous viral clearance, and 13 initiated antiviral therapy before meeting either definition. Distinct risk patterns emerged: all patients with an initial HBV DNA level ≥ 2.0 log IU/mL progressed to true reactivation, whereas only 2 of 20 with lower levels did so. Hematologic malignancy was also strongly associated with clinically significant reactivation, with true reactivation occurring in 6 of 12 patients compared with 1 of 13 patients with other diseases. These findings suggest that low-level HBV DNA reappearance under immunosuppression represents transient viremia rather than progressive reactivation. Risk stratification based on initial viral load and underlying disease may enable individualized management, reducing unnecessary antiviral therapy while maintaining patient safety.
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