Research Article

De Novo vs. Recurrent Hepatitis B After Liver Transplantation: Clinical Profiles And Functional Cure

DOI:

10.3791/70562

June 12th, 2026

In This Article

Summary

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This study evaluates 150 post-liver transplant patients and reveals distinct clinical profiles between de novo and recurrent hepatitis B virus infections. Rigorous multivariate analysis identifies hepatitis B immunoglobulin (HBIG) combination therapy as an independent predictor of accelerated functional cure, supporting optimized long-term antiviral strategies.

Abstract

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This study compares the clinical characteristics and functional cure rates of de novo (DNH) versus recurrent hepatitis B virus (HBV) infections following liver transplantation. Data from 150 adult patients diagnosed with post-transplant HBV between 2010 and 2024 were analyzed, explicitly excluding individuals receiving anti-HBc-positive donor grafts. Participants were stratified by pre-transplant serology into DNH (n = 36) and recurrent HBV (n = 114) cohorts. Clinically, the DNH group experienced more severe acute hepatic injury upon infection, evidenced by elevated median peak bilirubin levels and a remarkably higher incidence of hepatitis B e antigen (HBeAg) positivity at initial diagnosis (86.1% vs. 9.6%, p < 0.001). Despite this severe acute presentation, DNH patients exhibited robust hepatic recovery following antiviral intervention, achieving alanine aminotransferase (ALT) normalization rates comparable to the recurrent group (50.0% vs. 48.2%, p = 1.000). Functional cure, explicitly defined as sustained hepatitis B surface antigen (HBsAg) loss, was achieved in 20.67% (31/150) of the total cohort. Time-to-event Kaplan-Meier survival analysis demonstrated that the recurrent cohort achieved functional cure significantly earlier and at a higher cumulative probability (Log-rank p = 0.037). Crucially, multivariate Cox proportional hazards regression established that combination therapy with hepatitis B immunoglobulin (HBIG) served as a robust independent predictor of definitive functional cure (Adjusted Hazard Ratio = 4.21, p = 0.002), successfully overcoming initial baseline disparities. In conclusion, while DNH manifests as a severe acute infection due to pre-transplant immune naivety, recurrent HBV is associated with a more favorable trajectory toward functional cure. These findings support the implementation of personalized antiviral management, establishing that integrating nucleos(t)ide analogs with low-dose HBIG significantly optimizes definitive serological outcomes.

Introduction

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Liver transplantation (LT) stands as the definitive curative intervention for end-stage liver disease (ESLD)1. Among the leading global etiologies of ESLD requiring LT, chronic infection with the hepatitis B virus (HBV) remains a formidable challenge2. The World Health Organization estimates that in 2015, approximately 257 million people worldwide were living with chronic HBV infection, with the highest prevalence in Africa (6.1%) and the Western Pacific region (6.2%)3. In China, a region historically burdened by high endemicity, hundreds of thousands of cases continue to be reported annually, underscoring its persistent public health impact4. For these patients, LT offers a life-saving opportunity. However, the post-transplant course is uniquely complicated by the risk of HBV infection of the new graft, a significant complication that threatens both graft and patient survival1. This risk manifests in two distinct clinical entities: recurrent HBV infection, operationally defined as the re-emergence of hepatitis B surface antigen (HBsAg) and/or HBV DNA in recipients who were HBsAg-positive before transplantation; and de novo HBV infection (DNH), which refers to a new HBV infection in recipients who were HBsAg-negative before surgery5. In the context of the global pursuit to eliminate viral hepatitis by 2030, the successful management and ultimate functional cure of these post-transplant infections have become critical clinical imperatives.

The pathogenesis and risk profiles for recurrent and de novo HBV infections are fundamentally different, necessitating tailored preventive strategies. Recurrent HBV primarily stems from the persistence of the virus in extrahepatic reservoirs of the recipient, such as peripheral blood mononuclear cells, which are not removed during the hepatectomy6. Under the influence of post-transplant immunosuppression, this residual virus can reactivate and infect the new liver2. The introduction of potent, high-genetic-barrier nucleoside analogs (NAs) has revolutionized prophylaxis, dramatically reducing historical recurrence rates from over 80% to well below 10% when used in combination with hepatitis B immunoglobulin (HBIG)7,8. In contrast, DNH is predominantly linked to external sources. While historically associated with the utilization of grafts from anti-HBc-positive donors, modern rigorous screening protocols have shifted the paradigm. Today, true community-acquired or occult recipient-originated DNH (excluding donor-derived cases) represents a unique and poorly characterized clinical challenge. The clinical presentation can vary from an asymptomatic state to severe hepatitis, including fibrosing cholestatic hepatitis, a rapidly progressive form of liver injury2.

The contemporary management of post-LT HBV prophylaxis is an area of active research and evolving clinical paradigms, particularly concerning the role and duration of HBIG. While the combination of lifelong NAs and HBIG has been the long-standing standard of care, this regimen is burdened by high cost and the inconvenience of parenteral administration2. Consequently, significant efforts have focused on developing HBIG-sparing or HBIG-free protocols. Recent evidence, including a comprehensive 2023 meta-analysis, indicates that monotherapy with high-potency NAs alone may yield comparable long-term outcomes to combination therapy with HBIG in terms of both HBV recurrence rates and overall patient survival9. However, whether NA monotherapy is sufficient to drive functional cure, defined strictly as sustained HBsAg loss, the optimal therapeutic endpoint, remains highly controversial. The true independent value of HBIG in facilitating definitive serological clearance in the modern NA era is therefore underexplored.

Despite these strides, critical knowledge gaps persist. While the epidemiological and clinical profiles of recurrent HBV are well-documented, comprehensive comparative analyses of de novo versus recurrent infections in large, contemporary cohorts are lacking. Specifically, the distinct clinical characteristics at onset, virological and serological dynamics, long-term treatment responses, and ultimate functional cure rates between these two entities remain inadequately characterized. Furthermore, while complete viral eradication remains challenging, functional cure, defined strictly as sustained HBsAg loss with or without seroconversion, is currently recognized as the optimal and most pragmatic therapeutic surrogate endpoint in the post-transplant setting, as it signifies profound, sustained viral suppression and is strongly associated with improved long-term clinical outcomes. This led to the hypothesis that due to the fundamentally different pre-transplant immunological backgrounds, patients with DNH will exhibit more severe acute clinical presentations upon infection compared to those with recurrent HBV, whereas recurrent patients may achieve functional cure more rapidly. Furthermore, the adjunctive use of HBIG will serve as a critical catalyst for functional cure across both cohorts. This study, therefore, aims to perform a detailed retrospective analysis of a large single-center cohort of patients with post-LT HBV infection. This study seeks to systematically compare the clinical presentation and treatment efficacy between de novo and recurrent HBV, and to rigorously employ multivariate modeling to elucidate independent predictors of successful functional cure. The findings are intended to refine risk stratification and inform the development of more precise, evidence-based management algorithms for this complex patient population.

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Protocol

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Ethical approval for this retrospective research was granted by the Institutional Review Board (IRB) of Renji Hospital, School of Medicine, Shanghai Jiao Tong University. All procedures were executed in strict adherence to the guidelines outlined in the Declaration of Helsinki. Because the analysis exclusively utilized de-identified historical records, the review board explicitly exempted the study from requiring written informed consent. Patient privacy and data security were rigorously maintained throughout the investigation. The stepwise methodology employed to screen and classify the final analytical cohort from the primary transplant registry is detailed in Figure 1. The reagents and the equipment used are listed in the Table of Materials.

1. Study design and patient population

The analytical cohort was established by screening individuals who underwent liver transplantation between January 1, 2010, and July 31, 2024. Ultimately, 150 recipients were enrolled based on the following specific inclusion parameters: an age range of 18– 74 years, a confirmed LT procedure, and postoperative HBsAg quantification greater than 1 IU/mL. To guarantee that the de novo cases represented purely community-acquired or recipient-originated infections rather than graft-transmitted diseases, any recipient of an organ from an anti-HBc-positive donor was strictly excluded, along with individuals lacking continuous follow-up records. The finalized cohort was subsequently divided according to pre-surgical serology: the DNH cohort (n = 36) comprised initially HBsAg-negative patients who acquired a novel infection postoperatively, whereas the recurrent cohort (n = 114) consisted of individuals with pre-existing chronic HBV whose HBsAg and/or HBV DNA re-emerged post-transplantation.

2. Data collection, laboratory assays, and definitions

All patients were regularly followed up in the outpatient clinic after liver transplantation. The standardized postoperative surveillance protocol included intensive monitoring (e.g., weekly during the first month, monthly for the first 6 months, and every 3 – 6 months thereafter). A comprehensive review of medical records was conducted to collect data on demographic characteristics, primary liver disease (including indications for transplantation and baseline severity assessed via the Model for End-Stage Liver Disease [MELD] and FIB-4 scores), post-transplant immunosuppression regimens, time to HBsAg seroconversion, and final treatment outcomes.

To address perioperative viral management, standard antiviral prophylaxis was administered in accordance with institutional guidelines. All patients in the recurrent cohort (pre-transplant HBsAg-positive) received standard perioperative prophylaxis consisting of nucleos(t)ide analogs (NAs) initiated before or at the time of transplant, supplemented with an intraoperative anhepatic phase administration of hepatitis B immunoglobulin (HBIG). Postoperatively, these patients were maintained on NA therapy with or without low-dose HBIG based on individual risk stratification. Conversely, as patients in the DNH cohort were HBsAg-negative pre-transplantation and received grafts from anti-HBc-negative donors, they did not undergo routine HBV-specific antiviral prophylaxis before the serological confirmation of the de novo infection.

For serological testing, peripheral venous blood samples (5 mL) were collected, centrifuged at approximately 1,500 x g for 10 min to obtain serum, and stored at -70°C. Levels of HBsAg, hepatitis B surface antibody (anti-HBs), hepatitis B e antigen (HBeAg), hepatitis B e antibody (anti-HBe), and anti-HBc were quantitatively detected using generic/commercial enzyme-linked immunosorbent assay kits on an automated electrochemiluminescence immunoanalyzer. The established normal reference thresholds were: HBsAg < 1 IU/mL, anti-HBs & lt; 10 mIU/mL, HBeAg & lt; 1 IU/mL, anti-HBe >1 IU/mL, and anti-HBc & gt; 1 IU/mL. To mitigate the risk of overlooking occult HBV infections, which standard chemiluminescence immunoassays might miss, routine surveillance incorporated highly sensitive real-time polymerase chain reaction (PCR) testing for HBV DNA alongside standard serological panels. HBV DNA levels were quantified using commercial PCR assays with a lower limit of detection of 20 IU/mL. All viral load values were standardized and logarithmically transformed (log10 IU/mL) for statistical consistency. In line with contemporary treatment concepts and the global pursuit of viral hepatitis elimination by 203010,11, “ advantageous population ” was defined for finite-duration NA therapy as patients meeting the following criteria: HBsAg & lt; 100 IU/mL, HBeAg seroconversion (anti-HBe positivity), HBV DNA & lt; 10 IU/mL, and alanine aminotransferase (ALT) within the normal upper limit.

3. Statistical analysis

All statistical analyses were performed using R software and IBM SPSS Statistics. Categorical variables were presented as counts and percentages and compared between the DNH and recurrent groups using the Chi-square test or Fisher's exact test when expected cell counts were less than 5. Continuous variables were assessed for normality using the Shapiro-Wilk test. Recognizing the heavily skewed, non-normal distribution of clinical parameters (e.g., time to onset, peak biochemical markers), all continuous data are expressed as median [interquartile range, IQR] and compared using the non-parametric Mann-Whitney U test.

To rigorously evaluate the primary outcome of functional cure (defined as sustained HBsAg loss), time-to-event survival analyses were conducted using the Kaplan-Meier method, with differences between strata assessed via the log-rank test. To identify independent predictors of functional cure, a multivariate Cox proportional-hazards regression model was constructed to calculate adjusted hazard ratios (aHRs).

To ensure mathematical stability and model convergence, the final multivariate model incorporated core clinical variables, including age, infection type (DNH vs. recurrent), and HBIG combination therapy. Potential baseline confounders with quasi-complete separation, such as sex and initial HBeAg status, were evaluated in univariate analyses but excluded from the final multivariate model to maintain the robustness of the hazard ratio estimates. A two-tailed P-value of less than 0.05 was considered statistically significant for all tests.

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Results

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Study cohort and baseline characteristics

Out of 3,801 initial liver transplant procedures evaluated between January 2010 and July 2024, 258 individuals (6.79%) exhibited post-surgical HBsAg positivity. Following the strict exclusion of cases with fragmented monitoring data or those receiving grafts from anti-HBc-positive donors, 150 eligible patients formed the final analytical cohort (Figure 1). This population was stratified based on preoperati...

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Discussion

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The present investigation elucidates the divergent clinical trajectories and functional cure outcomes of de novo hepatitis B (DNH) and recurrent hepatitis B virus (HBV) infection following liver transplantation (LT)2,6. While DNH was associated with more severe acute hepatic injury at onset, recurrent infection achieved functional cure significantly earlier and at a higher rate. These differences may be fundamentally rooted in the pre-transplant immunological sta...

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Disclosures

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The authors have no conflicts of interest.

Acknowledgements

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The authors sincerely thank the clinical nurses, coordinators, and staff of the Liver Transplantation Center and Department of Infectious Diseases at Renji Hospital, Shanghai Jiao Tong University School of Medicine, for their dedicated patient care and meticulous data recording, which made this retrospective study possible. We are also grateful to the hospital’s medical records and statistics departments for their support in data retrieval.

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Materials

List of materials used in this article
NameCompanyCatalog NumberComments
Cobas e 602 AnalyzerRoche Diagnostics (Basel, Switzerland)4886826001Automated electrochemiluminescence immunoanalyzer
Cyclosporine AStandard hospital pharmacy formularyNMPA: H10960122Calcineurin inhibitor (CNI); adjunct or alternative
Elecsys anti-HBc II AssayRoche Diagnostics (Basel, Switzerland)11820559122ECLIA kit for total anti-HBc detection
Elecsys anti-HBe AssayRoche Diagnostics (Basel, Switzerland)11820613122ECLIA kit for anti-HBe quantification
Elecsys anti-HBs AssayRoche Diagnostics (Basel, Switzerland)2104316190ECLIA kit for anti-HBs quantification
Elecsys HBeAg AssayRoche Diagnostics (Basel, Switzerland)11820583122ECLIA kit for HBeAg quantification
Elecsys HBsAg II AssayRoche Diagnostics (Basel, Switzerland)4687785190ECLIA kit for HBsAg quantification
Entecavir (ETV)Standard hospital pharmacy formularyNMPA: H20100019Nucleos(t)ide analog; primary antiviral therapy
Hepatitis B Immunoglobulin (HBIG)Standard hospital pharmacy formularyNMPA: S20083007Used for passive immunization therapy
High-sensitivity HBV DNA PCR KitSansure Biotech (Changsha, China)S3062ERT-PCR with LOD of 20 IU/mL
IBM SPSS Statistics (version 26.0)IBM Corp. (Armonk, NY, USA)N/AUsed for baseline demographic comparisons and non-parametric tests (Mann-Whitney U, Fisher's exact)
Mycophenolate Mofetil (MMF)Roche (Basel, Switzerland)H20052083Anti-proliferative adjunct therapy
R Software (version 4.2.2)R Foundation for Statistical Computing (Vienna, Austria)N/AUsed for Kaplan-Meier curves, Multivariate Cox regression, and data visualization (ggplot2, survminer)
Sirolimus (Rapamycin)Pfizer (New York, NY, USA)HJ20130697mTOR inhibitor; used for oncology/nephrotoxicity risk
Software for Statistical Analysis
Systemic Steroids (Prednisone)Standard hospital pharmacy formularyNMPA: H12020689Corticosteroid; used for early post-transplant period
Tacrolimus (FK506)Astellas Pharma (Tokyo, Japan)J20150101Calcineurin inhibitor (CNI); backbone immunosuppression
Tenofovir Alafenamide (TAF)Standard hospital pharmacy formularyNMPA: H20180060Nucleos(t)ide analog; second-generation prodrug
Tenofovir Amibufenamide (TMF)Standard hospital pharmacy formularyNMPA: H20210011Novel nucleos(t)ide analog prodrug
Tenofovir Disoproxil (TDF)Standard hospital pharmacy formularyNMPA: H20171313Nucleos(t)ide analog; first-generation prodrug

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Tags

De Novo Hepatitis BRecurrent Hepatitis BLiver TransplantationFunctional CureHepatitis B VirusAntiviral TherapyHepatitis B ImmunoglobulinHBsAg LossKaplan Meier AnalysisCox Regression

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