Evidence map›Paper›PMID 42351169›Full record

ArticleJournal of translational medicine2026

Role of viral and host factors in determining the outcome of HBV-associated acute liver failure.

Patrizia Farci, Davide De Battista, Ronald E Engle, Eric Chu, Zhaochun Chen, Brendan Jeffrey, Jody Rule, Hanh Nguyen, Sandra Raini, Soichi Takeda and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Patrizia FarciHepatic Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 50, Room 6523, 50 South Drive-MSC, Bethesda, MD, 20892-8009, USA. patrizia.farci@nih.gov.
Davide De Battista *Hepatic Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 50, Room 6523, 50 South Drive-MSC, Bethesda, MD, 20892-8009, USA.
Ronald E Engle *Hepatic Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 50, Room 6523, 50 South Drive-MSC, Bethesda, MD, 20892-8009, USA.
Eric ChuClinical Monitoring Research Program Directorate Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
Zhaochun ChenHepatic Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 50, Room 6523, 50 South Drive-MSC, Bethesda, MD, 20892-8009, USA.
Brendan JeffreyBioinformatics and Computational Biosciences Branch, Office of Cyber Infrastructure and Computational Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, 20892, MD, USA.
Jody RuleDivision of Digestive and Liver Diseases, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.
Hanh NguyenHepatic Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 50, Room 6523, 50 South Drive-MSC, Bethesda, MD, 20892-8009, USA.
Sandra RainiHepatic Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 50, Room 6523, 50 South Drive-MSC, Bethesda, MD, 20892-8009, USA.
Soichi TakedaHepatic Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 50, Room 6523, 50 South Drive-MSC, Bethesda, MD, 20892-8009, USA.
Dean FollmanBiostatistics Research Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Harvey J AlterDepartment of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, MD, USA.
William M LeeDivision of Digestive and Liver Diseases, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute hepatitis B virus (HBV) infection encompasses a broad clinical spectrum, from self-limited hepatitis to acute liver injury (ALI), acute liver failure (ALF), subacute liver failure, and ALF on chronic HBV reactivation. This study investigates how host and viral factors interact to shape the clinical spectrum of HBV-associated ALF.

methodsWe analyzed 231 serial serum samples from 49 well-characterized patients including 36 with HBV-associated ALF and 13 with acute hepatitis B. Among ALF patients, 7 had ALI, 7 acute and 11 subacute liver failure, and 11 ALF on chronic HBV. Viral factors, including HBV replication, genotype, sequence diversity and viral evolution by next-generation sequencing (NGS) were assessed alongside host immune responses and cytokine profiles by proteomics.

resultsDemographics were similar across groups. Mortality was highest in subacute liver failure and ALF on chronic HBV (82%) and intermediate in acute liver failure (43%). The three forms of ALF differed by clinical, virologic, and immunologic features. Acute liver failure was characterized by markedly elevated alanine aminotransferase and high IgM anti-HBc titers, whereas ALF on CHB showed higher serum HBV DNA, HBV RNA and HBcrAg levels. HBV genotype A predominated (63%), followed by D (15%), C (9%), and others (2-6%). NGS of the basal core promoter and precore/core regions revealed highly homogeneous viral populations in acute and subacute liver failure throughout follow-up, while ALF on CHB showed marked viral heterogeneity. Genetic diversity was genotype-dependent, unrelated to disease severity, and significantly lower in genotype A than D. Acute liver failure was associated with broad type 1 cytokine response (i.e. IP-10, MIP-1α, MIP-1β, TNF-α, and IFN-γ), restricted type 2 cytokine response (i.e. IL-4 and sCD137), along with proinflammatory (i.e. MCP-1, Il-6, and IL-8) and homeostatic (i.e. IL-7) cytokines, whereas subacute liver failure and ALF on chronic HBV exhibited low and restricted, but distinct cytokine profiles. Elevated GM-CSF and PDGF-BB at admission predicted transplant-free survival.

conclusionsDistinct clinical, serologic, virologic, and cytokine profiles correlate with disease severity, highlighting differing pathogenic mechanisms across HBV-associated ALF forms. Early biomarkers, including GM-CSF and PDGF-BB, may help predict recovery and guide individualized management to improve survival.

Indexed as

Hepatitis BHepatitis B virusHost-Pathogen InteractionsLiver Failure, AcuteAdultCytokinesDNA, ViralFemaleGenotypeHumansMaleTreatment OutcomeCytokinesDNA, ViralAcute liver failureHBVHost immunityPathogenesisViral factors

Identifiers

PMID42351169
PMCPMC13326087

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.