Evidence map›Paper›PMID 41945394›Full record

Observational studyThe Journal of clinical investigation2026

HIV causes global B cell dysregulation and restricts HBV-specific B cell development in an incident HBV cohort.

Katherine E Cascino, Thomas Liechti, Eric C Seaberg, Kathleen Stevens, Steven M Wolinsky, Mallory D Witt, Robbie B Mailliard, Mario Roederer, Justin R Bailey, Chloe L Thio and 1 more

Abstract readMulticenter StudyObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in The Journal of clinical investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Katherine E CascinoDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Thomas LiechtiImmunoTechnology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, Maryland, USA.
Eric C SeabergDepartment of Epidemiology, Johns Hopkins University, Baltimore, Maryland, USA.
Kathleen StevensDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Steven M WolinskyDivision of Infectious Diseases, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Mallory D WittLundquist Research Institute at Harbor-UCLA Medical Center, Torrance, California, USA.
Robbie B MailliardDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Mario RoedererImmunoTechnology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, Maryland, USA.
Justin R BaileyDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Chloe L ThioDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Andrea L CoxDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Funding

Virology CoreU19AI188551 · NIAID · JOHNS HOPKINS UNIVERSITY · PI CHLOE L THIO · 2025 to 2026
$16.5M
NIAID NIH HHS U19 AI188551
6 · The paper itself

Abstract

BACKGROUNDFunctional B cell responses for both prevention and control of hepatitis B virus (HBV) infection remain poorly understood, including in the context of HBV/HIV coinfection.METHODSHere, we employed high-dimensional single-cell analysis to assess global and hepatitis B surface antigen-specific (HBsAg-specific) B cells in a longitudinal cohort of incident HBV from the Multicenter AIDS Cohort Study, with a subset of the cohort living with HIV-1.RESULTSWe observed that prior HIV infection has negative consequences for B cell function in early post-acute HBV infection, including increased frequencies of atypical memory B cells and regulatory B cells, expression of the activation marker CD86 on multiple B cell subsets in chronic HBV (CHB), and restricted expansion of HBsAg-specific B cells. In contrast, in HBV monoinfection, we observed no changes in the global B cell population from prior to infection and robust expansion of HBsAg-specific B cells. These expanded antigen-specific B cells resembled class-switched intermediate and resting memory B cells, with activation phenotypes that may contribute to ongoing HBV control.CONCLUSIONHIV infection has a significant impact on B cell responses to subsequent HBV infection that may promote development of CHB in HBV/HIV coinfection.FUNDINGVaccine Research Center, NIAID, Bill & Melinda Gates Foundation, and NIH.

Indexed as

B-LymphocytesHepatitis B, ChronicHepatitis B virusHIV-1HIV InfectionsMemory B CellsAdultCoinfectionFemaleHepatitis B Surface AntigensHumansMaleMiddle AgedHepatitis B Surface AntigensB cellsImmunologyVirology

Identifiers

PMID41945394
PMCPMC13221222

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Registered trials

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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.