Evidence map›Paper›PMID 38479361›Full record

ArticleImmunity2024

Epstein-Barr virus gp42 antibodies reveal sites of vulnerability for receptor binding and fusion to B cells.

Wei Bu, Ashish Kumar, Nathan L Board, JungHyun Kim, Kennichi Dowdell, Shu Zhang, Yona Lei, Anna Hostal, Tammy Krogmann, Yanmei Wang and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  10. Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025
    Review
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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 at 2 institutions in 1 country.

Wei BuMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Ashish KumarStructural Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Nathan L BoardMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
JungHyun KimMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Kennichi DowdellMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Shu ZhangMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Yona LeiMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Anna HostalMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Tammy KrogmannMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Yanmei WangClinical Services Program, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Stefania PittalugaLaboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Joseph MarcotrigianoStructural Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: joseph.marcotrigiano@nih.gov.
Jeffrey I CohenMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: jcohen@niaid.nih.gov.
National Institutes of Health · USLeidos (United States) · US

Funding

Herpesvirus Pathogenesis and Vaccine DevelopmentZIAAI000978 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI COHEN, JEFFREY · 2009 to 2025
$13.7M
Entry and replication of positive-sense, RNA virusesZIAAI001217 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MARCOTRIGIANO, JOSEPH · 2017 to 2025
$11.0M
Phase II SER-CAT Optimization: Acquisition of a next generation area detectorS10RR028976 · NCRR · UNIVERSITY OF GEORGIA · PI WANG, BI-CHENG · 2010 to 2010
$1.5M
Acquisition of a High Precision Micro Diffractometer to Support NIH funded Research at SER-CATS10OD027000 · OD · UNIVERSITY OF GEORGIA · PI ROSE, JOHN PATRICK · 2019 to 2019
$600k
Acquition of a microdiffractometer for SER-CATS10RR025528 · NCRR · UNIVERSITY OF GEORGIA · PI ROSE, JOHN PATRICK · 2009 to 2009
$414k
CCR NIH HHS HHSN261200800001CIntramural NIH HHS Z99 AI999999NCI NIH HHS HHSN261200800001ENCRR NIH HHS S10 RR025528NCRR NIH HHS S10 RR028976NIH HHS S10 OD027000
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) causes infectious mononucleosis and is associated with B cell lymphomas. EBV glycoprotein 42 (gp42) binds HLA class II and activates membrane fusion with B cells. We isolated gp42-specific monoclonal antibodies (mAbs), A10 and 4C12, which use distinct mechanisms to neutralize virus infection. mAb A10 was more potent than the only known neutralizing gp42 mAb, F-2-1, in neutralizing EBV infection and blocking binding to HLA class II. mAb 4C12 was similar to mAb A10 in inhibiting glycoprotein-mediated B cell fusion but did not block receptor binding, and it was less effective in neutralizing infection. Crystallographic structures of gH/gL/gp42/A10 and gp42/4C12 complexes revealed two distinct sites of vulnerability on gp42 for receptor binding and B cell fusion. Passive transfer of mAb A10 into humanized mice conferred nearly 100% protection from viremia and EBV lymphomas after EBV challenge. These findings identify vulnerable sites on EBV that may facilitate therapeutics and vaccines.

Indexed as

BenzeneacetamidesEpstein-Barr Virus InfectionsHerpesvirus 4, HumanPiperidonesAnimalsAntibodies, ViralGlycoproteinsMiceViral ProteinsAntibodies, Viralantineoplaston A10BenzeneacetamidesGlycoproteinsPiperidonesViral ProteinsEpstein-Barr virusfusion machineryglycoprotein 42herpesvirusHLA class IImonoclonal antibody therapy

Identifiers

PMID38479361
PMCPMC11000673
OpenAlexW4392716041

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.