Evidence map›Paper›PMID 41006833›Full record

ArticleNature microbiology2025

Epstein-Barr virus exploits desmocollin 2 as the principal epithelial cell entry receptor.

Hongbo Wang, Zongjun Mou, Yao Yu Yeo, Qianyun Ge, Xiang Liu, Yohei Narita, Zhixuan Li, Chong Wang, Wanyu Li, Katelyn Rs Zhao and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
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  5. Review
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

19 authors.

Hongbo WangDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. wanghb.hongbo@gmail.com.ORCID http://orcid.org/0000-0002-4333-4436
Zongjun MouDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Yao Yu YeoCenter for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-7604-2296
Qianyun GeComprehensive Cancer Center, College of Medicine, The Ohio State University, Columbus, OH, USA.
Xiang LiuDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Yohei NaritaDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-8867-3669
Zhixuan LiDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Chong WangDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Wanyu LiDepartment of Microbiology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-5964-1545
Katelyn Rs ZhaoDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Jenny LiDepartment of Pathology, Comprehensive Cancer Center, College of Medicine, The Ohio State University, Columbus, OH, USA.
Wei BuLaboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Benjamin GewurzDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-3965-3418
Jeffrey I CohenLaboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Mingxiang TengDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.ORCID http://orcid.org/0000-0002-8536-8941
Xinghong DaiDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.ORCID http://orcid.org/0000-0002-4102-3175
Xuefeng LiuDepartment of Pathology, Comprehensive Cancer Center, College of Medicine, The Ohio State University, Columbus, OH, USA.
Sizun JiangCenter for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. sjiang3@bidmc.harvard.edu.ORCID http://orcid.org/0000-0001-6149-3142
Bo ZhaoDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. bzhao@bwh.harvard.edu.ORCID http://orcid.org/0000-0002-8612-5597

Funding

Cancer Immune Monitoring and Analysis CenterU24CA224331 · NCI · DANA-FARBER CANCER INST · PI FRANK S HODI, Catherine Ju-Ying Wu · 2017 to 2026
$18.4M
Targeting Epstein-Barr Virus super-enhancersR01AI123420 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Bo Zhao · 2016 to 2026
$5.1M
Dissecting enhancer function through integrative genomicsR35GM155298 · NIGMS · H. LEE MOFFITT CANCER CTR & RES INST · PI MINGXIANG TENG · 2024 to 2026
$1.3M
NCI NIH HHS U24 CA224331NIAID NIH HHS R01 AI123420NIGMS NIH HHS R35 GM155298
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) infects B and epithelial cells, causing various lymphomas and epithelial malignancies. Although cell-free infection of epithelial cells is inefficient, direct B-epithelial cell contact infection is highly efficient and probably the dominant route. To identify mechanisms of contact-mediated infection, we implemented a genome-wide CRISPR screen and uncovered desmocollin 2 (DSC2) as an EBV epithelial receptor and DSC3 as a co-factor for infection. DSC2 and DSC3 double knockout significantly inhibited both cell-free and cell-cell contact EBV infection of normal oral keratinocytes, while their overexpression permitted infection in receptor-negative cells. Antibodies to DSC2 blocked infection across normal oral keratinocytes, primary oral keratinocytes, and head and neck epithelial organoids. Combining DSC2 and DSC3 antibodies efficiently blocked cell-cell contact infection. Mechanistically, DSC2 interacted with the EBV gH/gL glycoprotein and facilitated epithelial fusion. Notably, EphA2 overexpression failed to restore infection in DSC2/3-deficient cells, indicating its dependence on DSC2/3. Our findings establish DSC2 as a principal EBV entry receptor and target for vaccine and therapeutic development.

Indexed as

DesmocollinsEpithelial CellsHerpesvirus 4, HumanReceptors, VirusVirus InternalizationCell LineEpstein-Barr Virus InfectionsHumansKeratinocytesReceptor, EphA2DesmocollinsDSC2 protein, humanDSC3 protein, humanReceptor, EphA2Receptors, Virus

Identifiers

PMID41006833
PMCPMC13040475

What OpenQuestion holds

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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.