Evidence map›Paper›PMID 24893782›Full record

ArticleThe Journal of general virology2014

Epstein-Barr virus, the germinal centre and the development of Hodgkin's lymphoma.

Ghada Mohamed, Katerina Vrzalikova, Fathima Zumla Cader, Martina Vockerodt, Eszter Nagy, Patrik Flodr, Lee-Fah Yap, Arjan Diepstra, Philip M Kluin, Stefano Rosati and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of general virology, 2014. 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
0.9field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 13 citations in OpenAlex.

  1. 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

11 authors at 5 institutions in 4 countries.

Ghada MohamedCentre for Human Virology and the School of Cancer Sciences, University of Birmingham, Birmingham, UK.
Katerina VrzalikovaCentre for Human Virology and the School of Cancer Sciences, University of Birmingham, Birmingham, UK.
Fathima Zumla CaderCentre for Human Virology and the School of Cancer Sciences, University of Birmingham, Birmingham, UK.
Martina VockerodtCentre for Human Virology and the School of Cancer Sciences, University of Birmingham, Birmingham, UK.
Eszter NagyCentre for Human Virology and the School of Cancer Sciences, University of Birmingham, Birmingham, UK.
Patrik FlodrLaboratory of Molecular Pathology, Department of Pathology and Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacký University, 77900 Olomouc, Czech Republic.
Lee-Fah YapDepartment of Oral Biology and Biomedical Sciences & Oral Cancer Research and Coordinating Centre, Faculty of Dentistry, University of Malaya, Kuala Lumpur, Malaysia.
Arjan DiepstraUniversity of Groningen and University Medical Centre Groningen Department of Pathology and Medical Biology, Groningen, The Netherlands.
Philip M KluinUniversity of Groningen and University Medical Centre Groningen Department of Pathology and Medical Biology, Groningen, The Netherlands.
Stefano RosatiUniversity of Groningen and University Medical Centre Groningen Department of Pathology and Medical Biology, Groningen, The Netherlands.
Paul MurrayCentre for Human Virology and the School of Cancer Sciences, University of Birmingham, Birmingham, UK.
University of Birmingham · GBUniversity Medical Center Groningen · NLPalacký University Olomouc · CZUniversity of Groningen · NLUniversity of Malaya · MY

Funding

Cancer Research UK 12393
6 · The paper itself

Abstract

The relationship between Epstein-Barr virus (EBV) and the germinal centre (GC) of the asymptomatic host remains an enigma. The occasional appearance of EBV-positive germinal centres in some patients, particularly those with a history of immunosuppression, suggests that EBV numbers in the GC are subject to immune control. The relationship, if any, between lymphoid hyperplasia with EBV-positive germinal centres and subsequent or concurrent lymphomagenesis remains to be clarified. As far as the development of EBV-associated Hodgkin's lymphoma is concerned, the suppression of virus replication, mediated by LMP1 on the one hand, and the loss of B-cell receptor signalling on the other, appears to be an important pathogenic mechanism. A further important emerging concept is that alterations in the microenvironment of the EBV-infected B-cell may be important for lymphomagenesis.

Indexed as

AdultB-LymphocytesCell DifferentiationEpstein-Barr Virus InfectionsFemaleGerminal CenterHerpesvirus 4, HumanHodgkin DiseaseHumansMaleMiddle AgedPseudolymphomaReceptors, Antigen, B-CellViral Matrix ProteinsVirus ReplicationYoung AdultEBV-associated membrane antigen, Epstein-Barr virusReceptors, Antigen, B-CellViral Matrix Proteins

Identifiers

PMID24893782
PMCPMC7346593
OpenAlexW2126082150

What OpenQuestion holds

Textmetadata
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.