Evidence map›Paper›PMID 27096949›Full record

ArticlePLoS pathogens2016

Early T Cell Recognition of B Cells following Epstein-Barr Virus Infection: Identifying Potential Targets for Prophylactic Vaccination.

Jill M Brooks, Heather M Long, Rose J Tierney, Claire Shannon-Lowe, Alison M Leese, Martin Fitzpatrick, Graham S Taylor, Alan B Rickinson

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. A tonsil organoid model reveals Epstein-Barr virus-infected germinal center B cell states during primary infection.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  9. Identifying Epstein-Barr virus peptide sequences associated with differential IgG antibody response.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2022
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  19. Burkitt Lymphomas Evolve to Escape Dependencies on Epstein-Barr Virus.Frontiers in cellular and infection microbiology · 2020
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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

8 authors at 2 institutions in 2 countries.

Jill M BrooksInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
Heather M LongInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
Rose J TierneyInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
Claire Shannon-LoweInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
Alison M LeeseInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
Martin FitzpatrickBiomolecular Mass Spectrometry and Proteomics Group, Utrecht University, Utrecht, The Netherlands.
Graham S TaylorInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
Alan B RickinsonInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
University of Birmingham · GBUtrecht University · NL

Funding

Cancer Research UK 13174Cancer Research UK 15032Cancer Research UK C5575/A15032Cancer Research UK C8781/A13174Medical Research Council G0901755Medical Research Council MR/J002046/1Medical Research Council MR/N023781/1
6 · The paper itself

Abstract

Epstein-Barr virus, a B-lymphotropic herpesvirus, is the cause of infectious mononucleosis, has strong aetiologic links with several malignancies and has been implicated in certain autoimmune diseases. Efforts to develop a prophylactic vaccine to prevent or reduce EBV-associated disease have, to date, focused on the induction of neutralising antibody responses. However, such vaccines might be further improved by inducing T cell responses capable of recognising and killing recently-infected B cells. In that context, EBNA2, EBNA-LP and BHRF1 are the first viral antigens expressed during the initial stage of B cell growth transformation, yet have been poorly characterised as CD8+ T cell targets. Here we describe CD8+ T cell responses against each of these three "first wave" proteins, identifying target epitopes and HLA restricting alleles. While EBNA-LP and BHRF1 each contained one strong CD8 epitope, epitopes within EBNA2 induced immunodominant responses through several less common HLA class I alleles (e.g. B*3801 and B*5501), as well as subdominant responses through common class I alleles (e.g. B7 and C*0304). Importantly, such EBNA2-specific CD8+ T cells recognised B cells within the first day post-infection, prior to CD8+ T cells against well-characterised latent target antigens such as EBNA3B or LMP2, and effectively inhibited outgrowth of EBV-transformed B cell lines. We infer that "first wave" antigens of the growth-transforming infection, especially EBNA2, constitute potential CD8+ T cell immunogens for inclusion in prophylactic EBV vaccine design.

Indexed as

Antigens, ViralB-LymphocytesCD8-Positive T-LymphocytesEnzyme-Linked Immunospot AssayEpitopes, T-LymphocyteEpstein-Barr Virus InfectionsHumansImmunoblottingLymphocyte ActivationViral VaccinesAntigens, ViralEpitopes, T-LymphocyteViral Vaccines

Identifiers

PMID27096949
PMCPMC4838210
OpenAlexW2342226634

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.