Evidence map›Paper›PMID 24619311›Full record

ReviewImmunologic research2014

The interplay between Epstein-Barr virus and B lymphocytes: implications for infection, immunity, and disease.

Olivia L Hatton, Aleishia Harris-Arnold, Steven Schaffert, Sheri M Krams, Olivia M Martinez

Open access · bronzeAbstract readReview
In one paragraph

Review in Immunologic research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

126 citing papers in PubMed, 1 synthesis or guideline pooled it, 213 citations in OpenAlex.

  1. Pooled it
  2. The influence of Epstein-Barr virus and cytomegalovirus on childhood respiratory health: A population-based prospective cohort study.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2020
    Trial
  3. Review
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
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  14. Epstein-Barr Virus in Multiple Sclerosis: Past, Present, and Future.Neurology(R) neuroimmunology & neuroinflammation · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

66 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Olivia L HattonProgram in Immunology and Department of Abdominal Transplantation, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Aleishia Harris-Arnold
Steven Schaffert
Sheri M Krams
Olivia M Martinez
Stanford University · US

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
A Stanford - SJSU Postdoctoral Training Program to Enhance URM TeachingK12GM088033 · NIGMS · STANFORD UNIVERSITY · PI BOOTHROYD, JOHN C · 2010 to 2016
$4.1M
Cellular Mechanisms of PTLD in Transplant ResipientsR01AI041769 · NIAID · STANFORD UNIVERSITY · PI MARTINEZ, OLIVIA M · 1997 to 2012
$3.9M
NIAID NIH HHS R01 AI041769NIAID NIH HHS R01 AI41769NIAID NIH HHS T32 AI007290NIGMS NIH HHS K12 GM088033
6 · The paper itself

Abstract

Human B cells are the primary targets of Epstein-Barr virus (EBV) infection. In most cases, EBV infection is asymptomatic because of a highly effective host immune response, but some individuals develop self-limiting infectious mononucleosis, while others develop EBV-associated lymphoid or epithelial malignancies. The viral and immune factors that determine the outcome of infection are not understood. The EBV life cycle includes a lytic phase, culminating in the production of new viral particles, and a latent phase, during which the virus remains largely silent for the lifetime of the host in memory B cells. Thus, in healthy individuals, there is a tightly orchestrated interplay between EBV and the host that allows the virus to persist. To promote viral persistence, EBV has evolved a variety of strategies to modulate the host immune response including inhibition of immune cell function, blunting of apoptotic pathways, and interfering with antigen processing and presentation pathways. In this article, we focus on mechanisms by which dysregulation of the host B cell and immune modulation by the virus can contribute to development of EBV+ B cell lymphomas.

Indexed as

B-LymphocytesEpstein-Barr Virus InfectionsHerpesvirus 4, HumanHost-Pathogen InteractionsHumansImmune EvasionMicroRNAsOncogene Proteins, ViralViral Matrix ProteinsEBV-associated membrane antigen, Epstein-Barr virusMicroRNAsOncogene Proteins, ViralViral Matrix Proteins

Identifiers

PMID24619311
PMCPMC4199828
OpenAlexW1963527597

What OpenQuestion holds

Textmetadata
LicenceTDM
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.