Evidence map›Paper›PMID 31217170›Full record

ArticleAnnals of the rheumatic diseases2019

Association of Epstein-Barr virus serological reactivation with transitioning to systemic lupus erythematosus in at-risk individuals.

Neelakshi R Jog, Kendra A Young, Melissa E Munroe, Michael T Harmon, Joel M Guthridge, Jennifer A Kelly, Diane L Kamen, Gary S Gilkeson, Michael H Weisman, David R Karp and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
8.1field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. EBV Genome Variations and Association With Diseases.Journal of medical virology · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Lupus nephritis.Nature reviews. Disease primers · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. REDEFINING AUTOIMMUNE DISEASES: THE OPPORTUNITY FOR PRECISION AND PREVENTION.Transactions of the American Clinical and Climatological Association · 2025
    Review
  18. Article
  19. Review
  20. Article
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

15 authors at 6 institutions in 1 country.

Neelakshi R JogArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Kendra A YoungDepartment of Epidemiology, University of Colorado Anschutz Medical Campus, Colorado School of Public Health, Aurora, Colorado, USA.
Melissa E MunroeArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Michael T HarmonArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Joel M GuthridgeArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Jennifer A KellyArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Diane L KamenDepartment of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.
Gary S GilkesonDepartment of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.
Michael H WeismanDivision of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
David R KarpDivision of Rheumatic Diseases, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Patrick M GaffneyArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
John B HarleyCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Daniel J WallaceDivision of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Jill M NorrisDepartment of Epidemiology, University of Colorado Anschutz Medical Campus, Colorado School of Public Health, Aurora, Colorado, USA.
Judith A JamesArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA judith-james@omrf.org.ORCID 0000-0002-9574-7355
Oklahoma Medical Research Foundation · USCedars-Sinai Medical Center · USColorado School of Public Health · USMedical University of South Carolina · USCincinnati Children's Hospital Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Tracking and Evaluation CoreU54GM104938 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI PAUL G SPICER · 2013 to 2026
$68.2M
Oklahoma Rheumatic Disease Research Cores Center (Overall Application)P30AR073750 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JUDITH A JAMES · 2018 to 2026
$8.5M
Resource CoreP30AR072582 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAMES C OATES · 2017 to 2026
$8.5M
SLAM Genes-from Mouse to ManP50AR055503 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI KARP, DAVID R · 2007 to 2011
$8.3M
HLA GENE COMPLEMENTATION IN PRIMARY SJOGREN'S AND LUPUSR01AI024717 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI KOTTYAN, LEAH CLAIRE, WEIRAUCH, MATTHEW TYSON · 1987 to 2025
$7.8M
Gene Regulation as a Foundation for Autoimmune Disease PreventionU01AI130830 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI WEIRAUCH, MATTHEW TYSON · 2017 to 2021
$7.2M
SNP Confirmation and High Throughput Genotyping CoreP30AR053483 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GUTHRIDGE, JOEL MARVIN · 2007 to 2017
$6.7M
Pre-Clinical Studies to Identify SLE Therapeutic TargetsU19AI082714 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JAMES, JUDITH A · 2009 to 2018
$6.2M
Patient Resource CoreP60AR062755 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI GILKESON, GARY S · 2012 to 2016
$5.8M
Better Outcomes for Children: Promoting Excellence in Healthcare Genomics to Inform PolicyU01HG008666 · NHGRI · CINCINNATI CHILDRENS HOSP MED CTR · PI HARLEY, JOHN BARKER · 2015 to 2019
$4.2M
Genetic Linkage in LupusR37AI024717 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 2005 to 2014
$4.2M
Understanding early events in lupus autoimmunity to aid preventionU01AI101934 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JAMES, JUDITH A · 2012 to 2016
$2.3M
NHGRI NIH HHS U01 HG008666NIAID NIH HHS R01 AI024717NIAID NIH HHS R37 AI024717NIAID NIH HHS U01 AI101934NIAID NIH HHS U01 AI130830NIAID NIH HHS U19 AI082714NIAMS NIH HHS K24 AR068406NIAMS NIH HHS P30 AR053483NIAMS NIH HHS P30 AR072582NIAMS NIH HHS P30 AR073750NIAMS NIH HHS P50 AR055503NIAMS NIH HHS P60 AR062755NIGMS NIH HHS U54 GM104938
6 · The paper itself

Abstract

objectiveSystemic lupus erythematosus (SLE) is a systemic autoimmune disease with unknown aetiology. Epstein-Barr virus (EBV) is an environmental factor associated with SLE. EBV maintains latency in B cells with frequent reactivation measured by antibodies against viral capsid antigen (VCA) and early antigen (EA). In this study, we determined whether EBV reactivation and single nucleotide polymorphisms (SNPs) in EBV-associated host genes are associated with SLE transition.

methodsSLE patient relatives (n=436) who did not have SLE at baseline were recontacted after 6.3 (±3.9) years and evaluated for interim transitioning to SLE (≥4 cumulative American College of Rheumatology criteria); 56 (13%) transitioned to SLE prior to the follow-up visit. At both visits, detailed demographic, environmental, clinical information and blood samples were obtained. Antibodies against viral antigens were measured by ELISA. SNPs in

resultsMean baseline VCA IgG (4.879±1.797 vs 3.866±1.795, p=0.0003) and EA IgG (1.192±1.113 vs 0.7774±0.8484, p=0.0236) levels were higher in transitioned compared with autoantibody negative non-transitioned relatives. Increased VCA IgG and EA IgG were associated with transitioning to SLE (OR 1.28 95% CI 1.07 to 1.53, p=0.007, OR 1.43 95% CI 1.06 to 1.93, p=0.02, respectively). Significant interactions were observed between

conclusionHeightened serologic reactivation of EBV increases the probability of transitioning to SLE in unaffected SLE relatives.

Indexed as

AutoimmunityAntibodies, ViralAntigens, ViralCase-Control StudiesEnzyme-Linked Immunosorbent AssayFemaleFollow-Up StudiesHerpesviridae InfectionsHerpesvirus 4, HumanHumansLupus Erythematosus, SystemicMaleMiddle AgedRisk FactorsAntibodies, ViralAntigens, Viralautoimmunityepstein-barr virussystemic lupus erythematosus

Identifiers

PMID31217170
PMCPMC6692217
OpenAlexW2951407633

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.