Evidence map›Paper›PMID 35005588›Full record

ArticleJournal of translational autoimmunity2021

Serologic markers of Epstein-Barr virus reactivation are associated with increased disease activity, inflammation, and interferon pathway activation in patients with systemic lupus erythematosus.

Rebecca A Wood, Lauren Guthridge, Emma Thurmond, Carla J Guthridge, Joseph M Kheir, Rebecka L Bourn, Catriona A Wagner, Hua Chen, Wade DeJager, Susan R Macwana and 8 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational autoimmunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

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  7. Adoptive T-cell therapy for virus-associated diseases.Clinical microbiology reviews · 2025
    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

18 authors at 2 institutions in 1 country.

Rebecca A WoodArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Lauren GuthridgeArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Emma ThurmondArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Carla J GuthridgeArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Joseph M KheirArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Rebecka L BournArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Catriona A WagnerArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Hua ChenArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Wade DeJagerArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Susan R MacwanaArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Stan KampArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Rufei LuArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Cristina ArriensArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Eliza F ChakravartyArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Aikaterini ThanouArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Joan T MerrillArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Joel M GuthridgeArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Judith A JamesArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Oklahoma Medical Research Foundation · USUniversity of Oklahoma Health Sciences 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
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 GAFFNEY, PATRICK M · 2009 to 2018
$6.2M
Oklahoma ACE: Molecular Destruction of Autoimmune Disease to Aid Clinical Trail SuccessUM1AI144292 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JUDITH A JAMES · 2019 to 2026
$3.3M
Understanding early events in lupus autoimmunity to aid preventionU01AI101934 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JAMES, JUDITH A · 2012 to 2016
$2.3M
Mechanisms of Lupus Disease Transition and Hydroxychloroquine Immune ModulationR01AR072401 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JAMES, JUDITH A · 2017 to 2020
$1.8M
NIAID NIH HHS U01 AI101934NIAID NIH HHS U19 AI082714NIAID NIH HHS UM1 AI144292NIAMS NIH HHS P30 AR053483NIAMS NIH HHS P30 AR073750NIAMS NIH HHS R01 AR072401NIGMS NIH HHS U54 GM104938
6 · The paper itself

Abstract

SLE is a clinically heterogeneous disease characterized by an unpredictable relapsing-remitting disease course. Although the etiology and mechanisms of SLE flares remain elusive, Epstein-Barr virus (EBV) reactivation is implicated in SLE pathogenesis. This study examined the relationships between serological measures of EBV reactivation, disease activity, and interferon (IFN)-associated immune pathways in SLE patients. Sera from adult SLE patients (n = 175) and matched unaffected controls (n = 47) were collected and tested for antibodies against EBV-viral capsid antigen (EBV-VCA; IgG and IgA), EBV-early antigen (EBV-EA; IgG), cytomegalovirus (CMV; IgG), and herpes simplex virus (HSV-1; IgG). Serological evidence of EBV reactivation was more common in SLE patients compared to controls as demonstrated by seropositivity to EBV-EA IgG (39% vs 13%; p = 0.0011) and EBV-VCA IgA (37% vs 17%; p = 0.018). EBV-VCA, CMV1, and HSV-1 IgG seropositivity rates did not differ between SLE patients and controls. Furthermore, concentrations of EBV-VCA (IgG and IgA) and EBV-EA (IgG) were higher in SLE patients. SLE patients with high disease activity had increased concentrations of EBV-VCA IgA (mean ISR 1.34 vs. 0.97; p = 0.041) and EBV-EA IgG levels (mean ISR 1.38 vs. 0.90; p = 0.007) compared with those with lower disease activity. EBV reactivation was associated with enhanced levels of the IFN-associated molecule IP-10 (p < 0.001) and the soluble mediators BLyS (p < 0.001) and IL-10 (p = 0.0011). In addition, EBV-EA IgG responses were enriched in two previously defined patient clusters with robust expression of IFN and inflammatory or lymphoid and monocyte responses. Patients in these clusters were also more likely to have major organ involvement, such as renal disease. This study supports a possible role for EBV reactivation in SLE disease activity.

Indexed as

AntibodiesDisease activityEpstein-barr virusInterferonSystemic lupus erythematosus

Identifiers

PMID35005588
PMCPMC8716608
OpenAlexW3198826987

What OpenQuestion holds

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Registered trials

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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.