Evidence map›Paper›PMID 21035384›Full record

ArticleJournal of clinical virology : the official publication of the Pan American Society for Clinical Virology2011

Epstein-Barr virus replication linked to B cell proliferation in inflamed areas of colonic mucosa of patients with inflammatory bowel disease.

Sumathi Sankaran-Walters, Kanat Ransibrahmanakul, Irina Grishina, Jason Hung, Enrique Martinez, Thomas Prindiville, Satya Dandekar

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In one paragraph

Article in Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

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  20. Pathogenesis of Crohn's disease: Bug or no bug.World journal of gastrointestinal pathophysiology · 2015
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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

7 authors at 3 institutions in 1 country.

Sumathi Sankaran-WaltersDepartment of Medical Microbiology and Immunology, University of California, Davis, CA 95616, United States. ssankara@ucdavis.edu
Kanat Ransibrahmanakul
Irina Grishina
Jason Hung
Enrique Martinez
Thomas Prindiville
Satya Dandekar
University of California Davis Medical Center · USUniversity of California, Davis · USUniversity of California System · US

Funding

Building Interdisciplinary Research Careers in Womens Health at UC Davis - Administrative SupplementK12HD051958 · NICHD · UNIVERSITY OF CALIFORNIA DAVIS · PI LANE, NANCY E · 2005 to 2023
$9.6M
INTESTINAL CYTOKINE &TCELL HOMEOSTASIS IN SIV INFECTIONR01AI043274 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI DANDEKAR, SATYA · 1998 to 2013
$5.1M
HIV reservoir and CD4 repopulation in gut lymphoid tissueR01DK061297 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI DANDEKAR, SATYA · 2002 to 2012
$3.5M
NIAID NIH HHS AI43274NIAID NIH HHS R01 AI043274NICHD NIH HHS K12 HD051958NIDDK NIH HHS DK61297NIDDK NIH HHS R01 DK061297
6 · The paper itself

Abstract

backgroundInflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract. Epstein-Barr virus (EBV) infection is associated with increased disease severity in therapeutically immunosuppressed IBD patients. The role of EBV infection in patients with IBD who are unresponsive to medical therapy is unclear. Anti-viral strategies may be a viable treatment option if severity of EBV infection, reflected in peripheral blood, contributes to IBD progression.

objectivesWe investigated the role of EBV in IBD patients unresponsive to medical therapy by examining EBV reactivation and B-cell proliferation in colonic mucosa. STUDY

designEBV DNA copy numbers were measured by real-time PCR in peripheral blood mononuclear cells (PBMC) of 84 patients with IBD and 115 non-IBD controls in a retrospective cross-sectional study. EBV-infected cells in colonic mucosa were identified by immunohistochemistry.

resultsEBV load in PBMC was higher in patients with IBD than in non-IBD controls, especially in patients not responding to medication. Inflamed colonic mucosa of these patients had high levels of expression of lytic and latent EBV genes that localized to proliferating B-lymphocytes, which was not seen in patients responding to therapy.

conclusionsEBV replication was associated with severe IBD and mucosal inflammation. Increased proliferation and EBV infection of B-lymphocytes in inflamed colonic mucosa highlight the potential role of EBV in mucosal inflammation. The immunomodulatory effects of EBV could delay the resolution of the IBD associated inflammation, thus contributing to disease progression. These results indicate that anti-viral therapeutic strategies for the resolution of IBD may be useful.

Indexed as

ColonVirus ReplicationAdultAgedAged, 80 and overB-LymphocytesCell ProliferationCross-Sectional StudiesDNA, ViralEpstein-Barr Virus InfectionsFemaleHerpesvirus 4, HumanHumansInflammatory Bowel DiseasesMaleMiddle AgedDNA, Viral

Identifiers

PMID21035384
PMCPMC3052968
OpenAlexW1990852256

What OpenQuestion holds

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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.