Evidence map›Paper›PMID 26322262›Full record

ArticleSpringerPlus2015

Production of thyrotropin receptor antibodies in acute phase of infectious mononucleosis due to Epstein-Barr virus primary infection: a case report of a child.

Keiko Nagata, Keisuke Okuno, Marika Ochi, Keisuke Kumata, Hitoshi Sano, Naohiro Yoneda, Jun-Ichi Ueyama, Michiko Matsushita, Satoshi Kuwamoto, Masako Kato and 3 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in SpringerPlus, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. 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

13 authors at 1 institution in 1 country.

Keiko NagataDivision of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503 Japan.
Keisuke OkunoDivision of Pediatrics and Perinatology, Department of Multidisciplinary Internal Medicine, Tottori University, 36-1 Nishi-cho, Yonago, Tottori 683-8504 Japan.
Marika OchiDivision of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503 Japan.
Keisuke KumataDivision of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503 Japan.
Hitoshi SanoDivision of Pediatrics and Perinatology, Department of Multidisciplinary Internal Medicine, Tottori University, 36-1 Nishi-cho, Yonago, Tottori 683-8504 Japan.
Naohiro YonedaDivision of Pediatrics and Perinatology, Department of Multidisciplinary Internal Medicine, Tottori University, 36-1 Nishi-cho, Yonago, Tottori 683-8504 Japan.
Jun-Ichi UeyamaDivision of Pediatrics and Perinatology, Department of Multidisciplinary Internal Medicine, Tottori University, 36-1 Nishi-cho, Yonago, Tottori 683-8504 Japan.
Michiko MatsushitaDivision of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503 Japan.
Satoshi KuwamotoDivision of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503 Japan.
Masako KatoDivision of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503 Japan.
Ichiro MurakamiDivision of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503 Japan.
Susumu KanzakiDivision of Pediatrics and Perinatology, Department of Multidisciplinary Internal Medicine, Tottori University, 36-1 Nishi-cho, Yonago, Tottori 683-8504 Japan.
Kazuhiko HayashiDivision of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503 Japan.
Tottori University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Various autoantibodies have been reported to be detected during the progression of infectious mononucleosis. We observed a case of infectious mononucleosis due to Epstein-Barr virus primary infection for 2 months, and noticed the transiently increased titer of thyrotropin receptor autoantibodies detected at the acute phase on the 3rd day after admission. At that time, real-time quantitative PCR also revealed the mRNA expressions of an immediate early lytic gene, BZLF1, and a latent gene, EBNA2. The expression of BZLF1 mRNA means that Epstein-Barr virus infects lytically, and EBNA2 protein has an important role in antibody production as well as the establishment of Epstein-Barr virus latency. These results suggest that Epstein-Barr virus lytic infection is relevant to thyrotropin receptor autoantibody production. Thyrotropin receptor autoantibodies stimulate thyroid follicular cells to produce excessive thyroid hormones and cause Graves' disease. Recently, we reported the thyrotropin receptor autoantibody production from thyrotropin receptor autoantibody-predisposed Epstein-Barr virus-infected B cells by the induction of Epstein-Barr virus lytic infection in vitro. This case showed in vivo findings consistent with our previous reports, and is important to consider the pathophysiology of Graves' disease and one of the mechanisms of autoimmunity.

Indexed as

AutoantibodyEpstein–Barr virus (EBV)Graves’ diseaseInfectious mononucleosisLytic infectionReactivationThyrotropin receptor antibody (TRAb)

Identifiers

PMID26322262
PMCPMC4549369
OpenAlexW1849911255

What Socratic 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 Socratic graph.