Evidence map›Paper›PMID 23656710›Full record

ReviewCurrent opinion in rheumatology2013

Multiple sclerosis: autoimmunity and viruses.

Matthew F Cusick, Jane E Libbey, Robert S Fujinami

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  19. Neuroinvasion, neurotropic, and neuroinflammatory events of SARS-CoV-2: understanding the neurological manifestations in COVID-19 patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020
    Review
  20. Viral infections and multiple sclerosis.Drug discovery today. Disease models · 2020
    Review
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

3 authors at 1 institution in 1 country.

Matthew F CusickDepartment of Pathology, University of Utah, Salt Lake City, Utah 84132, USA.
Jane E Libbey
Robert S Fujinami
University of Utah · US

Funding

Training Program in Microbial PathogenesisT32AI055434 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MULVEY, MATTHEW A, PLANELLES, VICENTE · 2004 to 2025
$6.0M
Virus-Host Interactions that Lead to EpilepsyR01NS065714 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S · 2010 to 2018
$2.9M
NIAID NIH HHS T32 AI055434NIAID NIH HHS T32AI055434NINDS NIH HHS 5R01NS065714-03NINDS NIH HHS R01 NS065714
6 · The paper itself

Abstract

purpose of reviewThis review will explore two new aspects of the involvement of viruses in multiple sclerosis pathogenesis. The first aspect is the complex interactions between viruses. The second aspect is the proposal of a mechanism by which autoreactive T cells are able to escape thymic selection and potentially recognize self and a pathogen. RECENT

findingsWith regard to viruses, recent work has demonstrated that one virus may enhance the replication of another virus, potentially leading to an increase in inflammation and disease progression. Also, interactions between human endogenous retroviruses, which likely do not replicate, and certain herpes viruses, may also play a role in disease pathogenesis. Mechanistically, T cells expressing dual T-cell receptors would be able to recognize self and a foreign antigen specifically. Therefore, human endogenous retroviruses potentially play a role in multiple sclerosis pathogenesis, and both interactions between multiple viruses and autoreactive CD8(+) T cells with dual T-cell receptors may play a role in the pathogenesis of the disease. SUMMARY: The complex interactions between multiple viral infections, either within the central nervous system or in the periphery, and the host immune response to viral infection may be such that a variety of viral specificities result in the activation of T cells that recognize self and induce multiple sclerosis. Therefore, it is unlikely that any one microbe will be determined to be the causative agent of multiple sclerosis as reflected by the number of potential triggering mechanisms of the disease.

Indexed as

AutoimmunityCD8-Positive T-LymphocytesHumansLymphocyte ActivationMultiple SclerosisReceptors, Antigen, T-CellVirus DiseasesVirus ReplicationReceptors, Antigen, T-Cell

Identifiers

PMID23656710
PMCPMC4406397
OpenAlexW2063068284

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.