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Article

Latent virus infection upregulates CD40 expression facilitating enhanced autoimmunity in a model of multiple sclerosis.

Scientific reports - 10 Sept 2015

Casiraghi Costanza, Márquez Ana Citlali, Shanina Iryna, Horwitz Marc Steven

Abstract excerpt

Epstein-Barr virus (EBV) has been identified as a putative environmental trigger of multiple sclerosis (MS) by multiple groups working worldwide. Previously, we reported that when experimental autoimmune encephalomyelitis (EAE) was induced in mice latently infected with murine γ-herpesvirus 68 (γHV-68), the murine homolog to EBV, a disease more reminiscent of MS developed. Specifically, MS-like lesions developed...

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Topics

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Share to Antigen-Presenting Cells
Share to CD40 Antigens

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Encephalomyelitis, Autoimmune, Experimental

Share to Herpesviridae Infections

Share to Herpesvirus 4, Human

Share to STAT1 Transcription Factor

Share to T-Lymphocyte Subsets

Share to Virus Latency

Source

Open in PubMed Open full text

Identifiers

PMID: 26356194
DOI: 10.1038/srep13995
PMCID: PMC4564856

Genes

MOG
STAT1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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