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EBV in MS: guilty by association?


Lünemann, J D; Münz, C (2009). EBV in MS: guilty by association? Trends in Immunology, 30(6):243-248.

Abstract

Epstein-Barr Virus (EBV) is one of the most successful human viruses, infecting more than 90% of the adult population worldwide and persisting for the lifetime of the host. Individuals with a history of symptomatic primary EBV infection, called infectious mononucleosis, carry a moderately higher risk of developing multiple sclerosis (MS). In addition, EBV-specific immune responses, which crucially regulate the host-virus balance in healthy virus carriers, are altered in patients with MS. Although no data so far unequivocally support a direct etiologic role of the virus, recent studies allow for the development of testable hypotheses as to how EBV infection potentially promotes autoimmunity and central nervous system (CNS) tissue damage in MS.

Abstract

Epstein-Barr Virus (EBV) is one of the most successful human viruses, infecting more than 90% of the adult population worldwide and persisting for the lifetime of the host. Individuals with a history of symptomatic primary EBV infection, called infectious mononucleosis, carry a moderately higher risk of developing multiple sclerosis (MS). In addition, EBV-specific immune responses, which crucially regulate the host-virus balance in healthy virus carriers, are altered in patients with MS. Although no data so far unequivocally support a direct etiologic role of the virus, recent studies allow for the development of testable hypotheses as to how EBV infection potentially promotes autoimmunity and central nervous system (CNS) tissue damage in MS.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Health Sciences > Immunology and Allergy
Life Sciences > Immunology
Language:English
Date:2009
Deposited On:11 Jan 2010 08:32
Last Modified:27 Jun 2022 10:45
Publisher:Elsevier
ISSN:1471-4906
OA Status:Closed
Publisher DOI:https://doi.org/10.1016/j.it.2009.03.007
PubMed ID:19428300