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J Neurol Sci. 2016 Feb 15;361:213-9. doi: 10.1016/j.jns.2016.01.013. Epub 2016 Jan 6.

Epstein-Barr virus and multiple sclerosis. From evidence to therapeutic strategies.

Author information

1
Department of Neurology, Hospital Universitario Central de Asturias, Oviedo, Spain. Electronic address: sfmenendez@gmail.com.
2
Department of Neuropaediatrics, Hospital Universitario Central de Asturias, Oviedo, Spain.
3
Pathology department (Neuropathology division), Hospital Universitario Araba, Álava, Spain.
4
Department of Neurology, Hospital Universitario Central de Asturias, Oviedo, Spain.

Abstract

Multiple sclerosis is caused by a complex interaction between genetic predisposition and environmental factors. Epstein-Barr virus (EBV) is an environmental risk factor that is strongly related to multiple sclerosis (MS), since EBV seropositivity is linked to a significant risk of developing MS. EBV may be involved in the pathogenesis of the disease and it is possibly a prerequisite for the development of MS. EBV infection persists in B-cells during the lifetime of the host and can modulate their function. In addition, MS patients might have a deficient capacity to eliminate latent EBV infection in the central nervous system and this would promote the accumulation of infected B cells. Several mechanisms of pathogenesis, including a direct and indirect function of infected B cells, have been postulated in inflammation and neurodegeneration. A relationship between EBV and human endogenous retroviruses in the pathogenesis of MS has also been reported. If EBV is important in the pathogenesis of MS, different therapeutic strategies seem possible for MS treatment.

KEYWORDS:

B-cell; CD20; Epstein–Barr virus; Human endogenous retroviruses; Multiple sclerosis

PMID:
26810546
DOI:
10.1016/j.jns.2016.01.013
[Indexed for MEDLINE]

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