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PubMed · 16400268

Does epstein-barr virus cause multiple sclerosis?

Abstract

The etiology of multiple sclerosis (MS) remains unknown; however, both genetic and environmental influences undoubtedly are involved. In terms of the environment, infectious agents and random factors seem likely and there is growing evidence that MS may sometimes occur as an uncommon complication of an infection by the Epstein-Barr virus (EBV). Support for this concept, including epidemiologic considerations, persistent infection of B lymphocytes, known neurologic complications of EBV infection, serologic studies, and attempts at genome identification are reviewed. These data are consistent with EBV being a leading candidate agent in MS causation, but the evidence is not considered definitive at this time.

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BibTeXRIS

Stuart D Cook. 2004. Does epstein-barr virus cause multiple sclerosis?. https://pubmed.ncbi.nlm.nih.gov/16400268/

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A 51-year-old man developed anemia, and was diagnosed with pure red cell aplasia through the absence of erythroid progenitors. Initially, he was treated with cyclosporine and prednisolone for 6 months but they were ineffective. Large granular lymphocyte (LGL) leukemia with the T-cell gamma delta phenotype evolved after 6 months showing CD2+, CD3+, CD8- and CD56- with the T-cell receptor beta gene rearrangement, clonalities of gamma and delta genes and complex chromosome abnormality simultaneously with hemophagocytic syndrome (HPS). Epstein-Barr virus (EBV) genomic DNA was detected in the bone marrow cells. Administration of bolus methylprednisolone was ineffective, and the patient died one month later. In the present patient, it seemed that lymphoproliferative disease of large granular lymphocytes (LDGL) manifested initially as PRCA, gammadelta LGL leukemia evolved, and finally fatal HPS become complicated, presumably caused by the EBV reactivation in the immunodeficiency state with the administration of immunosuppressants.

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Epstein-Barr virus immunossuppression of innate immunity mediated by phagocytes.

Epstein-Barr virus (EBV) is an oncogenic human herpesvirus that persistently infects approximately 90% of the world's population. Such a remarkably sustained of viral infectivity relies on EBV's ability to evade the host immune defenses. A crucial part of this anti-EBV response is mediated by cytotoxic CD8+ T lymphocytes, which maintain a life-long control over proliferating latently-infected B cells in order to prevent these from giving rise to lymphomatous diseases. On the other hand, little has been done to assess the role of phagocytes-mediated innate immunity in the pathogenesis of EBV infection. In the course of primary EBV infection, episodes of neutropenia and monocytopenia can be observed during the acute phase of infection. According to the role of those cells in the non specific and specific immunity, such a decrease in circulating phagocytes may then temporarily affect the immune defense and potentially influence the outcome of EBV infection. Recent studies have demonstrated that EBV infects both neutrophils and monocytes and modulates several of their biological functions. This review covers the current state of our knowledge relative to the role of neutrophils and monocytes in EBV pathogenesis and describes the nature of countermeasures deployed by EBV against these cells.

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