epstein-barr virus causes arthritis

Posted on 01 Янв 20189

Epstein–Barr virus and rheumatoid arthritis: is there a link? - NCBI - NIH

Epstein–Barr virus and rheumatoid arthritis: is there a link? - NCBI - NIH
16 янв. 2006 г. - Rheumatoid arthritis is a systemic autoimmune disease characterized by chronic, destructive, debilitating arthritis. Its etiology is unknown; it is presumed that environmental factors trigger development in the genetically predisposed. Epstein–Barr virus, a nearly ubiquitous virus in the human population, has ...

These study designs have not been able to address the timing of these abnormalities with regard to the development of RA, nor have they been able to exclude the possibility that RA itself, or its treatment, is responsible for abnormally elevated EBV serologic responses and viral loads. Scotet E, David-Ameline J, Peyrat MA, Moreau-Aubry A, Pinczon D, Lim A, Even J, Semana G, Berthelot JM, Breathnach R, et al. Screening for family members of patients with nasopha-ryngeal carcinoma. Cooke SP, Rigby SP, Griffiths DJ, Venables PJ. Rheumatoid arthritis synovial membrane contains a 62,000-molecular-weight protein that shares an antigenic epitope with the Epstein-Barr virus-encoded associated nuclear antigen.

In nasopharyngeal carcinoma, for example, levels of IgA anti-VCA antibody 10-fold those in normal subjects are found years in advance of the onset of disease [ ], indicative of high levels of viral replication. Help for cytotoxic-T-cell responses is mediated by CD40 signalling. RA patients have more EBV-infected B cells than normal controls, leading to a 10-fold systemic EBV overload. Temporal relationship between elevation of Epstein-Barr virus antibody titers and initial onset of neurological symptoms in multiple sclerosis. B cell transformation by EBV also induces the expression of EBV-induced gene 3 ( ), which encodes a form of IL-12, responsible for the initiation of Th1-type immunity [ The host's cellular immune response has primary responsibility for the control of latent EBV infection within the B cells [ T cells activate the innate immune response to EBV and are required for the generation of robust memory responses by CD8 ].

The evidence linking Epstein–Barr virus and rheumatoid arthritis is reviewed. EBV, a widespread virus, highly recognized by antibodies but never eliminated, is an ideal candidate to trigger chronic immune complex disease. Rheumatology 1, IML, AP-HM, 270, boulevard de Sainte-Marguerite, 13009 Marseille, France; Inserm UMRs 1097, Aix-Marseille University, 163, avenue de Luminy, 13288 Marseille, France. Burkitt's lymphoma: its clinical course in relation to immunologic reactivities to Epstein-Barr virus and tumor-related antigens. Thus, in a normal adult, latent EBV infection is associated with moderate, stable and highly correlated levels of IgG antibodies against VCA, EBNA-1, and EA-R, with very low or undetectable levels of antibodies against EBNA-2 and EA-D [ Patterns of anti-Epstein–Barr virus (EBV) serologies observed in different disease states In situations of decreased cellular immunity, however, EBV reactivation, or the transition from latent to lytic infection, can occur. Linde A, Andersson J, Lundgren G, Wahren B. Rheumatoid arthritis (RA) is one of the most common autoimmune diseases, with a 0. Autoreactive B cells also have a central role in the development of RA, producing autoantibodies that might be involved in tissue damage in RA [ Genetic factors are important in disease susceptibility, but environmental exposures are probably crucial as well. Neel HB, Pearson GR, Weiland LH, Taylor WF, Goepfert HH, Pilch BZ, Goodman M, Lanier AP, Huang AT, Hyams VJ, et al. The costs of rheumatoid arthritis: absolute, incremental, and marginal estimates.

Epstein-Barr virus and rheumatoid arthritis. - NCBI
9 мая 2017 г. - Rheumatoid arthritis (RA) is one of the most common autoimmune diseases, with a 0.5% worldwide prevalence. The cause of RA remains unknown, however both genetic and environmental factors may contribute to its development. Among these is the Epstein-Barr virus (EBV). Here, we discuss several ...

The cause of rheumatoid arthritis (RA) still eludes us, though we know from twin studies that both genetic and environmental factors are important contributory components to disease susceptibility1; the latter is estimated to account for about one half of this risk.2 At least one major RA susceptibility gene resides within the ...

The development of antibodies targeting Epstein-Barr virus closely parallels autoimmune progression near the onset of SLE [abstract] Kang I, Quan T, Nolasco H, Park SH, Hong MS, Crouch J, Pamer EG, Howe JG, Craft J. Should infection still be considered as the most likely triggering factor for rheumatoid arthritis? Fairweather D, Frisancho-Kiss S, Rose NR. Hutchinson D, Shepstone L, Moots R, Lear JT, Lynch MP. Hence the need to monitor EBV load when treating RA patients with immunosuppressors. Several studies have shown that levels of EBV DNA and mRNA are much higher in the synovium of patients with RA than in that of healthy controls [ ].

Exposure to a common virus would explain the ubiquity of RA worldwide. Application of Epstein-Barr virus serology to the diagnosis and staging of North American patients with nasopharyngeal carcinoma. Epstein-Barr virus-specific IgA serum antibodies as an outstanding feature of nasopharyngeal carcinoma. Elevated levels of antibodies to Epstein-Barr virus antigens in sera and synovial fluids of patients with rheumatoid arthritis. These autoantibodies are directed against citrullinated proteins in the rheumatoid synovium, including fibrin, filaggrin, perinuclear factor, and keratin [ ] and in prospective cohort studies are present several years before the onset of RA [ ].

Elevated anti-EBV antibody titers have also been found in other autoimmune diseases, including Sjögren's syndrome [ ]. Dominant clonotypes in the repertoire of peripheral CD4+ T cells in rheumatoid arthritis. Different defects of T cell regulation of Epstein-Barr virus-induced B cell activation in rheumatoid arthritis. The cause of RA remains unknown, however both genetic and environmental factors may contribute to its development. Temporal relationship between elevation of Epstein-Barr virus antibody titers and initial onset of neurological symptoms in multiple sclerosis. Synovial Epstein-Barr virus infection increases the risk of rheumatoid arthritis in individuals with the shared HLA-DR4 epitope. These study designs have not been able to address the timing of these abnormalities with regard to the development of RA, nor have they been able to exclude the possibility that RA itself, or its treatment, is responsible for abnormally elevated EBV serologic responses and viral loads. Klatt T, Ouyang Q, Flad T, Koetter I, Buhring HJ, Kalbacher H, Pawelec G, Muller CA. Diet and rheumatoid arthritis in women: a possible protective effect of fish consumption. Epstein-Barr virus-specific cytotoxic T cell responses in rheumatoid arthritis patients.

Viral Arthritis: Practice Essentials, Pathophysiology, Etiology

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