Parvovirus B19 in the acute arthropathies and juvenile rheumatoid arthritis

Oğuz, Fatma; Akdeni̇z, Celal; Ünüvar, Emin; Küçükbasmacı, Ömer; Sıdal, Müjgan

doi:10.1046/j.1440-1754.2002.00789.x

Cited by 39 publications

(22 citation statements)

References 22 publications

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“…All children were followed over time to assess the progress of arthropathy to JIA: seropositive cases significantly drifted to progress to chronic arthritis and more likely to receive a final diagnosis of JIA than seronegative ones. These data suggested a role of parvovirus B19 for the development of JIA [37].…”

Section: The Potential Role Of Viruses In Juvenile Idiopathic Arthritismentioning

confidence: 75%

The Etiology of Juvenile Idiopathic Arthritis

Rigante

Bosco

Esposito

2014

Clinic Rev Allerg Immunol

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Over the years, the commonly used term to describe juvenile idiopathic arthritis (JIA) has changed. By definition, JIA includes all types of arthritis with no apparent cause, lasting more than 6 weeks, in patients aged less than 16 years at onset. JIA pathogenesis is still poorly understood: the interaction between environmental factors and multiple genes has been proposed as the most relevant working mechanism to the development of JIA. The concept that various microbes that colonize or infect not only the mucosal surfaces, like the oral cavity, but also the airways and gut might trigger autoimmune processes, resulting in chronic arthritides, and JIA was first drafted at the outset of last century. JIA development might be initiated and sustained by the exposure to environmental factors, including infectious agents which affect people at a young age, depending on the underlying genetic predisposition to synovial inflammation. Many data from patients with JIA suggest a scenario in which different external antigens incite multiple antigen-specific pathways, cytotoxic T cell responses, activation of classical complement cascade, and production of proinflammatory cytokines. In this review, emphasis is paid not only to the potential role of parvovirus B19 and Epstein-Barr virus in primis but also to the general involvement of different bacteria as Salmonella spp., Shigella spp., Campylobacter spp., Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bartonella henselae, and Streptococcus pyogenes for the development of immune-mediated arthritides during childhood. No unequivocal evidence favoring or refuting these associations has been clearly proved, and today, the strict definition of JIA etiology remains unknown. The infection can represent a random event in a susceptible individual, or it can be a necessary factor in JIA development, always in combination with a peculiar genetic background. Further studies are needed in order to address the unsolved questions concerning this issue.

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Section: The Potential Role Of Viruses In Juvenile Idiopathic Arthritismentioning

confidence: 75%

The Etiology of Juvenile Idiopathic Arthritis

Rigante

Bosco

Esposito

2014

Clinic Rev Allerg Immunol

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“…The virus may represent a trigger for both autoinflammation and autoimmunity. There are only few reports of parvovirus B19-induced autoimmunity, including rheumatoid arthritis, [16][17][18] systemic lupus erythematosus, 19,20 antiphospholipid syndrome, 21 systemic sclerosis and vasculitis. Lehmann et al 22 suggested that, in persistent parvovirus B19 infection, production of proinflammatory cytokines as a result of nonstructural protein 1 (nonstructural protein of parvovirus B19) may transactivate cellular promoter for the expansion of tumor necrosis factor-α and interleukin-6.…”

Section: Discussionmentioning

confidence: 99%

Successful Immunotherapy in Life-threatening Parvovirus B19 Infection in a Child

Butin¹,

Mekki

Phan³

et al. 2013

Pediatric Infectious Disease Journal

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We report a case of an immunocompetent child who developed parvovirus B19 infection complicated by autoinflammatory disease with myocarditis, tamponade and macrophage activation syndrome. He recovered with immunotherapy including prednisone, immunoglobulins, cyclosporin and anakinra (anti-interleukin-1). The report shows that parvovirus can provoke severe systemic inflammation with acute heart injury and that anti-interleukin-1 might be considered in such parvovirus-related inflammation.

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“…A number of studies link evidence of a previous Parvovirus B19 infection and parvo B19 viral persistence with the development of JIA and the presence of active disease. [20][21][22][23] Enteric and genitourinary tract organisms may play a triggering role in ERA, though none have been proven. Masi and Walsh 24 studied ERA patients with evidence of active synovitis.…”

Section: Environmental Triggers Of Jiamentioning

confidence: 99%