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Transient anticardiolipin antibody syndrome in a patient with parvovirus b19 infection

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  • HUMAN PARVOVIRUS B19

    2009, Feigin and Cherry's Textbook of Pediatric Infectious Diseases, Sixth Edition
  • Human parvovirus B19 infection and autoimmunity

    2008, Autoimmunity Reviews
    Citation Excerpt :

    To confirm the role of the virus in inducing an autoimmune response, BALB/c mice were immunized with the viral peptide: autoantibodies against keratin, collagen type II, cardiolipin and ssDNA were detected in the majority of the mice which developed a strong anti-virus response [22]. Several reports have described the association of parvovirus infection and the induction of antiphospholipid antibodies [20,21,23,24] through different mechanisms including the phospholipase-A2-like activity observed in the VP1 unique region of the structural protein VP1 [23] and a molecular mimicry mechanism [24]. Another possible mechanism in the induction of chronic autoimmune inflammation is the increased expression of TNF-alpha and IL-6 genes by the cytotoxic NS-protein that behaves as transactivator of the two gene promoter regions.

  • Antiphospholipid syndrome (APS): Where does it come from?

    2007, Best Practice and Research: Clinical Rheumatology
    Citation Excerpt :

    Some of these are summarized in Table 1. A few representative examples to this association include the finding of higher prevalence of IgM anticytomegalovirus antibodies among patients positive for aPL10, APS-related manifestations following parvovirus infection11,12, and very high prevalence of aPL following an infection with the human immunodeficiency virus.13,14 Perhaps the most impressive association of APS with infections can be found in its rare variant, catastrophic APS.15

  • Human parvovirus B19 infection and antiphospholipid antibodies

    2007, Autoimmunity Reviews
    Citation Excerpt :

    This enzyme activity may contribute to the inflammatory processes induced by the production of leukotrienes and prostaglandins, but may also lead to the generation of unnatural complexes with cellular proteins or unusual cleavage products from cellular phospholipid compounds that may induce aPL-antibodies in combination with a distinct genetic background. These effects may be combined with mechanisms based on molecular mimicry that have been discussed as a major cause for the formation of anti-phospholipid antibodies [33,34]. Results supporting this hypothesis have been demonstrated by Blank and coworkers in an experimental study, using peptides from different bacteria for the induction of the antiphospholipid syndrome in a mouse model [35].

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