Abstract
Erythema infectiosum is the main manifestation of human parvovirus B19 infections. Further B19-related diseases commonly associated with the acute infection are flue-like symptoms, transient aplastic crisis, transient arthralgias, leukopenia and thrombocytopenia, spontaneous abortion and hydrops fetalis in pregnant women. Hepatitis, myocarditis, meningitis, encephalitis as well as pure red cell anemia may occur occasionally. In addition parvovirus B19 infections have been frequently described as cause or trigger of various forms of autoimmune diseases affecting all blood cell lines, joints, connective tissue, uvea, large and small vessels. In some autoimmunopathias the data are conflicting. Despite these controversial results recent research revealed insights that may explain the molecular mechanisms for the observed autoimmune phenomena. The viral transactivator protein NS1 induces enhanced TNF and IL-6 production and activates mitochondria related and TNFα-induced apoptosis. The viral phospholipase A2-like (PLA2) activity exerted by the capsid protein VP1 contributes to the generation of elevated amounts of inflammatory eicosanoids such as prostaglandins and leukotrienes during acute and peristent infection. Additional phenomena may be caused by the formation and deposition of immunocomplexes. Molecular mimicry may contribute to the appearance of autoimmune antibodies, f.e. antiphospholipid and anti-neutrophil cytoplasmic antibodies as well as antinuclear antigens. All these mechanisms implicated in the pathogenesis of parvovirus B19 triggered autoimmune diseases will be discussed in this review.
Keywords: Parvovirus B19 infection, viral persistence, autoimmunity, rheumatic disease, pathogenesis
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