Lehmann Hartwig W, von Landenberg Philipp, Modrow Susanne
Klinik für Kinder- und Jugendmedizin, Sächsisches Krankenhaus Hubertusburg, 04779 Wermsdorf, Germany.
Autoimmun Rev. 2003 Jun;2(4):218-23. doi: 10.1016/s1568-9972(03)00014-4.
Human parvovirus B19 infections may cause a widespread benign and self-limiting disease in children and adults, known as erythema infectiosum or fifth disease. A variety of further manifestations are associated with the infection such as arthralgias, arthritis, leukopenia and thrombocytopenia, anemia and vasculitis, spontaneous abortion and hydrops fetalis in pregnant women. Both in children and adults parvovirus B19 infections have been frequently implicated as a cause or trigger of various forms of autoimmune diseases affecting joints, connective tissue and large and small vessels. In addition, autoimmune neutropenia, thrombocytopenia and hemolytic anemia are known as sequelae of B19 infection. The molecular basis of the autoimmune phenomena and resultant pathogenesis is unclear. The involvement of molecular mimicry between cellular and viral proteins, the induction of enhanced cytokine production via the viral transactivator protein NS1 and the phospholipase A2-like activity of the capsid protein VP1 may contribute to the induction of autoimmune reactions. All the known data and the potential mechanisms involved in the pathogenesis will be discussed in this review.
人细小病毒B19感染可在儿童和成人中引起一种广泛的良性自限性疾病，称为传染性红斑或第五病。该感染还伴有多种其他表现，如关节痛、关节炎、白细胞减少、血小板减少、贫血和血管炎，孕妇可出现自然流产和胎儿水肿。在儿童和成人中，细小病毒B19感染常被认为是影响关节、结缔组织以及大小血管的各种自身免疫性疾病的病因或触发因素。此外，自身免疫性中性粒细胞减少、血小板减少和溶血性贫血是B19感染的后遗症。自身免疫现象及由此产生的发病机制的分子基础尚不清楚。细胞蛋白与病毒蛋白之间的分子模拟、病毒反式激活蛋白NS1诱导细胞因子产生增加以及衣壳蛋白VP1的磷脂酶A2样活性可能都有助于自身免疫反应的诱导。本综述将讨论所有已知数据及发病机制中涉及的潜在机制。
