Lunardi Claudio, Tinazzi Elisa, Bason Caterina, Dolcino Marzia, Corrocher Roberto, Puccetti Antonio
Department of Clinical and Experimental Medicine, Section of Internal Medicine, University of Verona, Verona, Italy.
Autoimmun Rev. 2008 Dec;8(2):116-20. doi: 10.1016/j.autrev.2008.07.005.
Human parvovirus B19 infection is responsible for a wide range of human diseases ranging from mild erythema infectiosum in immunocompetent children to fetal loss in primary infected pregnant women and aplastic anemia or lethal cytopenias in adult immunocompromised patients. Since persistent viral infection is responsible for an autoimmune response and clinical symptoms can mimic autoimmune inflammatory disorders, parvovirus B19 is the object of intense efforts to clarify whether it is also able to trigger autoimmune diseases. Indeed the virus has been implicated as the causative or the precipitating agent of several autoimmune disorders including rheumatoid arthritis, systemic lupus, antiphospholipid syndrome, systemic sclerosis and vasculitides. Molecular mimicry between host and viral proteins seems to be the main mechanism involved in the induction of autoimmunity. By means of a random peptide library approach, we have identified a peptide that shares homology with parvovirus VP1 protein and with human cytokeratin. Moreover the VP peptide shares similarity with the transcription factor GATA1 that plays an essential role in megakaryopoiesis and in erythropoiesis. These new data sustain the role played by molecular mimicry in the induction of cross-reactive (auto)antibodies by parvovirus B19 infection.
人细小病毒B19感染可导致多种人类疾病，从免疫功能正常儿童的轻度传染性红斑到初次感染的孕妇流产，以及成年免疫功能低下患者的再生障碍性贫血或致死性血细胞减少。由于持续性病毒感染会引发自身免疫反应，且临床症状可类似自身免疫性炎症疾病，因此细小病毒B19成为人们深入研究其是否也能引发自身免疫性疾病的对象。事实上，该病毒已被认为是包括类风湿性关节炎、系统性红斑狼疮、抗磷脂综合征、系统性硬化症和血管炎在内的多种自身免疫性疾病的病因或诱发因素。宿主蛋白与病毒蛋白之间的分子模拟似乎是诱导自身免疫的主要机制。通过随机肽库方法，我们鉴定出一种与细小病毒VP1蛋白和人细胞角蛋白具有同源性的肽。此外，VP肽与在巨核细胞生成和红细胞生成中起关键作用的转录因子GATA1具有相似性。这些新数据支持了分子模拟在细小病毒B19感染诱导交叉反应性（自身）抗体中所起的作用。
