Research for human parvovirus and rheumatoid arthritis.

类风湿性关节炎（RA）的病因不明。我们已经证明了人细小病毒B19（B19）在B19感染患者和急性B19感染后发展为活动性RA的病例中持续存在超过6年。在30例RA患者中，23例滑膜组织中检测到B19-DNA和B19抗原VP-1，而在骨关节炎（OA）和关节创伤患者中较少见。VP-1在RA活动性滑膜病变中有特异性表达。原位杂交和免疫组化研究表明，VP-1的靶细胞为巨噬细胞、滤泡树突状细胞、T细胞和B细胞，而非滑膜衬里细胞。B19阴性的骨髓细胞、巨噬细胞与RA滑膜细胞共培养后，VP-1表达阳性，IL-6和TNF-α表达增加。加入B19中和抗体可显著抑制VP-1的表达以及IL-6和TNF α的产生，表明在RA滑膜细胞中检测到的B19具有感染性。这些数据表明，B19可能参与RA滑膜炎的发生和持续，导致关节病变。

The etiology of rhumatoid arthritis (RA) is unknown. We have shown the persistence of human parvovirus B19 (B19) for more than 6 years in a patients with B19 infections and also the cases, who developed into active RA after an acute B19 infection. B19-DNA and the B19 antigen VP-1 were detected in the synovial tissues in 23 out of 30 patients with RA,and infrequently in those with osteoarthrits (OA) and traumatic joints. The expression of VP-1 was specific in active synoviaI lesions of RA.In situ hybridization and immunohistochemical studies revealed that the target cells of B19 were macrophages, foIIicular dendritic cells, T Cells and B cells, but not synoviaI lining cells in the snovium. B19-negative bone marrow cells, anc macrophage ceIls became positive for the expression of VP-1, and more productive for IL-6 and tumor necrosis factor alpha (TNF alpha) when cocultured with RA synovial cells. The expression of VP-1 and the production of IL-6 and TNF alpha was significantly inhibited by the addition of neutralizing antibody for B19, suggesting that B19 detected in RA synovial cells are infective. These data indicate that B19 may be involved in the initiation and perpetuation of RA synovitis, leading to joint lesions.