THE PATHOGENETICAL ROLE OF VIRUS INFECTION AND ACTIVATION OF ONCOGENES.

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In order to clarify the role of virus infection and subsequent activation of protooncogenes on the triggering process of collagen disease,, the sera from 66 patients with SLE were analyzed by the immunoblotting method to detect antibodies to the antigens on the EB virus genome positive Raji and P3HR-1 cells, as well as on the cultured myeloid cell lines of various stages of differentiation. The sera from SLE patients were found to contain the antibodies to the antigens with Mr of 66K, 70K, 90K, 140K and 160K daltons on Raji cells which were identified as c-myc protein and EB virus nuclear antigen (EBNA) subtypes 1, 2, 3 and 4, respectively. The frequency and amount of antibodies against EBNA-2 and -3 were significantly higher than in 60 control normal sera. Further, the sera from SLE patient were found to have the antibodies to the antigens with Mr of 60K on K-562, KG-1 and HL-60 cells, which are also known to be c-myc product. After an incubation of HL-60 cells with TPA or vitamin D3 to induce their macrophage differentiation, the SLE sera became to detect the 55K and 39K antigens on the differentiated HL-60 cells, while the 60K antigen turned to undetectable or only faintly detected. Polyclonal antibodies to myc-specific and fos-specific peptides were applied to react with these antigens including cross experiments. The results of these studies confirmed that the sera from SLE patients contain antibodies to c-myc, c-fos and possibly c-Jun/AP-1 protooncogen products. In addition, SLE patients were found to show EBNA positive B cells at 3 times higher frequencies than that of B cells from normal subjects. It was suggested that EB virus infection with subsequent activation of several oncogenes may have an important pathogenetical role on the triggering process of SLE.