The human T-cell lymphoma virus, HTLV-I, has been found to be associated with patients with adult T-cell leukemia. Studies are underway to understand the mechanism of malignant transformation of cells infected with this virus and the immunologic response of individuals who are infected with this virus that demonstrate malignancies or those who are carriers of the virus but have not developed malignancies. Monoclonal antibodies were developed against protein products produced by a murine cell line which had been transfected with the recombinant plasmic clone containing HTLV-I proviral DNA sequences in regions coding for part of the env px and 3'LTR. Monoclonal antibodies reacted with different patterns when tested by Western blotting on proteins derived from purified HTLV-I and HTLV-II particles. The predominant pattern observed was binding into a p21 and p43 glycopeptide from both HTLV-I and/or HTLV-I, -II, and -III. Experiments were carried out to examine the effect of purified human HTLV-I, -II, and -III retroviruses on normal human lymphocytes of PHA-induced plastogenesis. The inactivated virus induced exaggerated concanavalin A proliferation and suppressed the PHA response. The purified virus causes inhibition of blastogenesis by PHA as did the virus preparations from HTLV-I, -II, and -III. B-cell chronic lymphocytic leukemia (CLL) cells were obtained from patients who were HTLV seropositive, however, whose malignant B-cells did not contain the HTLV-I retrovirus. Using hybridoma technology CLL cells were fused with a B lymphoblastoid cell line and the immunoglobulin captured. In one instance the captured immunoglobulin reacted with the HTLV-I p24 gag proteins and in the other instance the large envelope protein from HTLV-I. Immunoglobulin gene rearrangement present in the B CLL cells was demonstrated in the hybridoma cell line. The results indicate that the CLL cells were antigen committed cells prior to malignant transformation.
