Human T-lymphotropic virus-I (HTLV-I)-specific T-cell lines were established and cloned. An OKT8+ cytotoxic clone (K5) was specifically reactive against HTLV-I-bearing autologous tumor cells, and it retained a normal dependence on interluekin 2 (IL-2). We observed multiple proviral integration sites in K5 cells (i.e., there was no dominant proviral integration site), suggesting that the number of integration sites which, when occupied, result in T-cell transformation is finite. An OKT4+ HTLV-I-infected clone (R2) mounted a specific proliferative response to HTLV-I; however, its IL-2-independent proliferation increased with time and the antigen-specificity was eventually lost. All HTLV-I-infected clones tested including another OKT8+ transformed cytotoxic clone (K7) which had lost its reactivity against HTLV-I, expressed T-cell receptor B chain (TCR-B) messenger RNA at comparable levels. Two clones (K5 and K7) had the same rearrangement of the TCR-B gene, suggesting that they have the same clonal origin, even though they exhibited different functional properties following HTLV-I infection. These data indicate that HTLV-I-specific immune T-cell clones with a range of functions can be infected with HTLV-I, retain their immune reactivity for variable periods of time in culture, and lose it, although in some cases no alteration in function following HTLV-I infection can be detected. In addition, the data suggest that different consequences can take place in the same clone depending on the pattern of retroviral infection.
