Abstract

Human myeloid cell lines at different stages of differentiation (K562, HL60 and U937) were used to analyze the permissivity of the myelomonocytic lineage to acute infection with human T-cell leukemia virus type-I (HTLV-I) after cell-to-cell transmission and to evaluate the effect of cyclopentenone prostaglandins (PG)A1 and PGJ2 on virus transmission, proliferation of recipient cells and cell-mediated cytotoxicity against virus-donor cells. Exposure to HTLV-I delayed the growth rate of recipient cells, especially in U937 cells. This effect was related to the phase of cell cycle when cells were exposed to HTLV-I. Treatment of control and virus-exposed cells with these PGs, both inducing growth arrest prevalently at the G1/S interphase of the cell cycle, inhibited cell proliferation in a concentration-dependent way. The antiproliferative effect of both PGs increased progressively from pluripotent K562 to promyelocytic HL60 and monoblastoid U937 cells, suggesting that differentiated cells were more susceptible to PG-mediated inhibition of growth than pluripotent cells. PG treatment influenced the permissivity of recipient cells to HTLV-I, with different effects on less differentiated myeloid cells in comparison with more differentiated monoblastoid cells. In fact, the percentage of cells positive for the p19gag protein was increased among PG-treated K562 or HL60 cells, although it was reduced in PG-treated U937 cells. To this respect, PGA1 was more effective on asynchronous and PGJ2 on synchronous U937 cells.(ABSTRACT TRUNCATED AT 250 WORDS)