CD8(+) T cell supernatants of HIV type 1-infected individuals have opposite effects on long terminal repeat-mediated transcription in T cells and monocytes

CD8(+) T lymphocytes of HIV-1-infected individuals can efficiently suppress HIV-1 replication in CD4(+) T lymphocytes via soluble factors, We compared the effect of CD8(+) T cell-derived supernatants on HIV-1 LTR-driven gene expression in T cells and monocytic cell lines, Our results demonstrate that CD8(+) T cell supernatants that suppressed HIV-1 LTR-driven gene expression in Jurkat T cells significantly enhanced expression in Tat-activated U38 monocytic cells in the presence and absence of mitogenic stimulation, Examination of a panel of CD8(+) T cell-derived supernatants from HIV-infected individuals demonstrated that the extent of enhancement of transcription in U38 cells was mirrored in most cases by a similar level of suppression of transcription in Jurkat T cells, In latently infected U1 cells treated with TNF-alpha culture with CD8(+) T cell supernatants markedly enhanced virus production, In addition, the percentage increase in the enhancement of HIV-1 LTR-driven CAT expression by CD8(+) T cell supernatants correlated strongly (r = 0.911) with the level of p24 detected. The level of LTR-mediated gene expression in U38 cells was not influenced by rhMIP-1 alpha rhMIP-1 beta, or rhRANTES over a wide range of chemokine concentration, Treatment of CD8(+) T cell supernatant with a combination of antibodies to these chemokines resulted in a further augmentation of LTR-mediated CAT expression in U38 cells, Taken together, these results demonstrate that CD8(+) T cell suppressive factors may have opposite effects on HIV-1 LTR-driven gene expression and replication dependent on target cell type and further suggest that the beta-chemokines do not influence HIV-1 LTR-mediated gene expression in monocytic cells.