Abstract
The repression of the HIV-1 LTR by an unknown cellular protein which binds to the regulatory motif AAGGAG may account for the low transcription and replication of HIV-1 in resting naive T-cells. To identify this repressor we applied a decision theoretic procedure to a public gene expression database. The oncogene ets-2, previously found to repress IL-2 gene expression in naive T-cells, was the transcriptional repressor of HIV-LTR suggested by the statistical bioinformatics analysis. RT-PCR analysis and transfection experiments, confirmed the reciprocal relation between ets-2 and IL-2 transcripts and HIV-LTR in naive resting and activated T-cells. De-repression of the two loci could provide an additional trigger of viral activation and at the same time explain the multitude of autoimmune phenomena in HIV-1 patients.