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Human T-lymphotropic virus type I (HTLV-I), is the pathogenic agent of adult T-cell leukemia-lymphoma (ATLL), which always shows monoclonal HTLV-I provirus DNA integration. HTLV-I is rarely associated with B-cell disorders. The gen Tax of a human T-cell leukemia virus type I (HTLV-I) induces the expression of several cellular genes that are involved in T cell activation and proliferation. In the current study was to analyze prospectively HTLV-I proviral DNA presence in peripheral blood mononuclear cells (PBMCs) in patients with leukemia or lymphoma which are different to ATLL. Following this pattern we have studied in 61 patients with T and B-cell malignancies the presence of the virus HTLV-I on the during our service between April 2004 and May 2006. A real time PCR assay using SYBR Green intercalation was established. Primer and hybridization probes targeting tax region were standardized against MT2 cell line DNA for HTLV-I. The assay reliably detected a single copy of HTLV-I proviral genome in DNA from 1X106 PBMCs. Also included for each sample the HLA-DQ alpha gene (a measure of genomic DNA), We have detected the presence of HTLV-I in five patients: 2 patients with B-CLL (lymphocytes count: 1.3 x 109/L and 16,8 respectly), one patient with T-ALL CD4 and CD8 positive; other with NHL and one with B-ALL Ph+. As an interesting data, one of the patients with B-CLL presented as complication a immune thrombocytopenia after Fludarabine therapy. Two patients were died and the two cases with B-CLL show stable sickness. Only the patient with T-ALL achieved complete remission after chemotherapy. In conclusion, we have detected on our series, in a unsuspected way, the presence of HTLV-I on some of the patients with lymphoid malignancies, which are different to the ATLL, showing in these cases an atypical clinic course. After knowing the repercussion of HTLV-I over the immune competition of the infected patients it seems suggestive speculate on the possible implication of the virus in a deterioration of the immunity favouring the progress of neoplasia and/or a greater propensity to infections and immunological upheavals, like the observed ones in our series.