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The process of HTLV-I integration was analyzed under different approaches. These included the phylogenetic analyses of the integrase, their structural characteristics, and the structural genomics of the proviruses in lymphocytic cells of infected patients. Structurally, it was observed that the HHCC amino acid residues at the N terminus and DDE in the catalytic core were consensus in the integrases of HTLV-I, ASV, and HIV-1 viruses. The level of clonal expansion in infected lymphocytes of healthy carriers, TSP/HAM, and ATL patients was variable. The number of IPCR amplicons was significantly higher in TSP/HAM patients (8.6 ± 2.5) than in healthy carriers (5.0 ± 1.7) or ATL patients (2.8 ± 3.0) (P<0.004). The human genome sequences of 50 bp that flank the 3'-LTR of HTLV-I provirus had variable levels of homology with cDNA of tumor cell lines and normal tissues. Alignments of such sequences facilitated the chromosomal location of several proviruses. In general, the integration sites in HTLV-I seropositive individuals were non-randomly distributed in G:C rich domains of the human genome. In chromosomes 8, 9, and 16 were recorded more integrated sequences. The substractive hybridization of AFLP fragments permitted the fingerprinting of the integration process in the human genome. This methodology would be used in other molecular systems.
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References
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