Peripheral blood mononulear cells (PBMC) derived from 10 asymptomatic human T lymphotropic virus type I (HTLV-I) carriers were cultured for a short term (10-14 days) in the absence of exogenous antigens. In 5 carriers, when compared with 5 HTLV-I non-carriers an apparent increase in the proportion of CD8+ DR+ cells was observed. The clonality of cultured lymphocytes was then examined by analyzing the usage of Vbeta families of T cell receptor genes. In three of the 5 carriers with an increased CD8+ population, two to four Vbeta genes were dominant in the CD8+ population but not in the CD4+ population. No dominance of Vbeta gene usage was observed in lymphocytes derived from the 5 noncarriers. The sequence of cDNA from Vbeta families which were especially dominant revealed their oligoclonal characteristics. These results were quite similar to our previous findings from HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients in whom the same oligoclonal CD8+ cells were expanded cytotoxic T lymphocyte clones for HTLV-I genome products. We posed the question of whether the dominance of TCR Vbeta usage in cultured PBMC was associated with the HTLV-I genome dose in the PBMC or with anti-HTLV-I antibody titers. The three carriers who showed an increased CD8+ population mentioned above all showed a rather high HTLV-I genome dose, which again was similar to HAM/TSP patients. These three carriers however, did not necessarily show high anti-HTLV-I antibody titers in contrast with HAM/TSP patients, who generally do.

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