HTLV-1 clonal structure in the blood of subjects with HTLV-1 infection alone and those with co-infections.

<p><b>A.</b> The mean proviral load of patients with IDH or <i>Strongyloides</i> co-infection was higher than the proviral load of asymptomatic carriers (ACs) (Mann Whitney, respectively p = 0.0001 and p = 0.002). <b>B.</b> The estimated total number of clones in the blood of co-infected patients was comparable to the total number of clones of ACs (Mann Whitney, respectively for IDH and <i>Strongyloides</i> co-infected vs AC, p = 0.27 and p = 0.81). By contrast, the estimated total number of clones in the blood of HAM-TSP patients was higher than those of ACs (Mann Whitney, p = 0.03) <b>C.</b> On average, the infected clones in the blood of IDH and <i>Strongyloides</i> co-infected patients were more abundant than those in ACs (Mann Whitney, respectively for IDH and <i>Strongyloides</i> co-infected vs AC, p = 0.02, and p = 0.02) and those in HAM/TSP patients (Mann Whitney, respectively for IDH and St vs HAM/TSP, p = 0.006, and p = 0.002). <b>D.</b> The oligoclonality index in the blood of IDH patients was not significantly different from that in ACs (Mann Whitney, p = 0.08). On the contrary, the oligoclonality index in peripheral blood of <i>Strongyloides</i> co-infected patients was higher than that in ACs (Mann Whitney, p = 0.01). <b>E.</b> proviral load and oligoclonality index were not correlated in any of the cohorts except ATLL (Spearman, respectively for AC, HAM/TSP, IDH, <i>Strongyloides</i> co-infected and ATLL, p = 0.34, p = 0.27, p = 0.92, p = 0.58 and p = 0.004). <b>F.</b> Proviral load was correlated with the total number of clones in the blood in each cohort (Spearman, respectively for AC, HAM-TSP, IDH and St, p = 0.02, p = 0.0008, p = 0.05 and p = 0.04). <b>G.</b> oligoclonality index and total number of clones in the blood did not correlate in any cohorts (Spearman, respectively for AC, HAM-TSP, IDH and St, p = 0.46, p = 0.27, p = 0.64 and p = 0.58). In panels A, D and E, data on patients infected with HTLV-1 infection alone are shown for comparison purposes and were originally published in <i>Blood</i>. Gillet <i>et al.</i> The host genomic environment of the provirus determines the abundance of HTLV-1-infected T-cell clones. Blood. 2011; 117: 3113–3122. These data are shown by empty whiskers or grey symbols to distinguish them from new data in color.