Figure 2
Figure 2. HTLV-1 clonal structure in naturally infected patients. (A) The clonal distribution in each genomic DNA sample is depicted by a histogram. Each segment represents one UIS; the width of the segment is proportional to the relative abundance of that UIS. The 3 most abundant UISs are colored. (B) The OCI did not correlate with PVL in ACs or in patients with HAM/TSP, but this correlation was significant in patients with ATLL (Spearman rank, P = .0065, R = 0.57). The mean coefficient of variation of OCI was 4.3% (N = 11 samples). The OCI was greater in patients with ATLL than in patients with nonmalignant HTLV-1 infection (box-plot insert, Mann-Whitney, P < .0001). (C) The total number of UISs calculated using the Chao1-bc estimator. The total number of UISs correlated positively with PVL, both in ACs (Spearman rank, P = .035, R = 0.50) and in patients with HAM/TSP (Spearman rank, P = .003, R = 0.57). The mean coefficient of variation of Chao1-bc estimator was 9.5% (N = 11 samples). The adjacent box-plot shows that the number of UISs was significantly greater in patients with HAM/TSP than in ACs (unpaired t test with Welch correction, P = .0002). (D) Low-abundance UISs made up the large majority of all UISs, regardless of disease status. Only ATLL patients had very large UISs (right-hand extremity of the curve). The relative frequency distribution of UIS abundance in ATLL patients showed a shift to the right: asterisks denote the significance of the difference in the proportion of UISs at a given abundance between ATLL patients and ACs (χ2 test). (E) ACs had fewer UISs in each abundance category compared with patients with HAM/TSP: asterisks denote the significance of the difference in the mean number of UISs of a given abundance between patients with HAM/TSP and ACs (Mann-Whitney). ***P < .001. **P < .01. *P < .05. NS indicates not significant (P > .05).

HTLV-1 clonal structure in naturally infected patients. (A) The clonal distribution in each genomic DNA sample is depicted by a histogram. Each segment represents one UIS; the width of the segment is proportional to the relative abundance of that UIS. The 3 most abundant UISs are colored. (B) The OCI did not correlate with PVL in ACs or in patients with HAM/TSP, but this correlation was significant in patients with ATLL (Spearman rank, P = .0065, R = 0.57). The mean coefficient of variation of OCI was 4.3% (N = 11 samples). The OCI was greater in patients with ATLL than in patients with nonmalignant HTLV-1 infection (box-plot insert, Mann-Whitney, P < .0001). (C) The total number of UISs calculated using the Chao1-bc estimator. The total number of UISs correlated positively with PVL, both in ACs (Spearman rank, P = .035, R = 0.50) and in patients with HAM/TSP (Spearman rank, P = .003, R = 0.57). The mean coefficient of variation of Chao1-bc estimator was 9.5% (N = 11 samples). The adjacent box-plot shows that the number of UISs was significantly greater in patients with HAM/TSP than in ACs (unpaired t test with Welch correction, P = .0002). (D) Low-abundance UISs made up the large majority of all UISs, regardless of disease status. Only ATLL patients had very large UISs (right-hand extremity of the curve). The relative frequency distribution of UIS abundance in ATLL patients showed a shift to the right: asterisks denote the significance of the difference in the proportion of UISs at a given abundance between ATLL patients and ACs (χ2 test). (E) ACs had fewer UISs in each abundance category compared with patients with HAM/TSP: asterisks denote the significance of the difference in the mean number of UISs of a given abundance between patients with HAM/TSP and ACs (Mann-Whitney). ***P < .001. **P < .01. *P < .05. NS indicates not significant (P > .05).

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