Figure 2
Kinetic analysis of HTLV-1 provirus in infected IBMI-huNOG mice. (A) Quantification of leukocyte numbers in the peripheral blood of HTLV-1–infected mice. Peripheral blood was routinely collected from mock- and HTLV-1–infected mice every 2 weeks. Human CD45+ leukocytes were enumerated by FACS. Results from mock-infected mice (n = 10) are presented as mean ± standard deviation (SD), and representative results of 3 HTLV-1–infected mice are shown. (B) Quantification of HTLV-1 PVL in the peripheral blood of HTLV-1–infected mice. The PVL was determined by real-time PCR. Number at the top of each bar represents the number of analyzed HTLV-1–infected mice at each time point. (C) Expansion of CD3+ T-cell populations in the peripheral blood of HTLV-1–infected mice. PBMCs from mock-infected (n = 3) and HTLV-1–infected mice (n = 18) were stained for human CD3 when sacrificed; the median value was 8 wpi. Results are presented as the average percentages ± SD of human CD45+ cells. (D) Expansion of CD25+ CD4 T cells in the spleen of HTLV-1–infected mice. Splenocytes were stained for human CD3, CD4, and CD25 and analyzed by FACS. Representative results from mock-infected (mouse ID: 8X20) and HTLV-1–infected (mouse ID: 8X01) mice are shown. (E) Correlation between the percentages of CD25+ T cells and PVLs in the spleen. HTLV-1–infected mice (n = 37) were sacrificed to determine PVL and CD25+ T-cell frequency in CD4+ splenocytes. One dot represents the result of an individual HTLV-1–infected mouse. Spearman’s rank-correlation coefficient (r) was adopted to identify statistically significant correlations between values. Daggers indicate that flower cells were observed in the peripheral blood of HTLV-1–infected mice.

Kinetic analysis of HTLV-1 provirus in infected IBMI-huNOG mice. (A) Quantification of leukocyte numbers in the peripheral blood of HTLV-1–infected mice. Peripheral blood was routinely collected from mock- and HTLV-1–infected mice every 2 weeks. Human CD45+ leukocytes were enumerated by FACS. Results from mock-infected mice (n = 10) are presented as mean ± standard deviation (SD), and representative results of 3 HTLV-1–infected mice are shown. (B) Quantification of HTLV-1 PVL in the peripheral blood of HTLV-1–infected mice. The PVL was determined by real-time PCR. Number at the top of each bar represents the number of analyzed HTLV-1–infected mice at each time point. (C) Expansion of CD3+ T-cell populations in the peripheral blood of HTLV-1–infected mice. PBMCs from mock-infected (n = 3) and HTLV-1–infected mice (n = 18) were stained for human CD3 when sacrificed; the median value was 8 wpi. Results are presented as the average percentages ± SD of human CD45+ cells. (D) Expansion of CD25+ CD4 T cells in the spleen of HTLV-1–infected mice. Splenocytes were stained for human CD3, CD4, and CD25 and analyzed by FACS. Representative results from mock-infected (mouse ID: 8X20) and HTLV-1–infected (mouse ID: 8X01) mice are shown. (E) Correlation between the percentages of CD25+ T cells and PVLs in the spleen. HTLV-1–infected mice (n = 37) were sacrificed to determine PVL and CD25+ T-cell frequency in CD4+ splenocytes. One dot represents the result of an individual HTLV-1–infected mouse. Spearman’s rank-correlation coefficient (r) was adopted to identify statistically significant correlations between values. Daggers indicate that flower cells were observed in the peripheral blood of HTLV-1–infected mice.

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