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Figure 1 | Virology Journal

Figure 1

From: HTLV-1 proviral integration sites differ between asymptomatic carriers and patients with HAM/TSP

Figure 1

Host disease status and HBZ-binding capacity do not alter total unique HTLV-1-infected clones or oligoclonality. HTLV-1 infected Japanese asymptomatic carriers (AC; triangles) from Kagoshima and Kumamoto prefectures and HAM/TSP patients (circles) from Kagoshima were stratified on the basis of predicted HBZ peptide binding affinity of host HLA class I alleles (strong binders, sHBZ, filled symbols; weak binders, wHBZ, open symbols). Each symbol represents one individual. Genomic DNA samples were processed by sonication-based LM-PCR and samples passing data quality checks were analysed further, as previously described ([23, 24]). (A) The DivE method was used to estimate the total number of clones in the blood in each subject; the total clone number was positively correlated (Spearman correlation) with proviral load in each cohort both HAM (blue, p = 0.0004) and AC (black, p = 0.0001)). There was no significant difference in slope of the linear regression line between AC and HAM/TSP cohorts (likelihood ratio test, p = 0.30) or between sHBZ (continuous line) and wHBZ (dashed line) in the combined AC and HAM/TSP cohorts (likelihood ratio test, p = 0.06) indicating that there is no systematic difference in total clone number by disease status or HBZ binding status. (B) The oligoclonality index (OCI), which quantifies the diversity in observed clone abundance in each sample, was not significantly correlated with proviral load in ACs or HAM/TSP (Spearman correlation) and there was no significant difference in slope of the linear regression line between AC and HAM/TSP cohorts. (C) The median OCI did not differ significantly by HBZ binding status within individual cohorts (Mann-Whitney U test). Bars denote median +/- interquartile range.

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