Increased HIV-1 transcriptional activity and infectious burden in peripheral blood and gut-associated CD4+ T cells expressing CD30 (original) (raw)
Fig 1
Assessment of CD30 expression on CD4+ T cells.
(A) Percentage of CD4+ T cells expressing CD30 in samples from HIV-1-uninfected (n = 10) ART suppressed (n = 17) and viremic donors (n = 9) are shown. Surface expression was higher in ART suppressed and viremic HIV-1-infected individuals (p = 0.0023 and p = 0.045 respectively). (B) sCD30 (IU) in plasma was highest in viremic (n = 4) compared with HIV-1-uninfected (n = 10) and ART suppressed donors (n = 9) (p<0.001 and p<0.001 respectively). (C) No significant correlations were identified between the percentage of CD4+CD30+ T cells and sCD30 levels (r = 0.20, P = 0.35 by Spearman rank correlation analysis). The percentage of CD4+ T cells co-expressing CD69 in each cohort are shown in (D) and the percentage of CD69+CD4+ T cells expressing CD30 are shown in (E). The percentage of CD4+ T cells co-expressing HLA-DR (F) and HLA-DR+CD4+ T cells expressing CD30 (G) are shown. Despite significant increases in CD30+ cells expressing CD38/HLA-DR, there were no significant differences in the frequency of CD30 expression in CD38/HLA-DR-expressing CD4+ T cell populations. (H) The highest frequency of CD30+ T cells observed in HIV-1-infected individuals were of transitional/effector memory phenotype, compared to naïve T cells in healthy controls. (I) CD30+CD4+ and CD30-CD4+ T cells from viremic donors expressed significantly more PD1 than healthy controls (p = 0.02 and p = 0.02 respectively), CD30+CD4+ and CD30-CD4+ T cells from ART suppressed donors also expressed significantly more PD1 than healthy controls (p = 0.002 and p = 0.002 respectively). (J) Conversely, very few CD4+PD1+ T cells co-expressed CD30, but ART suppressed donors had significantly higher expression compared to healthy controls (p = 0.01). T Bars represent median ± interquartile range for all data. *p<0.05; **P < 0.01; ***P < 0.001. Significant intergroup differences were determined using rank Kurskal-Wallis tests incorporating Dunn's tests for multiple comparisons. Wilcoxon matched-pairs signed rank tests were used to determine statistical significant between CD30 intergroup, paired samples.