Fig 1: Correlation and receiver operating characteristic (ROC) analyses of plasma factors. (A) Spearman correlations among plasma CFI, C4, HLA, and C4b peptide levels. (B) ROC area under the curve (AUC) values, 95% confidence intervals, and p values for discrimination between EC and AT cases for each of the analyzed factors and a composite factor (C4b) derived from the plasma level of three C4b peptides. ROC graphs indicating the relative performance of candidate single-factor (C) and multifactor (D) ROC analyses. C4b represents a composite value formed by all of C4b peptides.
Fig 2: Plasma levels of CFI, C3, C4, and C4b-derived peptides in EC, VC, AT, and HN patients. Plasma concentrations of CFI (A), C3 (B), and C4 (C) as quantified by ELISA. (D) Relative C4b peptide (m/z 1896.04, 1739.94, and 1626.88) signal measured by Nanotrap-coupled MALDI-TOF-MS. Error bars indicate the standard error of the mean. EC, n = 48; VC, n = 45; AT, n = 35; HN, n = 34. *p < 0.05, **p < 0.01 by one-way ANOVA with a Kruskal-Wallis post-test for comparisons between each subgroup.
Fig 3: Model of CFI-mediated HIV regulation in AT and EC HIV patients. Left panel: Low CFI levels in AT patients allow C3b/C4b bound to HIV gp120/gp41 to interact with CR1 on the surface of CD4+ T cells and other HIV targets, promoting HIV infection and replication. Right panel: High CFI levels in EC patients favor CFI-mediated cleavage of C3b/C4b to iC3b/C4d and C3b/C4b-derived peptides, blocking CR1-mediated HIV associations with target cells.
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