Comprehensive characterization of homeostatic cellular immune signatures in VNPs can provide unique insights into mechanisms responsible for coping with viral pathogenesis as well as identifying strategies for immune restoration under clinically relevant settings such as antiretroviral therapy ART failure.
Thus, the homeostatic immune signatures reported in our study suggest a complex multifactorial mechanism accounting for non-progression in VNPs. An additional feature of SIV infection of natural hosts is low peripheral immune activation However, there are conflicting reports with respect to levels of immune activation in VNPs 11 β Delineation of unique characteristics of VNPs in halting immune deficiency despite high viral replication may provide valuable insights into immune compensatory mechanisms employed to cope with viral pathogenesis, a scenario that may develop under ART through acquired or transmitted resistance.
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These immune signatures may provide novel strategies for disease management and immune restoration following therapy. Group of Hospitals, Mumbai. The clinical characteristics of all the recruited participants are summarized in Table 1. All the recruited participants were ART naive. Figure 1. A 18 VNPs were recruited following stringent criteria. The last time point, for each sample, is the time of recruitment of participants for the study.
Each line represents one individual. B,C Absolute T cell count in blood as measured by flow cytometry. E Plasma viral load Log 10 VL. Table 1. Clinical, immunological, and viral characteristics of the study population. Fluorescence minus one FMO control was used to identify and gate cells.
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The quality of DNA was assessed by spectrophotometry. The data are represented as scatter plots, and bars indicate median values. MannβWhitney non-parametric test was performed for comparison between different study groups. Bivariate associations were determined by Spearman's rank correlation test.
