Relationship between CD38 expression on peripheral blood T‐cells and monocytes, and response to antiretroviral therapy: A one‐year longitudinal study of a cohort of chronically infected ART‐naive HIV‐1+ patients

Abstract

Background: HIV-1 infection has been associated with high expression of CD38 on peripheral blood (PB) CD81 and CD41 T-cells, which has been related with poor prognosis in untreated HIV-11 patients. In turn, CD38 expression on PB monocytes from HIV-11 individuals and its behavior after starting antiretroviral therapy (ART) have been poorly studied.Methods: CD38 expression on PB CD81 and CD41 T-lymphocytes and monocytes was prospectively analyzed in 30 ART-naive HIV-11 patients, using a quantitative multiparameter flow cytometry approach. Patients were tested prior to therapy, and at weeks 12, 14, 18, 112, and 152 after ART.Results: Prior to ART, CD38 expression was significantly increased on PB CD81 and CD41 T-cells and monocytes; despite a significant decrease after ART, CD38 expression remained abnormally high on PB CD81 T-cells and monocytes, even after one year of therapy, in the absence of detectable plasma viral load. The ART-induced early changes on CD38 expression by PB T-cells and monocytes differed among the cell subsets analyzed and patient groups, probably reflecting an interaction between the direct effects of therapy and a redistribution of the PB compartments of T-cells and monocytes. Hierarchical clustering analysis showed that the overall pattern of changes in CD38 expression observed early after starting ART was predictive of a better response to therapy, not only for PB CD81 T-cells, but also for CD41 T-cells and monocytes. Accordingly, those HIV-11 patients, who experienced a more pronounced increase in CD38 expression on both PB CD41 T-cells and monocytes after 2 weeks of ART, showed a more rapid viral clearance, which might reflect decreased HIV-1 replication in lymph nodes and other tissues, and a partial restoration of hematopoiesis.Conclusions: Combined quantitative measurement of CD38 expression on PB monocytes, and CD81 and CD41 T-cells is a more useful tool for monitoring HIV-11 patients under ART, rather than quantitation of CD38 expression on PB CD81 T-lymphocytes alone. q

Activation and maturation of peripheral blood T cells in HIV‐1‐infected and HIV‐1‐uninfected adults in Burkina Faso: a cross‐sectional study

“…CD38, the most extensively studied activation marker in HIV-1-infected subjects, had been reported to be upregulated on CD8 + T cells in association with disease progression [12-14,35-38]. The degree of correlation between CD38 expression on CD8 + T cells and HIV-1 plasma viral load in our study was moderate but comparable to other African studies [12,14].…”

The effect of HIV infection and HAART on inflammatory biomarkers in a population-based cohort of women

“…HAART has been shown to correct much of the inflammation induced by HIV at the level of CD4+ and CD8+ T cells [31]. Abnormalities in a number of serum markers have been shown to improve but not resolve on HAART [32, 33], so it was of interest to see if these changes extended to a broader panel of soluble mediators of inflammation.…”

Neutrophils in antiretroviral therapy–controlled HIV demonstrate hyperactivation associated with a specific IL-17/IL-22 environment

“…Previous studies have reported higher circulating levels of proinflammatory cytokines and monocyte activation in various cohorts of HIV-infected patients treated for a maximum of 2 years and with inclusion criteria for the plasma viral load that were higher than in our study. [33][34][35][36][37][38][39] These less strict viral load criteria suggest the possibility of incomplete viral suppression. The data obtained from our HIV cohort (median treatment duration, 9.4 years/viral load < _20 RNA copies/mL) suggest that a longer duration of ART and consequently of viral suppression can restore some HIV-associated immunologic abnormalities, such as increased proinflammatory cytokine levels and monocyte hyperactivation.…”