Chemokine Receptors Expression on T Cells and Response to HAART Among Chronic HIV-1-Infected Subjects

Abstract

Chemokines receptors are used by HIV-1 for entry into CD4(+) T cells. The beta-chemokines are capable of inhibiting HIV replication. This study determined the CCR5 and CXCR4 expression on T cells in HIV-1-infected patients treated with HAART. The successfully treated group (plasma viral load <400 copies/mL), when compared with the failure group (plasma viral load >400 copies/mL), had higher median CD4(+) T cells count (583 and 245 cells/mm(3); respectively, p< 0.0001). The failure patients had higher numbers and intensity of CCR5 and CXCR4-expressing T cells. Successfully treated patients were able to normalize the co-receptors expression-over on T cells. The viremic group showed higher CCR5 expression on CD4(+) T cells and lower number of cells; CCR5 expression was normalized in the aviremic group; the naïve group showed lower CCR5 expression and higher numbers of CD4 T cells; all groups showed normal CXCR4 expression compared to healthy controls. These findings may have clinical implications, since down-regulation of these co-receptors could be an adjuvant strategy for anti-HIV treatment.

GB virus C coinfection in advanced HIV type-1 disease is associated with low CCR5 and CXCR4 surface expression on CD4+ T-cells

“…We found this effect of CXCR4 up-regulation to be compensated by HAART treatment. This is in accordance with a recent study reporting down-regulation of CCR5 and CXCR4 in HIV patients receiving HAART [15]. Xiang et al .…”

“…We found this effect of CXCR4 up-regulation to be compensated by HAART treatment. This is in accordance with a recent study reporting down-regulation of CCR5 and CXCR4 in HIV-1 patients receiving HAART [15]. Xiang et al [7] previously reported that Jurkat cells stably expressing GBV-C non-structural 5A phosphoprotein inhibited HIV-1 replication by decreasing surface density of CXCR4 in vitro.…”

Effects of progesterone on the content of CCR5 and CXCR4 coreceptors in PBMCs of seropositive and exposed but uninfected Mexican women to HIV-1

“…3). The stage of infection, degree of cell activation, and use of antiretroviral treatment can influence the difference in the basal expression of CCR5 and CXCR4 between HIV positive and negative subjects [33][34][35][36]. In early infection, patients exhibit a greater percentage of CCR5 expressing CD4 + T cells, and a lower percentage of CXCR4 expressing CD4 + and CD8 + T cells, and CD14 + monocytes compared with healthy controls [27].…”

“…Brito et al reported that the HIV infected group showed higher CCR5 expression in CD4 + T cells but lower number of cells without differences in CXCR4 content [34]. There are no reports that compare CCR5 (without mutation CCR5 32) or CXCR4 expression of EU women with healthy controls or HIV-1 TP.…”

HIV induced suppression of host immunity: relevance to <i>Mycobacterium tuberculosis</i> infections

“…It is observed that the increase in plasma load of HIV-1 coincided with massive burst in the chemokine expression. Importantly, IP-10, MCP-1, IL-8 etc., were found to be increased in the periphery of HIV infected individuals [131][132][133][134]. The heightened levels of chemokines are believed to cause immune activation, followed by viral replication, and thereafter more destruction of CD4+ T cells.…”