Abstract
In Human immunodeficiency virus infected (HIV+) patients, deregulation of regulatory T (Treg) cells can be deleterious for the development of an efficient anti-HIV specific immune response with an inappropriate immune activation despite anti-retroviral therapy (ART). In addition, infection and ART have the potential to cause hematological and biochemical abnormalities that can lead to the discontinuation of ART. The aim of this study was to assess hematological, biochemical and immunological abnormalities in HIV+ patients’ naïve to ART and 6 months after ART initiation. In a cross-sectional study, 11 HIV+ patients and 09 healthy individuals (control group) were voluntarily recruited. At inclusion, blood samples were taken before administration of ART. All hematological, biochemical, immunological parameters and viral load were measured and assessed at inclusion (M0) and three and/or six months later (M3, M6). Higher level of white blood cells and CD4+ T lymphocytes (p = 0.032, 0.038 respectively) were observed in HIV+ patients. ART also had significantly effect on the level of red blood cells (p = 0.04) and Hb (p = 0.015). The inflammatory markers, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) that were significantly increased by HIV infection, tended to decrease for ESR and revert to levels similar to those of control for CRP. Analysis of CD4+CD25+ cells and CD4+Foxp3+CD25+ showed significantly elevated levels of activated form of all CD4+ cells and Treg cells. Interestingly, six months after initiation of ART, the average percentage of CD4+CD25+ was not significantly different from control group (p = 0.382). Our study provides information about the evolution of the activated form of all CD4 cells and Treg cells and points out the necessity to monitor hematological and biochemical parameters in order to detect and prevent toxicity, improve the quality of life and reduce the risk of mortality.
Highlights
Human immunodeficiency virus (HIV) is an RNA retrovirus that infects immune cells and uses the host cell transcriptional and translational machineries to proliferate and undermine the health of the host
Participants were visited at entry (M0), 3 mouths (M3) and/or 6 mouths (M6) after anti-retroviral therapy (ART) initiation with nucleoside reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs) and measurements were taken at the same time point
HIV+ individuals were recruited at the time of diagnosis just before starting antiretroviral treatment
Summary
Human immunodeficiency virus (HIV) is an RNA retrovirus that infects immune cells and uses the host cell transcriptional and translational machineries to proliferate and undermine the health of the host. Infection with HIV is characterized by progressive immunodeficiency, immune activation and depletion of CD4+ cells [1]. This virus causes progressive impairment of the immune system, leading to increased susceptibility to infections, tumors and the fatal condition, called acquired immunodeficiency syndrome (AIDS) [2]. Disease progression in HIV-infected patients can be delayed by treatment with anti-retroviral therapy (ART). It results in diminished viral replication and increased number of CD4+ cells [4]. ART is known to be toxic to liver and bone marrow, in several studies the relationship of HIV viruses and anti-retroviral drug effect on several parameters has been reported [7] [8]. The abnormalities may be caused by opportunistic infections, neoplasms that cause bone marrow suppression or haemolysis though that can be corrected, prevented and improved by treatment with ART [9]
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