scholarly journals Niveau des CD4+ CD38+ HLA-DR+ comme évolution des biomarqueurs de l'infection par le VIH indépendamment de la thérapie antirétrovirale

2017 ◽  
Vol 4 (2) ◽  
pp. 155-158
Author(s):  
Yanis Meddour ◽  
◽  
Imène Zerrouk ◽  
Fatma Zohra Souid ◽  
Mohamed Amine ◽  
...  
Keyword(s):  
T Cells ◽  
Viral Load ◽  
Hiv Infection ◽  
Cd4 T Cells ◽  
Therapy Response ◽  
Activation Markers ◽  
Color Flow ◽  
Disease Evolution ◽  
Cytokines And Chemokines ◽  
Hla Dr

Introduction. HIV infection is characterized by an enhanced synthesis of cytokines and chemokines, a quantitative T cells disequilibrium and increased Turn over that signs a chronic activation of the immune system. Phenotype change in CD4+ T cells by over-expression of activation antigens CD38 and HLA-DR are suggested as markers of this process. Materials and methods. We investigated by four-color flow cytometry the expression of both activation markers on peripheral CD4+ T cells in 106 HIV-1 Algerian infected patients and 34 uninfected controls. Percentage’s expression of CD4+CD38+HLA-DR+ cells was compared with clinical stages, viral load and anti-retroviral treatment (ARV). Results. The proportion of CD4+ T cells coexpressing HLA-DR and CD38 was higher in infected patients than in controls (respectively, 14.2 % ± 3.6 vs. 5.8 % ± 4.1, P=0.01), in symptomatic HIV patients than asymptomatic (13 % ± 3 vs. 15.9 % ± 4.6, P=0.01) and followed viral load kinetics. In matched treated and untreated patients, activated CD4+T proportion does not show any statical difference (respectively, 13 % and 14 %, p=0.09). Conclusion. In our cohort, CD4+ T cells expressing CD38 and HLA-DR were associated with HIV infection and correlated with disease progression, regardless of ARV treatment. As CD4+ count and viral load, this lymphocyte subset may be an interesting disease evolution marker; its value remains to be determined in prognostic or as therapy response indicator.

scholarly journals Differential Expression of Activation Markers by Mycobacterium tuberculosis-specific CD4+ T Cell Distinguishes Extrapulmonary From Pulmonary Tuberculosis and Latent Infection

2019 ◽  
Vol 71 (8) ◽  
pp. 1905-1911 ◽  
Author(s):  
Paulo S Silveira-Mattos ◽  
Beatriz Barreto-Duarte ◽  
Beatriz Vasconcelos ◽  
Kiyoshi F Fukutani ◽  
Caian L Vinhaes ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Hiv Infection ◽  
Cd4 T Cells ◽  
Cell Activation ◽  
Cd4 T Cell ◽  
Activation Markers ◽  
Timely Initiation ◽  
Latent Tb

Abstract Background Diagnosis of active tuberculosis (ATB) currently relies on detection of Mycobacterium tuberculosis (Mtb). Identifying patients with extrapulmonary TB (EPTB) remains challenging because microbiological confirmation is often not possible. Highly accurate blood-based tests could improve diagnosis of both EPTB and pulmonary TB (PTB) and timely initiation of anti-TB therapy. Methods A case-control study was performed using discriminant analyses to validate an approach using Mtb-specific CD4+T-cell activation markers in blood to discriminate PTB and EPTB from latent TB infection (LTBI) as well as EPTB from PTB in 270 Brazilian individuals. We further tested the effect of human immunodeficiency virus (HIV) coinfection on diagnostic performance. Frequencies of interferon-γ +CD4+T cells expressing CD38, HLADR, and/or Ki67 were assessed by flow cytometry. Results EPTB and PTB were associated with higher frequencies of CD4+T cells expressing CD38, HLADR, or Ki67 compared with LTBI (all P values < .001). Moreover, frequencies of HLADR+ (P = .03) or Ki67+ (P < .001) cells accurately distinguished EPTB from PTB. HIV infection did not affect the capacity of these markers to distinguish ATB from LTBI or EPTB from PTB. Conclusions Cell activation markers in Mtb-specific CD4+T cells distinguished ATB from LTBI and EPTB from PTB, regardless of HIV infection status. These parameters provide an attractive approach for developing blood-based diagnostic tests for both active and latent TB.

Abstract P167: Title: Prediction of Arterial Stiffness from Early T-cell Activation among HIV and HCV Co-infected Women in the Women's Interagency HIV Study (WIHS)

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Roksana Karim ◽  
Naoko Kono ◽  
Robert Kaplan ◽  
Wendy J Mack ◽  
Howard N Hodis ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Arterial Stiffness ◽  
Hiv Infection ◽  
T Cell Activation ◽  
Cell Activation ◽  
Infection Status ◽  
Activation Markers ◽  
Color Flow ◽  
The Impact

Introduction: Activation of T-lymphocytes, a hallmark of HIV infection, reaches a set point early in HIV infection and persists even after viral suppression with highly active antiretroviral therapy (HAART). Early T-cell activation predicts subsequent CD4 depletion, progression to AIDS and survival. HIV-infected subjects are at high risk for premature atherosclerosis. Little is known regarding the impact of early T cell activation on arterial stiffness. While Kaplan et al. (2011) were the first and only group to show a cross-sectional association, we investigate here if early T cell activation can predict future arterial stiffness. Hypothesis: High early T cell activation will predict increased arterial stiffness, measured 5.5 (IQR=2.5-7.5) years later, in HIV and HCV co-infected women. Methods: A longitudinal study nested within the WIHS, an ongoing prospective cohort study. Percentages of CD4 and CD8 T cell activation, assessed by CD38 and HLA-DR co-expression using 3-color flow cytometry, were measured on average 5.5 years before arterial stiffness assessments (carotid artery distensibility, and Young’s elastic modulus for elasticity) using B-mode carotid ultrasound. Multiple linear regression models evaluated the association between log-transformed T cell activation markers (independent variables) and arterial stiffness (dependent variable). Analyses were stratified by HCV co-infection status and by pre- and post-HAART assessment of T cell activation. Results: A total of 376 HIV+ women (185 HCV+) were included in the analysis. Participants were on average 46(SD=9) years old, 59% Black, and 49% were current smokers. Activation of both CD4 and CD8 T cells significantly univariately predicted reduced distensibility and elasticity among HIV-infected women. CD4 activation continued to significantly predict distensibility (β(SEM)= −3.51(1.30) 10 −6* N −1* m 2 , p=0.01), and elasticity (0.11(0.04)10 5* N * m 2 , p=0.004) with adjustment for age, race, BMI, smoking, ART, CD4 count, and HIV RNA. CD8 activation was no longer associated after adjustment. When stratified by HCV co-infection status, the prediction of arterial stiffness parameters from early CD4 activation was somewhat stronger among the HIV+/HCV+ women compared to HIV+/HCV- women (β(SEM)= −4.44(1.93), p=0.02 vs. −3.04(1.84), p=0.10 for distensibility, and 0.17(0.06), p=0.003 vs. 0.09(0.05), p=0.09 for elasticity); however the test for interaction was not statistically significant. In a subset of 188 women, CD4 activation measured both pre- and post-HAART significantly predicted later arterial stiffness. Conclusions: CD4 activation level predicts future arterial stiffness in HIV-infected women, perhaps more markedly among HCV co-infected women. These data confirm the proinflammatory impact of activated T cells that can cause vascular dysfunction and shed light on the early onset of atherogenesis.

scholarly journals Fractional Dynamics of HIV with Source Term for the Supply of New CD4+ T-Cells Depending on the Viral Load via Caputo–Fabrizio Derivative

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1806
Author(s):  
Zahir Shah ◽  
Rashid Jan ◽  
Poom Kumam ◽  
Wejdan Deebani ◽  
Meshal Shutaywi
Keyword(s):  
T Cells ◽  
Viral Load ◽  
Hiv Infection ◽  
Cd4 T Cells ◽  
Source Term ◽  
Chaotic Behavior ◽  
Numerical Study ◽  
Public Health Problem ◽  
Fractional Dynamics ◽  
Global Public Health

Human immunodeficiency virus (HIV) is a life life-threatening and serious infection caused by a virus that attacks CD4+ T-cells, which fight against infections and make a person susceptible to other diseases. It is a global public health problem with no cure; therefore, it is highly important to study and understand the intricate phenomena of HIV. In this article, we focus on the numerical study of the path-tracking damped oscillatory behavior of a model for the HIV infection of CD4+ T-cells. We formulate fractional dynamics of HIV with a source term for the supply of new CD4+ T-cells depending on the viral load via the Caputo–Fabrizio derivative. In the formulation of fractional HIV dynamics, we replaced the constant source term for the supply of new CD4+ T-cells from the thymus with a variable source term depending on the concentration of the viral load, and introduced a term that describes the incidence of the HIV infection of CD4+ T-cells. We present a novel numerical scheme for fractional view analysis of the proposed model to highlight the solution pathway of HIV. We inspect the periodic and chaotic behavior of HIV for the given values of input factors using numerical simulations.

scholarly journals Raltegravir Inclusion Decreases CD4 T-Cells Intra-Cellular Viral Load and Increases CD4 and CD28 Positive T-Cells in Selected HIV Patients

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 208
Author(s):  
Gaurav Kumar ◽  
Jacqueline Cottalorda-Dufayard ◽  
Rodolphe Garraffo ◽  
Francine De Salvador-Guillouët ◽  
Eric Cua ◽  
...  
Keyword(s):  
T Cells ◽  
Viral Load ◽  
Cd4 T Cells ◽  
Pcr Assay ◽  
Hiv Patients ◽  
Hla Dr ◽  
Immune Phenotypes ◽  
The Impact ◽  
To Receive ◽  
Plasmatic Viral Load

Raltegravir (RLT) prevents the integration of HIV DNA in the nucleus, but published studies remain controversial, suggesting that it does not decrease proviral DNA. However, there are only a few studies focused on virus-targeted cells. We aimed our study on the impact of RLT inclusion on total intra-cellular viral DNA (TID) in cellular subsets and immune effects in patients with newly acquired undetectable plasmatic viral load (UVL). Six patients having UVL using an antiretroviral combination for 6 months and CD4 T-cells > 350/mL and <500/mL were selected to receive RLT for 3 months from M0 to M3. Patients had 7 sequential viro-immunological determinations from M-1 to M5. Immune phenotypes were determined by flow cytometry and TID quantification was performed using PCR assay on purified cells. TID (median values) at the initiation of RLT in CD4 T-cells was 117 copies/millions of cells, decreased to 27.5 on M3, and remained thereafter permanently under the cut-off (<10 copies/millions of cells) in 4 out of 6 patients. This was associated with an increase of CD4 and CD4 + CD28+ T-cells and a decrease of HLA-DR expression and apoptosis of CD4 T-cells. RLT inclusion led to decreases in the viral load along with positive immune reconstitution, mainly for CD4 T-cells in HIV patients.

scholarly journals Mathematical Models of the Complete Course of HIV Infection and AIDS

2002 ◽  
Vol 4 (4) ◽  
pp. 215-221 ◽  
Author(s):  
R. Paul Duffin ◽  
Richard H. Tullis
Keyword(s):  
T Cells ◽  
Viral Load ◽  
T Cell ◽  
Hiv Infection ◽  
Mathematical Models ◽  
Cd4 T Cells ◽  
Opportunistic Infections ◽  
Viral Clearance ◽  
Viral Production ◽  
Reservoir Models

Mathematical models of HIV infection are important to our understanding of AIDS. However, most models do not predict both the decrease in CD4+ T cells and the increase in viral load seen over the course of infection. By including terms for continuous loss of CD4+ T cells and incorporating alteration in viral clearance and viral production, two new models have been created that accurately predict the dynamics of the disease. The first model is a clearance rate reduction model and is based on a 10% per year decrease in both viral clearance and CD4+ T cell levels. A macrophage reservoir model incorporating the observation that macrophage viral production increases up to 1000 fold in the presence of opportunistic infections that become increasingly common as disease progresses. Both viral clearance and macrophage reservoir models predict the expected decrease in T cell levels and rise in viral load observed at the onset of AIDS.

scholarly journals HIV and Tuberculosis co-infection impacts T-cell activation markers but not the numbers subset of regulatory T-cells in HIV-1 infected patients

2013 ◽  
Vol 2 (1) ◽  
Author(s):  
Moustapha Mbow ◽  
Ndèye S.S. Santos ◽  
Makhtar Camara ◽  
Awa Ba ◽  
Aliou Niang ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
Hiv Infection ◽  
T Cell Activation ◽  
Cell Activation ◽  
Treg Cells ◽  
Activation Markers ◽  
Hla Dr ◽  
Hiv 1

Background: Tuberculosis (TB) has been shown to accelerate the clinical course of HIV infection, but the mechanisms by which this occurs are not well understood. Regulatory T-cells (Tregs)are known to dampen hyperactivation of the immune cells, but it remains unclear whether hyperactivation of T-cells in HIV infection is associated with a decrease of Tregs and what the effect Mycobacterium tuberculosis (MTB) co-infection has on T-cell activation and Tregs.Objectives: In this study, we aim to evaluate whether active TB is associated with the increased expression of T-cell activation markers and reduced number of Treg cells in HIV-1-infected patients.Methods: This study was conducted on 69 subjects consisting of 20 HIV-infected patients,20 HIV and MTB co-infected patients, 19 MTB-infected patients and 10 uninfected control subjects negative for both MTB and HIV. The frequencies of T-cell activation markers (CD38 and HLA-DR) and Treg cells (CD4+CD25+CD127-) were measured by flow cytometry.Results: Significantly higher expression of CD38 and HLA-DR on CD4+ and CD8+ T-cells was found in MTB and HIV co-infected patients compared with HIV-infected patients. However,no significant difference in the percentage of Treg cells was reported between HIV patients with TB and those without. The study also showed a negative correlation between regulatoryT-cells frequency and CD4+ T-cell counts.Conclusion: These results suggest that TB enhances the expression of peripheral T-cell activation markers during HIV infection, whilst having no impact on the percentages of Tregcells.

scholarly journals Clinicopathological Manifestations and Immune Phenotypes in Adult-onset Immunodeficiency With Anti-interferon-γ Autoantibodies

2021 ◽  
Author(s):  
Yi-Chun Chen ◽  
Shao-Wen Weng ◽  
Chen-Hsiang Lee ◽  
Wen-Chi Huang ◽  
Huey-Ling You ◽  
...  
Keyword(s):  
T Cells ◽  
Nk Cells ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Cytokine Production ◽  
Adult Onset ◽  
Activation Markers ◽  
Color Flow ◽  
Neutrophilic Dermatoses ◽  
Ifn Γ

Abstract Purpose Adult-onset immunodeficiency with anti-interferon (IFN)-γ autoantibodies (anti-IFN-γ Abs) is an immunodeficiency syndrome. Immune dysfunction in this distinct disorder remains to be clarified. Methods We prospectively collected blood samples of 20 patients with anti-IFN-γ Abs and 65 healthy normal subjects. Percentages of lymphocyte subpopulations, most relevant to T-, B-, and NK-cells, and percentages of stimulated lymphocytes with cytokine production were assessed using eight-color flow cytometry. The results were adjusted to age and absolute lymphocyte counts.Results Most (85%) patients presented non-tuberculous mycobacterial infection. Skin lesions were predominantly manifested by neutrophilic dermatoses. Involved lymph nodes had granulomatous inflammation, except 22.2% showing atypical lymphoid hyperplasia without granuloma formation. In the multiple linear regression model, CD4+ T cells and non-activated subpopulations (recent thymic emigrants and naïve subtypes) were significantly decreased with increased expression of activation markers and polarization to Th1, Th17, and Treg. The percentage of NK cells was increased, but two major NK subpopulations, CD56bright and CD56+CD16+ subsets were decreased. Furthermore, NK cells diminished expression of NKp30 and NKp46 with increased CD57 expression. The cytokine production was significantly lower, namely TNF-α in CD4+ T cells (P = 0.009), CD8+ T cells (P < 0.001), and NK cells (P = 0.002); IFN-γ in CD8+ T cells (P = 0.002) and NK cells (P = 0.001); and IL-2 in CD4+ (P < 0.001), and CD8+ (P = 0.005) T cells. Conclusion We conclude that the immune system in patients with anti–IFN-γ Abs could be exhausted which may contribute to the distinct clinicopathologic features.

scholarly journals SUN2 Silencing Impairs CD4 T Cell Proliferation and Alters Sensitivity to HIV-1 Infection Independently of Cyclophilin A

2017 ◽  
Vol 91 (6) ◽  
Author(s):  
Daniel A. Donahue ◽  
Françoise Porrot ◽  
Norbert Couespel ◽  
Olivier Schwartz
Keyword(s):  
T Cells ◽  
T Cell ◽  
Hiv Infection ◽  
T Cell Activation ◽  
Cd4 T Cells ◽  
Cyclophilin A ◽  
Host Protein ◽  
Cd4 T Cell ◽  
Linc Complex ◽  
Activation Markers

ABSTRACT Linker of nucleoskeleton and cytoskeleton (LINC) complexes connect the nucleus to the cytoskeleton in eukaryotic cells. We previously reported that the overexpression of SUN2, an inner nuclear membrane protein and LINC complex component, inhibits HIV infection between the steps of reverse transcription and nuclear import in a capsid-specific manner. We also reported that SUN2 silencing does not modulate HIV infection in several cell lines. Silencing of SUN2 was recently reported to decrease HIV infection of CD4 T cells, an effect which was suggested to result from modulation of cyclophilin A (CypA)-dependent steps of HIV infection. We confirm here that HIV infection of primary CD4 T cells is compromised in the absence of endogenous SUN2, and we extend these findings to additional viral strains. However, we find that CypA is not required for the decreased infection observed in SUN2-silenced cells and, conversely, that endogenous SUN2 is not required for the well-documented positive modulation of HIV infection by CypA. In contrast, CD4 T cells lacking SUN2 exhibit a considerable defect in proliferative capacity and display reduced levels of activation markers and decreased viability. Additionally, SUN2-silenced CD4 T cells that become infected support reduced levels of viral protein expression. Our results demonstrate that SUN2 is required for the optimal activation and proliferation of primary CD4 T cells and suggest that the disruption of these processes explains the contribution of endogenous SUN2 to HIV infection in primary lymphocytes. IMPORTANCE Linker of nucleoskeleton and cytoskeleton (LINC) complexes connect the nucleus to the cytoskeleton. We previously reported that the overexpression of the LINC complex protein SUN2 inhibits HIV infection by targeting the viral capsid and blocking infection before the virus enters the nucleus. A recent report showed that the depletion of endogenous SUN2 in primary CD4 T cells results in decreased HIV infection and that this involves cyclophilin A (CypA), a host protein that interacts with the capsid of HIV to promote infection. We confirm that HIV infection is reduced in CD4 T cells lacking SUN2, but we find no role for CypA. Instead, SUN2 silencing results in CD4 T cells with decreased viability and much lower proliferation rates. Our results show that SUN2 is required for optimal CD4 T cell activation and proliferation and explain the reduced level of HIV infection in the absence of SUN2.

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