scholarly journals Relationship Between CD4+ T-Cell Counts/HIV-1 RNA Plasma Viral Load and AIDS-Defining Events Among Persons Followed in the ACTG Longitudinal Linked Randomized Trials Study

2010 ◽  
Vol 55 (1) ◽  
pp. 117-127 ◽  
Author(s):  
Marlene Smurzynski ◽  
Kunling Wu ◽  
Constance A Benson ◽  
Ronald J Bosch ◽  
Ann C Collier ◽  
...  
2016 ◽  
Vol 1 (2) ◽  
pp. 260 ◽  
Author(s):  
Yolanda D. Mahnke ◽  
Kipper Fletez-Brant ◽  
Irini Sereti ◽  
Mario Roederer

Background. Highly active antiretroviral therapy induces clinical benefits to HIV-1 infected individuals, which can be striking in those with progressive disease. Improved survival and decreased incidence of opportunistic infections go hand in hand with a suppression of the plasma viral load, an increase in peripheral CD4+ T-cell counts, as well as a reduction in the activation status of both CD4+ and CD8+ T cells.Methods. We investigated T-cell dynamics during ART by polychromatic flow cytometry in total as well as in HIV-1-specific CD4+ and CD8+ T cells. We also measured gene expression by single cell transcriptomics to assess functional state.Results. The cytokine pattern of HIV-specific CD8+ T cells was not altered after ART, though their magnitude decreased significantly as the plasma viral load was suppressed to undetectable levels. Importantly, while CD4+ T cell numbers increased substantially during the first year, the population did not normalize: the increases were largely due to expansion of mucosal-derived CCR4+ CD4+ TCM; transcriptomic analysis revealed that these are not classical Th2-type cells.Conclusion. The apparent long-term normalization of CD4+ T-cell numbers following ART does not comprise a normal balance of functionally distinct cells, but results in a dramatic Th2 shift of the reconstituting immune system.


AIDS ◽  
2010 ◽  
Vol 24 (2) ◽  
pp. 195-204 ◽  
Author(s):  
Kavidha Reddy ◽  
Cheryl A Winkler ◽  
Lise Werner ◽  
Koleka Mlisana ◽  
Salim S Abdool Karim ◽  
...  

2001 ◽  
Vol 28 (1) ◽  
pp. 99-101 ◽  
Author(s):  
John N. Nkengasong ◽  
Marie-Yolande Borget ◽  
Chantal Maurice ◽  
Emmanuel Boateng ◽  
Mireille Kalou ◽  
...  

2018 ◽  
Vol 10 (02) ◽  
pp. 162-167
Author(s):  
Sakshee Gupta ◽  
Bharti Malhotra ◽  
Jitendra Kumar Tiwari ◽  
Prabhu Dayal Khandelwal ◽  
Rakesh Kumar Maheshwari

ABSTRACT BACKGROUND: Coinfections of human immunodeficiency virus (HIV) with hepatitis viruses may affect the progress of disease and response to therapy. OBJECTIVES: To study the incidence of hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfections in HIV–positive patients and their influence on HIV–1 viral load and cluster of differentiation 4+ (CD4+) T–cell counts. MATERIALS AND METHODS: This pilot study was done on 179 HIV–positive patients attending antiretroviral therapy (ART) centre. Their blood samples were tested for HIV-1 viral load, CD4+ T–cell counts, hepatitis B surface antigen, anti–HCV antibodies, HBV DNA and HCV RNA polymerase chain reaction. RESULTS: Among the 179 patients, 7.82% (14/179) were coinfected with HBV and 4.46% (8/179) with HCV. Median CD4+ T–cell count of HIV monoinfected patients was 200 cells/µl and viral load was 1.67 log10 copies/µl. Median CD4+ T–cell counts of 193 cells/µl for HBV (P = 0.230) and 197 cells/µl for HCV (P = 0.610) coinfected patients were similar to that of HIV monoinfected patients. Viral load was higher in both HBV and HCV infected patients but statistically significant only for HCV (P = 0.017). Increase in CD4+ T–cell counts and decrease in HIV–1 viral load in coinfected patients on 2 years of ART were lower than that in HIV monoinfected patients. CONCLUSION: HBV/HCV coinfected HIV patients had similar CD4+ T–cell counts as in HIV monoinfected patients, higher HIV viral load both in chemo–naive patients and in those on ART as compared to HIV monoinfected patients. However, this study needs to be done on a large scale to assess the impact of coinfection on CD4 count and HIV viral load with proper follow–up of patients every 6 months till at least 2 years.


2001 ◽  
Vol 28 (1) ◽  
pp. 99-101
Author(s):  
John N. Nkengasong ◽  
Marie-Yolande Borget ◽  
Chantal Maurice ◽  
Emmanuel Boateng ◽  
Mireille Kalou ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rute Marcelino ◽  
Filipa Gramacho ◽  
Francisco Martin ◽  
Pedro Brogueira ◽  
Nuno Janeiro ◽  
...  

AbstractThe ectodomain of gp41 is the target of potent binding and neutralizing antibodies (NAbs) and is being explored in new strategies for antibody-based HIV vaccines. Previous studies have suggested that the W164A-3S (3S) and EC26-2A4 (EC26) peptides located in the gp41 ectodomain may be potential HIV vaccine candidates. We assessed 3S- and EC26-specific binding antibody responses and related neutralizing activity in a large panel of chronic HIV-1-infected Portuguese individuals on ART. A similar proportion of participants had antibodies binding to 3S (9.6%) and EC26 (9.9%) peptides but the level of reactivity against 3S was significantly higher compared to EC26, except in the rare patients with double peptide reactivity. The higher antigenicity of 3S was unrelated with disease stage, as assessed by CD4+ T cell counts, but it was directly related with plasma viral load. Most patients that were tested (89.9%, N = 268) showed tier 1 neutralizing activity, the potency being inversely associated with plasma viral load. In the subset of patients that were tested for neutralization of tier 2 isolates, neutralization breadth was inversely correlated with plasma viral load and directly correlated with CD4+ T cell counts. These results are consistent with a role for neutralizing antibodies in controlling viral replication and preventing the decline of CD4+ T lymphocytes. Importantly, in patients with 3S-specific antibodies, neutralizing titers were inversely correlated with viral RNA levels and proviral DNA levels. Moreover, patients with 3S and/or EC26-specific antibodies showed a 1.9-fold higher tier 2 neutralization score than patients without antibodies suggesting that 3S and/or EC26-specific antibodies contribute to neutralization breadth and potency in HIV-1 infected patients. Overall, these results suggest that antibodies targeting the S3 and EC26 epitopes may contribute to reduce viral burden and provide further support for the inclusion of 3S and EC26 epitopes in HIV-1 vaccine candidates.


2018 ◽  
Vol 34 (10) ◽  
Author(s):  
Ingridt Hildegard Vogler ◽  
Daniela Frizon Alfieri ◽  
Heloisa Damazio Bruna Gianjacomo ◽  
Elaine Regina Delicato de Almeida ◽  
Edna Maria Vissoci Reiche

Abstract: The latest Brazilian guideline recommended the reduction of routine CD4+ T cell counts for the monitoring of patients with human immunodeficiency virus type 1 (HIV-1) under combination antiretroviral therapy (cART). The aim of this study was to evaluate the safety of monitoring response to cART in HIV-1 infection using routine viral load at shorter intervals and CD4+ T cell count at longer intervals. CD4+ T cell counts and HIV-1 viral load were evaluated in 1,906 HIV-1-infected patients under cART during a three-year follow-up. Patients were stratified as sustained, non-sustained and non-responders. The proportion of patients who showed a CD4+ T > 350cells/µL at study entry among those with sustained, non-sustained and non-responders to cART and who remained with values above this threshold during follow-up was 94.1%, 81.8% and 71.9%, respectively. HIV-1-infected patients who are sustained virologic responders and have initial CD4+ T cell counts > 350cells/µL showed a higher chance of maintaining the counts of these cells above this threshold during follow-up than those presenting CD4+ T ≤ 350cells/µL (OR = 39.9; 95%CI: 26.5-60.2; p < 0.001). This study showed that HIV-1-infected patients who had sustained virologic response and initial CD4+ T > 350cells/µL were more likely to maintain CD4+ T cell counts above this threshold during the next three-year follow-up. This result underscores that the evaluation of CD4+ T cell counts in longer intervals does not impair the safety of monitoring cART response when routine viral load assessment is performed in HIV-1-infected patients with sustained virologic response.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Prashant Malhotra ◽  
Patrick Haslett ◽  
Barbara Sherry ◽  
David H. Shepp ◽  
Paul Barber ◽  
...  
Keyword(s):  
T Cell ◽  

Viruses ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 764
Author(s):  
Melissa Stunnenberg ◽  
Lisa van Pul ◽  
Joris K. Sprokholt ◽  
Karel A. van Dort ◽  
Sonja I. Gringhuis ◽  
...  

The mitochondrial antiviral protein MAVS is a key player in the induction of antiviral responses; however, human immunodeficiency virus 1 (HIV-1) is able to suppress these responses. Two linked single nucleotide polymorphisms (SNPs) in the MAVS gene render MAVS insensitive to HIV-1-dependent suppression, and have been shown to be associated with a lower viral load at set point and delayed increase of viral load during disease progression. Here, we studied the underlying mechanisms involved in the control of viral replication in individuals homozygous for this MAVS genotype. We observed that individuals with the MAVS minor genotype had more stable total CD4+ T cell counts during a 7-year follow up and had lower cell-associated proviral DNA loads. Genetic variation in MAVS did not affect immune activation levels; however, a significantly lower percentage of naïve CD4+ but not CD8+ T cells was observed in the MAVS minor genotype. In vitro HIV-1 infection of peripheral blood mononuclear cells (PBMCs) from healthy donors with the MAVS minor genotype resulted in decreased viral replication. Although the precise underlying mechanism remains unclear, our data suggest that the protective effect of the MAVS minor genotype may be exerted by the initiation of local innate responses affecting viral replication and CD4+ T cell susceptibility.


Sign in / Sign up

Export Citation Format

Share Document