Background: Plasma HIV p24 is considered a significant predictor of CD4 T cell decline and progression to AIDS in HIV-infected patients. We evaluated the p24 levels in patients on triple therapy and after switching to ritonavir-boosted protease inhibitor monotherapy (mtPI/rtv), as well as the relationships with virological and immunological evolution.

Materials And Methods: Plasma samples from patients participating in two studies of simplification to mtPI/rtv were analysed for presence of p24, using a boosted enzyme-linked immunosorbent assay specific for mature p24. Only patients with available samples at baseline (on triple therapy) and during a follow-up of at least 12 months after switching to mtPI/rtv were included.

Results: A total of 233 samples from 51 patients were analysed. After switching to mtPI/rtv and a median follow-up of 24 months, 14 patients maintained continuous undetectable viraemia, and 37 patients experienced a total of 49 transient viraemic episodes. Unexpectedly, the evolutionary p24 patterns were uniform for most patients, both before and after switching to mtPI/rtv, independently of the virological behaviour, fitting into one of three categories: persistent undetectable p24 levels, positive p24, matching only with the viraemic episodes, and persistent detectable p24 levels. The last group showed lower CD4 T cell counts and percentages, as well as lower CD4/CD8 T cell ratios after 12 and 24 months of follow up.

Conclusion: Treatment simplification to mtPI/rtv does not influence the behaviour of p24 in plasma. Patients with continuous positive p24, despite undetectable viraemia, showed worse immunological evolution.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.eimc.2016.02.001DOI Listing

Publication Analysis

Top Keywords

cd4 cell
12
p24 levels
12
switching mtpi/rtv
12
patients
10
p24
10
hiv-infected patients
8
triple therapy
8
samples patients
8
simplification mtpi/rtv
8
follow-up months
8

Similar Publications

Recent studies have suggested that sVEGFR3 is involved in cardiac diseases by regulating lymphangiogenesis; however, results are inconsistent. The aim of this study was to investigate the function and mechanism of sVEGFR3 in myocardial ischemia/reperfusion injury (MI/RI). sVEGFR3 effects were evaluated in vivo in mice subjected to MI/RI, and in vitro using HL-1 cells exposed to oxygen-glucose deprivation/reperfusion.

View Article and Find Full Text PDF

Aim: Regulatory T cells (Tregs) play a crucial role in the development and progression of atherosclerosis. However, the specific association between Treg immune traits and atherosclerosis and related cardiovascular diseases remains unclear, impeding their potential for clinical therapeutic application.

Method: Fifty-eight Treg-related immune traits were obtained from the latest summary level genome-wide association study, which included 3,757 individuals from Sardinia.

View Article and Find Full Text PDF

Potential therapeutic effect of dimethyl fumarate on Treg/Th17 cell imbalance in biliary atresia.

Clin Immunol

January 2025

Department of Pediatric Surgery, Children's Hospital of Fudan University, Shanghai Key Laboratory of Birth Defect, and Key Laboratory of Neonatal Disease, Ministry of Health, Shanghai 201102, China. Electronic address:

The imbalance between Tregs and proinflammatory Th17 cells in children with biliary atresia (BA) causes immune damage to cholangiocytes. Dimethyl fumarate (DMF), an immunomodulatory drug, regulates the Treg/Th17 balance in diseases like multiple sclerosis (MS). This study explores DMF's effect on Treg/Th17 balance in BA and its potential mechanism.

View Article and Find Full Text PDF

Background: Circulating levels of the female hormone estrogen has been associated with the development of Parkinson's disease (PD), although the underlying mechanism remains unclear. Immune homeostasis mediated by peripheral regulatory T cells (Treg) is a crucial factor in PD. The aim of this study was to explore the effects of estrogen deficiency on neuroinflammation and neurodegeneration in a rodent model of PD, with particular reference to Treg.

View Article and Find Full Text PDF

Myasthenia gravis (MG) is a T cell-dependent, B cell-mediated disorder strongly associated with antigen presentation by dendritic cells (DCs). In MG, mucosal tolerance is linked to increased expression of TGF-β mRNA in monocytes. Additionally, monocytic myeloid-derived suppressor cells (M-MDSCs) exhibit negative immunomodulatory effects by suppressing autoreactive T and B cells.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!