Research Paper Volume 13, Issue 14 pp 18094—18105
Subclinical atherosclerosis and immune activation in young HIV-infected patients with telomere shortening
- 1 Servicio de Medicina Interna, Sección de Enfermedades infecciosas, Hospital General Universitario Reina Sofía and Universidad de Murcia, Murcia 30003, Spain
- 2 Centro Regional de Hemodonación de Murcia, Servicio de Hematología y Oncología Médica, Hospital Universitario Morales Meseguer, IMIB-Arrixaca, Red CIBERER CB15/00055, Murcia 30003, Spain
- 3 Servicio de Inmunología, Virgen de la Arrixaca Clinical University Hospital (HCUVA) and Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia 30120, Spain
Received: March 23, 2021 Accepted: July 13, 2021 Published: July 26, 2021
https://doi.org/10.18632/aging.203350How to Cite
Copyright: © 2021 Alcaraz et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background: To date, available data on premature aging in young HIV-infected adults are scarce and no reports offer comprehensive assessment of telomere shortening (TS) in relation to subclinical atherosclerosis (SCA). In this study, we investigate if telomere shortening and immune activation markers are associated with SCA, which is one of the main degenerative diseases in young HIV-infected adults.
Methods: A descriptive cross-sectional study was carried out in 149 HIV-infected patients on stable antiretroviral regimen (ART). Carotid intima-media thickness (cIMT) was estimated by carotid ultrasound. Quantitative singleplex PCR was performed to evaluate TS. The expression of activation/senescence markers was evaluated by multiparametric flow cytometry.
Results: TS was observed in 73 patients (49%). Higher cIMT was observed in patients with TS than those without it (0.86 vs. 0.80 mm; p=0.041). Patients under the age of 50 (defined as young adults) with TS showed higher absolute numbers of activated lymphocyte T cells CD8+CD38+ (3.94 vs. 2.34 cell/μl; p=0.07) and lymphocyte B cells CD19+CD38+ (3.07 vs. 2.10 cell/μl; p=0.004) compared to those without TS. In the multivariate analysis, the only factor independently associated with TS was the absolute number of lymphocyte T cells CD8+CD38+ T cells (OR = 1.18; 95%-CI = 1.00-1.39; p = 0.05).
Conclusion: Young HIV-infected adults show premature biological aging with accentuated immune activation. Chronic inflammation with excessive T-cells activation could be associated to TS, premature aging, and SCA in young HIV-infected adults.