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HLA-C*07 is associated with symptomatic HIV-1-associated neurocognitive disorders (HAND) and immune dysregulation.

Authors :
Pons-Fuster, Eduardo
Bernal, Enrique
Guillamón, Concepción F.
Gimeno, Lourdes
Martínez-Sánchez, María V.
Ruiz-Lorente, Inmaculada
Campillo, José A.
Ceballos, Diana
Torres, Ana
Tomás, Cristina
Muñoz, Ángeles
Alcaraz, Antonia
Selma, Pedro
Ruiz-Nicolas, Carlos
Muro, Manuel
Minguela, Alfredo
Source :
Infectious Diseases. Oct2024, Vol. 56 Issue 10, p818-829. 12p.
Publication Year :
2024

Abstract

Background: HIV-1-associated neurocognitive disorders (HAND) in stable patients undergoing antiretroviral therapy (ART) may result from ongoing immune dysregulation and chronic inflammation. A contributing factor may result from the unstable HLA class I allele, HLA-C*07. Objective: To assess the genetic profile of killer-cell immunoglobulin-like receptors (KIR), human leukocyte antigens (HLA), and immune activation or senescence markers and their association with HAND in stable HIV-1 patients receiving ART. Methods: An observational cross-sectional study was carried out with 96 patients with asymptomatic or symptomatic HAND. HLA and KIR as well as immune activation/senescence biomarkers in peripheral blood cells were assessed by SSO-Luminex typing and flow cytometry, respectively. Results: HLA-C*07 is associated with symptomatic HAND. The frequency of two copies of HLA-C*07 was higher in patients with symptomatic than with asymptomatic HAND (12.0 vs. 2.2%, ρ < 0.001). The percentage of senescent CD8+CD28- T-cells was higher in patients with two copies of HLA-C*07 (ρ < 0.05). In patients with symptomatic HAND, the percentages of non-senescent CD8+CD28+ T cells were inversely proportional to the number of copies of the HLA-C*07 (ρ < 0.05). Conclusion: Patients with symptomatic HAND showed a higher frequency of the homozygotic unstable HLA-C*07 allotype, which could be associated with neurocognitive complications. Two copies of HLA-C*07 were associated with immune senescent T lymphocyte profiles characterized by the loss of CD28 expression. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
23744235
Volume :
56
Issue :
10
Database :
Academic Search Index
Journal :
Infectious Diseases
Publication Type :
Academic Journal
Accession number :
179995784
Full Text :
https://doi.org/10.1080/23744235.2024.2351047