T-LYMPHOCYTE IMMUNOPHENOTYPING AND THE PATHOGENESIS OF BONE LOSS IN HIV PATIENTS WITH VIRAL SUPPRESSION
DOI:
https://doi.org/10.63330/aurumpub.061-040Keywords:
Bone Mineral Density, HIV/AIDS, Chronic Inflammation, T Lymphocytes, OsteoimmunologyAbstract
With the introduction of combination antiretroviral therapy (cART), the life expectancy of people living with HIV/AIDS (PLWHA) has increased significantly, transforming the infection into a chronic condition. However, the aging of this population has brought to light a high incidence of comorbidities, such as premature bone loss, exacerbated by persistent systemic inflammation and chronic immune activation. Phenotypic assessment of CD4+ and CD8+ T-cell subpopulations is associated with reduced bone mineral density (BMD) in patients living with HIV who have controlled viral loads. Evaluating bone densitometry (DXA) scans and performing flow cytometry-based immunophenotyping are viable methods for detecting the lymphocytes directly linked to reduced bone density in HIV patients. It is essential to investigate markers of regulation (PD-1, CTLA-4), activation (HLA-DR), proliferation (Ki-67), and cytokine production. A high prevalence of bone abnormalities, such as osteopenia and osteoporosis, is observed in HIV patients with controlled viral loads. Studies demonstrate that patients with osteopenia exhibit higher T-cell proliferative activity and reduced numbers of regulatory cells (CD4+CD3+CTLA-4+ and CD8+CD3+PD-1+) compared to patients with normal BMD. Furthermore, increased expression of activation markers (HLA-DR and CD69) and an imbalance in the production of inflammatory cytokines, such as TNF-α and IFN-γ, are observed. Specific circulating lymphocyte profiles and regulatory dysfunction are understood to play a significant role in the pathogenesis of bone loss in PLWHA (patients living with controlled HIV).
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