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Updated: May 7, 2026
High-Resolution Fluorespirometry to Assess Dynamic Changes in Mitochondrial Membrane Potential in Human Immune Cells
Published on: May 24, 2024
Mitochondrial function and apoptosis of peripheral mononuclear cells (PBMCs) in the HIV infected patients
Monika Bociąga-Jasik1, Joanna Góralska, Anna Polus
1Chair of Gastroenterology, Hepatology and Infectious Diseases, Department of Infectious Diseases Jagiellonian University, Collegium Medicum, Sniadeckich 5, 31-531 Kraków, Poland. monika.bociagajasik@gmail.com.
Abstract:
HIV infection results in the development of immunodeficiency mainly due to the apoptosis of infected and by stander CD4 cells. The aim of the study was to follow the mitochondrial dependent pathway of apoptosis, one of the suggested mechanisms of above process. The inner mitochondrial membrane potential (MMP), Adenosine-5'-triphosphate (ATP) generation, apoptosis and necrosis markers of peripheral mononuclear cells (PBMCs) were compared in HIV infected patients and HIV negative control group. The correlation of blood viral load, TNFα concentration, CD4 cells count and duration of ARV therapy was considered. Additionally, group of HIV infected ARV-naive patients was involved for the follow-up study and the effects of one year of ARV therapy on measured parameters were studied. PBMCs of HIV infected individuals (especially without ARV therapy) demonstrated lower MMP and ATP generation and higher percentage of apoptotic/necrotic PBMCs. Correlation between blood TNFα level and mitochondrial dysfunction was observed. The first months of ARV therapy resulted in most significant restoration of mitochondrial function and living PBMCs count. HIV infection and ARV therapy have significant impact on mitochondrial function and apoptosis of PBMCs. They are driven by abnormal mitochondrial function apoptosis of immune cells which seems to be the key element leading to immunosuppression, thus an early intervention in this process by therapy can be beneficial for symptomatology of HIV infected patients.
Insights
HIV infection causes immune deficiency by triggering CD4 cell apoptosis. Antiretroviral therapy (ARV) can restore mitochondrial function and boost immune cells, improving patient outcomes.
Area of Science:
- Immunology
- Cell Biology
- Virology
Background:
- HIV infection leads to immunodeficiency primarily through CD4 cell apoptosis.
- Mitochondrial dysfunction is a proposed mechanism driving this immune cell death.
- Understanding apoptosis pathways is crucial for managing HIV.
Purpose of the Study:
- To investigate the mitochondrial-dependent pathway of apoptosis in HIV-infected individuals.
- To compare mitochondrial function and cell death markers in PBMCs between HIV-infected and HIV-negative groups.
- To assess the impact of antiretroviral therapy (ARV) on these parameters.
Main Methods:
- Measured inner mitochondrial membrane potential (MMP) and Adenosine-5'-triphosphate (ATP) generation in peripheral mononuclear cells (PBMCs).
- Assessed apoptosis and necrosis markers in PBMCs.
- Correlated findings with viral load, TNFα concentration, CD4 cell count, and ARV therapy duration.
Main Results:
- HIV-infected individuals, particularly those treatment-naive, showed reduced MMP and ATP generation, with increased apoptotic/necrotic PBMCs.
- A correlation was observed between elevated blood TNFα levels and mitochondrial dysfunction.
- Early ARV therapy significantly restored mitochondrial function and increased viable PBMCs.
Conclusions:
- HIV infection and ARV therapy profoundly impact PBMC mitochondrial function and apoptosis.
- Abnormal mitochondrial function driving immune cell apoptosis is a key factor in HIV-induced immunosuppression.
- Early therapeutic intervention targeting mitochondrial dysfunction may benefit HIV-infected patients.
