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Cell cycle distribution of CD4+ lymphocytes in HIV-1-infected subjects
Mariana Melillo Sauer Chaves1, Esper Georges Kallas
1Infectious Diseases Division, Federal University of São Paulo, São Paulo, Brazil.
Insights
HIV-1 infection alters CD4(+) lymphocyte cell cycle, increasing S phase and decreasing G(1) phase. This finding may help understand CD4(+) T-cell depletion in HIV patients.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Apoptosis is a potential cause of CD4(+) T-lymphocyte loss in human immunodeficiency virus (HIV) infection.
- HIV infection may disrupt normal lymphocyte cell cycle distribution.
- This study investigates CD4(+) and CD8(+) lymphocyte cell cycle in HIV-infected individuals.
Purpose of the Study:
- To evaluate the cell cycle distribution of CD4(+) and CD8(+) lymphocytes in HIV-1-infected subjects.
- To compare cell cycle analysis methods for lymphocyte evaluation.
Main Methods:
- Two methods for lymphocyte identification were assessed: magnetic beads and concurrent staining.
- Propidium iodide DNA labeling was used for cell cycle analysis.
- The selected method was applied to HIV-1 patients and controls.
Main Results:
- No significant difference was found between magnetic bead and concurrent staining methods, though magnetic beads showed higher variability.
- HIV-1 patients exhibited a higher proportion of CD4(+) lymphocytes in S phase (2.69% vs. 1.19%) and a decrease in G(1) phase (96.11% vs. 98.10%).
- These cell cycle changes were not observed in CD8(+) lymphocytes and did not correlate with T-lymphocyte counts or viral load.
Conclusions:
- A novel approach for evaluating lymphocyte cell cycle distribution was developed and applied to HIV-1 infection.
- The findings may enhance understanding of CD4(+) T-lymphocyte depletion in HIV-1 patients.
Background:
Apoptosis is one of the possible explanations for the progressive loss of CD4(+) T lymphocytes in infection with the human immunodeficiency virus (HIV), which may interfere with cell cycle distribution. This study evaluated the cell cycle of CD4(+) and CD8(+) lymphocytes in HIV-infected subjects and controls.
Methods:
Two methods to identify lymphocytes for cell cycle analysis were evaluated, magnetic beads and concurrent staining, and both were followed by propidium iodide DNA labeling. The chosen method was used to evaluate the cell cycle of lymphocytes in HIV-1-infected subjects and controls.
Results:
There was no significant difference between the two methods, although a higher variability was observed with the magnetic bead cell separation method. A higher proportion of cells in the S phase was observed in HIV-1 patients (2.69% vs. 1.19%, P = 0.016), coupled with a decrease in G(1) (96.11% vs. 98.10%, P = 0.005) in CD4(+) lymphocytes, a phenomenon not observed in CD8(+) lymphocytes. No correlation was detected between the different cell cycle phases and T-lymphocyte counts or viral load.
Conclusions:
The present work developed a new approach to evaluate lymphocyte cell cycle distribution, applied in the setting of HIV-1 infection. It may contribute to the understanding of the CD4(+) T-lymphocytes depletion seen in these patients.
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