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Published on: October 31, 2010
CD14(high)CD16(+) rather than CD14(low)CD16(+) monocytes correlate with disease progression in chronic HIV-infected
Junyan Han1, Beibei Wang, Ning Han
1Institute of Infectious Diseases, Capital Medical University, Beijing, China.
Insights
HIV infection affects distinct CD14(+)CD16(+) monocyte subsets differently. The CD14(high)CD16(+) subset, linked to disease progression, recovers with antiretroviral therapy, unlike the CD14(low)CD16(+) subset.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- CD14(+)CD16(+) monocytes are a key target for HIV-1 entry.
- These monocytes are heterogeneous, comprising CD14(high)CD16(+) and CD14(low)CD16(+) subsets.
- Understanding subset-specific responses is crucial for HIV pathogenesis.
Purpose of the Study:
- To investigate the differential effects of HIV infection on CD14(high)CD16(+) and CD14(low)CD16(+) monocyte subsets.
- To correlate monocyte subset proportions with HIV disease markers (viral load, CD4(+) T-cell count).
- To assess the impact of highly active antiretroviral therapy (HAART) on these monocyte subsets.
Main Methods:
- Recruitment of untreated HIV-infected patients.
- Analysis of monocyte subset proportions in relation to plasma viral loads and CD4(+) T-cell counts.
- Longitudinal and cross-sectional studies of patients on HAART.
Main Results:
- CD14(high)CD16(+) monocytes exhibit distinct immunoregulatory phenotypes (higher CD64, HLA-DR) compared to CD14(low)CD16(+).
- Elevated CD14(high)CD16(+) monocytes correlate with higher viral loads and lower CD4(+) counts in untreated patients.
- HAART effectively restored CD14(high)CD16(+) monocyte proportions, while CD14(low)CD16(+) monocytes remained unaffected.
Conclusions:
- HIV infection differentially impacts CD14(+)CD16(+) monocyte subsets.
- The CD14(high)CD16(+) subset is a potential biomarker for HIV disease progression.
- Antiretroviral therapy influences innate immune responses by modulating specific monocyte subsets.
Objective:
CD14(+)CD16(+) monocytes are an important cellular target for HIV-1 entry and expand in the peripheral blood of HIV-infected individuals. Because CD14(+)CD16(+) monocytes are a heterogeneous population and consist of CD14(high)CD16(+) and CD14(low)CD16(+) subsets, we evaluated the effects of HIV infection on distinct subsets of CD16(+) monocytes.
Methods:
Untreated HIV-infected patients were recruited to investigate the relationship between the proportions of monocyte subsets with plasma viral loads and CD4(+) T-cell counts. Patients receiving highly active antiretroviral therapy (HAART) were followed up in a cross-sectional and a longitudinal study.
Results:
Compared with CD14(low)CD16(+), CD14(high)CD16(+) monocytes showed higher levels of CD64 and HLA-DR antigens, which imply that these 2 distinct subsets have different immunoregulatory phenotypes. In HAART-naive patients, elevated proportions of CD14(high)CD16(+) monocytes were correlated with increased viral loads and decreased CD4(+) T-cell counts, whereas CD14(low)CD16(+) monocytes did not show such correlation with disease progression. Of importance, HAART recovered the proportion of CD14(high)CD16(+) monocytes, whereas CD14(low)CD16(+) monocytes did not decrease during 1 year of antiviral therapy.
Conclusions:
Taken together, our observations elucidate distinct immune responses of monocyte subsets during HIV infection and antiviral therapy and provide new insight into the roles of innate immunity in HIV-related pathogenesis.
