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Updated: May 1, 2026
Preparation and Use of HIV-1 Infected Primary CD4+ T-Cells as Target Cells in Natural Killer Cell Cytotoxic Assays
Published on: March 14, 2011
Natural killer cell and T-cell subset distributions and activation influence susceptibility to perinatal HIV-1
Melanie A Gasper1, Pratima Kunwar, Grace Itaya
1aSeattle Biomedical Research Institute bDepartment of Global Health cDepartment of Medicine dDepartment of Epidemiology eDepartment of Pediatrics, University of Washington fFred Hutchinson Cancer Research Center, Seattle, Washington, USA gCenter for Public Health Research, Kenya Medical Research Institute hDepartment of Paediatrics and Child Health, University of Nairobi, Nairobi, Kenya.
Insights
Neonatal immune cells in cord blood, specifically natural killer (NK) and T-cells, correlate with mother-to-child HIV-1 transmission. Infant immune cell profiles at birth may predict HIV-1 acquisition risk.
Area of Science:
- Immunology
- Virology
- Pediatrics
Background:
- Mother-to-child transmission (MTCT) remains a significant route of HIV-1 acquisition in infants.
- Understanding neonatal immune factors influencing HIV-1 susceptibility is crucial for prevention strategies.
Purpose of the Study:
- To identify specific neonatal immunologic factors in cord blood that correlate with the risk of mother-to-child HIV-1 transmission.
- To investigate the role of natural killer (NK) and T-cell populations and their activation status in infant HIV-1 acquisition.
Main Methods:
- A case-control study comparing cord blood immune cells of HIV-1 exposed infants who acquired infection versus those who remained uninfected.
- Multiparameter flow cytometry was used to analyze NK and T-cell subsets and activation markers.
- A viral suppression assay evaluated the capacity of NK cells to inhibit HIV-1 replication in autologous CD4 T cells.
Main Results:
- Infants who acquired HIV-1 had a higher proportion of CD16-CD56 NK cells and lower NK cell activation.
- A greater number of mature CD4 and CD8 T cells were observed in infants who acquired HIV-1.
- NK cell's ability to suppress HIV-1 replication ex vivo correlated with the proportion of activated CD68+CD16+CD56 NK cells.
Conclusions:
- Infant HIV-1 acquisition is associated with distinct cord blood NK and T-cell phenotypes and activation states, even when maternal viral load is controlled.
- Both innate (NK cells) and adaptive (T cells) immune system characteristics at birth may influence an infant's susceptibility to HIV-1 infection.
Objective:
To determine neonatal immunologic factors that correlate with mother-to-child-transmission of HIV-1.
Design:
This case-control study compared cord blood natural killer (NK) and T-cell populations of HIV-1 exposed infants who subsequently acquired infection by 1 month (cases) to those who remained uninfected by 1 year of life (controls). Control specimens were selected by proportional match on maternal viral load.
Methods:
Cryopreserved cord blood mononuclear cells (CBMCs) were thawed and stained for multiparameter flow cytometry to detect NK and T-cell subsets and activation status. CBMCs were also used in a viral suppression assay to evaluate NK cell inhibition of HIV-1 replication in autologous CD4 T cells.
Results:
Cord blood from cases contained a skewed NK cell repertoire characterized by an increased proportion of CD16CD56 NK cells. In addition, cases displayed less-activated CD16CD56 NK cells and CD8 T cells, based on HLA-DRCD38 costaining. NK cell suppression of HIV-1 replication ex vivo correlated with the proportion of acutely activated CD68CD16CD56 NK cells. Finally, we detected a higher proportion of CD27CD45RA effector memory CD4 and CD8 T cells in cord blood from cases compared with controls.
Conclusion:
When controlled for maternal viral load, cord blood from infants who acquired HIV-1 had a higher proportion of CD16CD56 NK cells, lower NK cell activation and higher levels of mature T cells (potential HIV-1 targets) than control infants who remained uninfected. Our data provide evidence that infant HIV-1 acquisition may be influenced by both innate and adaptive immune cell phenotypes and activation status.
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