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AIDS. 2014 May 15;28(8):1115-24. doi: 10.1097/QAD.0000000000000263.

Natural killer cell and T-cell subset distributions and activation influence susceptibility to perinatal HIV-1 infection.

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aSeattle 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.



To determine neonatal immunologic factors that correlate with mother-to-child-transmission of HIV-1.


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.


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.


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.


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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