Affiliations 

  • 1 Institute of Infectious Disease and Molecular Medicine and Division of Medical Virology, University of Cape Town, Cape Town, South Africa
  • 2 Dept. Obstetrics and Gynaecology, Jalan Taming Sari, Taiping Hospital, Perak, Malaysia
  • 3 Institute of Infectious Disease and Molecular Medicine and Division of Medical Virology, University of Cape Town, Cape Town, South Africa; Desmond Tutu HIV Foundation, Cape Town, South Africa
  • 4 Department of Biology, Medgar Evers College, The City University of New York, NY, USA
  • 5 Institute of Infectious Disease and Molecular Medicine and Division of Medical Virology, University of Cape Town, Cape Town, South Africa; National Health Laboratory Services, Cape Town, South Africa
  • 6 Dept Obstetrics and Gynaecology, University of Cape Town and Groote Schuur Hospital, Cape Town, South Africa
  • 7 Institute of Infectious Disease and Molecular Medicine and Division of Medical Virology, University of Cape Town, Cape Town, South Africa; National Health Laboratory Services, Cape Town, South Africa. Electronic address: Jo-ann.Passmore@uct.ac.za
Clin Immunol, 2014 Feb;150(2):210-9.
PMID: 24440646 DOI: 10.1016/j.clim.2013.12.005

Abstract

HIV-infected individuals experience more persistent HPV infections and are less likely to resolve genital warts. This study compared phenotype and functions of NK and T cells from genital warts and blood from 67 women. We compared in vitro functional responses of NK and T cells by multiparametric flow cytometry. HIV+ women had significantly lower frequencies of CD4 T cells in warts (p = 0.001) and blood (p = 0.001). While the distribution of NK cell subsets was similar, HIV+ women tended to have lower frequencies of CD56(Dim) NK cells in both blood (p = 0.0001) and warts (p = 0.006) than HIV- women. Wart NK cells from HIV+ women expressed significantly lower CD107a and produced IFN-γ. HAART status was not associated with differences in NK cell functionality. We conclude that wart NK cells from HIV+ women have defects in their ability to degranulate and/or secrete IFN-γ, which may provide insights into why HIV+ women fail to spontaneously resolve genital warts.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.