Genetic variants in nonclassical major histocompatibility complex class I human leukocyte antigen (HLA)-E and HLA-G molecules are associated with susceptibility to heterosexual acquisition of HIV-1

Julie Lajoie, John Hargrove, Lynn S. Zijenah, Jean Hawes Humphrey, Brian J. Ward, Michel Roger

Research output: Contribution to journalArticle

Abstract

Human leukocyte antigen (HLA)-E and HLA-G molecules act as powerful modulators of the innate immune response. The present study shows that the HLA-EG genetic variant (the HLA-E*0103 allele) alone is significantly (P = .001) associated with a 4.0-fold decreased risk of human immunodeficiency virus 1 (HIV-1) infection in Zimbabwean women. Furthermore, women carrying the combination of the protective HLA-EG homozygote and HLA-G*0105N heterozygote genotypes had a 12.5-fold decreased risk of HIV-1 infection (P = .03), compared with women carrying neither genotype. These associations remained significant after adjustment was made for other significant sociodemographic risk factors for HIV prevalence in this population. In conclusion, HLA-E and HLA-G polymorphisms can independently and synergistically influence susceptibility to heterosexual acquisition of HIV-1.

Original languageEnglish (US)
Pages (from-to)298-301
Number of pages4
JournalJournal of Infectious Diseases
Volume193
Issue number2
DOIs
StatePublished - Jan 15 2006

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Heterosexuality
HLA Antigens
Major Histocompatibility Complex
HIV-1
Virus Diseases
Genotype
Social Adjustment
Homozygote
Heterozygote
Innate Immunity
Alleles
HIV
Population

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Immunology

Cite this

Genetic variants in nonclassical major histocompatibility complex class I human leukocyte antigen (HLA)-E and HLA-G molecules are associated with susceptibility to heterosexual acquisition of HIV-1. / Lajoie, Julie; Hargrove, John; Zijenah, Lynn S.; Humphrey, Jean Hawes; Ward, Brian J.; Roger, Michel.

In: Journal of Infectious Diseases, Vol. 193, No. 2, 15.01.2006, p. 298-301.

Research output: Contribution to journalArticle

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