HIV-1 evades a Gag mutation that abrogates killer cell immunoglobulin-like receptor binding and disinhibits natural killer cells in infected individuals with KIR2DL2+/HLA-C*03: 04+ genotype

AIDS. 2021 Jan 1;35(1):151-154. doi: 10.1097/QAD.0000000000002721.

Abstract

: HIV-1 sequence variations impact binding of inhibitory killer cell immunoglobulin-like receptors (KIRs) to human leukocyte antigen class I (HLA-I) molecules modulating natural killer cell function. HIV-1 strains encoding amino acids that mediate binding of inhibitory KIRs might therefore have a selective benefit in individuals expressing the respective KIR/HLA genotypes. Here, we demonstrate that HIV-1 clade C avoids a p24 Gag mutation that abolishes binding of KIR2DL2 to HLA-C03:04 and disinhibits natural killer cells in individual encoding for this genotype.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Genes, gag
  • Genotype
  • HIV Infections*
  • HIV-1* / genetics
  • HLA-C Antigens / genetics
  • Humans
  • Killer Cells, Natural / immunology
  • Mutation
  • Receptors, KIR / genetics
  • Receptors, KIR2DL2 / genetics

Substances

  • HLA-C Antigens
  • KIR2DL2 protein, human
  • Receptors, KIR
  • Receptors, KIR2DL2