Increased proportion of KIR3DS1 homozygotes in HIV-exposed uninfected individuals

Abstract

Homozygosity for the activating NK receptor KIR3DS1, may contribute to the more active NK cell function observed in EU and their relative resistance to HIV infection.

HIV Protective KIR3DL1 and HLA-B Genotypes Influence NK Cell Function Following Stimulation with HLA-Devoid Cells

“…These subtle variations could explain why NK cells from individuals with certain KIR-ligand combinations seem better able to activate NK cell responses in the presence of specific pathogens (8)(9)(10)(11). This has been highlighted by a number of epidemiologic studies linking the generic KIR3DS/ L1 haplotypes with HIV disease progression or resistance to infection (8,9,(12)(13)(14)(15).…”

“…These were recruited from amongst the participants of the St. Luc injection drug user (IDU) cohort or were the seronegative partner in a serodiscordant couple (13,32,33). Twenty-nine met the criteria for inclusion in an HIV EU population because they had at least five documented parenteral or mucosal exposures to HIV.…”

“…Assign software was used to interpret sequence information for allele typing (Conexio Genetics, Perth, Australia). KIR3DL/S1 generic genotyping was performed by PCR using two pairs of specific primers for amplification of either KIR3DL1 or KIR3DS1 as previously described (13). KIR3DL1 allotyping was peformed by sequencing KIR3DL1 exons as previously described (12).…”

Phenotypical and functional profiles of natural killer cells exhibiting matrix metalloproteinase-mediated CD16 cleavage after anti-HIV antibody-dependent activation

“…Assign 3Á51 software was used to interpret sequence information for allele assignment (Conexio Genetics, Perth, Australia). KIR3DL/S1 generic genotyping was performed by polymerase chain reaction (PCR) using two pairs of primers specific for amplification of either KIR3DL1 or KIR3DS1 alleles, as described previously [22]. KIR3DL1 allotyping was performed by sequencing KIR3DL1 exons, as described previously [23].…”

Early viral replication in lymph nodes provides HIV with a means by which to escape NK‐cell‐mediated control

“…This alternative mechanism of antiviral control may reflect a homeostatic preference to prevent immunopathology within tissues, where cytotoxicity could potentially cause non-specific destruction that could adversely affect these critical inductive sites. Epidemiologic data suggest that particular KIRs, when co-expressed with their HLA ligands, are associated with differential risk of infection [44,45] and protection from disease progression [10,18,19,46,47]. However, we were surprised that KIR 1 NK cells were not detectable in the LN during early HIV infection.…”