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.

Maja C Ziegler, Kewreshini Naidoo, Anais Chapel, Sindiswa Nkotwana, Jaclyn Mann, Zenele Mncube, Nasreen Ismael, Philip Goulder, Thumbi Ndung'u, Marcus Altfeld, Christina F Thobakgale

Journal: AIDS (London, England) 2021;35(1):151-154

PMID: 33273184

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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.

DOI: 10.1097/QAD.0000000000002721

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MeSH Terms: Genes, gag, Genotype, HIV Infections, HIV-1, HLA-C Antigens, Humans, Killer Cells, Natural, Mutation, Receptors, KIR, Receptors, KIR2DL2