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

AIDS (London, England) 2021 Jan 01

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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.

Citation

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. 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 (London, England). 2021 Jan 01;35(1):151-154