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.
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.
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HIV-1逃避了一种插科打突变，该突变消除了杀手细胞免疫球蛋白样受体结合，并在感染的具有KIR2DL2+/HLA-C*03：04+基因型的受感染个体中的天然杀伤细胞中。
DOI：
10.1097/qad.0000000000002721
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发表时间：
2021-01-01
期刊：
影响因子：
--
通讯作者：
Thobakgale CF
中科院分区：
文献类型：
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作者：
Ziegler MC;Naidoo K;Chapel A;Nkotwana S;Mann J;Mncube Z;Ismael N;Goulder P;Ndung'u T;Altfeld M;Thobakgale CF
HIV-1 sequence variations impact binding of inhibitory killer cell immunoglobulin-like receptors (KIRs) to human leucocyte class I (HLA-I) molecules modulating NK 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-C*03:04 and disinhibits NK cells in individual encoding for this genotype.
