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
Year: 2020
Type: article
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.
Source: AIDS
Authors: 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
Institutions: Leibniz Institute of Virology (LIV), University of KwaZulu-Natal, University of Oxford, Harvard University, Ragon Institute of MGH, MIT and Harvard, Max Planck Institute for Infection Biology, Africa Health Research Institute, University College London, Massachusetts Institute of Technology, University of the Witwatersrand, National Institute for Communicable Diseases
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W3092574047