PMID- 33273184
OWN - NLM
STAT- MEDLINE
DCOM- 20210302
LR  - 20240214
IS  - 1473-5571 (Electronic)
IS  - 0269-9370 (Print)
IS  - 0269-9370 (Linking)
VI  - 35
IP  - 1
DP  - 2021 Jan 1
TI  - 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.
PG  - 151-154
LID - 10.1097/QAD.0000000000002721 [doi]
AB  - : 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.
FAU - Ziegler, Maja C
AU  - Ziegler MC
AD  - Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for 
      Experimental Virology, Hamburg, Germany.
FAU - Naidoo, Kewreshini
AU  - Naidoo K
AD  - HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University 
      of KwaZulu-Natal, Durban, South Africa.
FAU - Chapel, Anais
AU  - Chapel A
AD  - Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for 
      Experimental Virology, Hamburg, Germany.
FAU - Nkotwana, Sindiswa
AU  - Nkotwana S
AD  - HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University 
      of KwaZulu-Natal, Durban, South Africa.
FAU - Mann, Jaclyn
AU  - Mann J
AD  - HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University 
      of KwaZulu-Natal, Durban, South Africa.
FAU - Mncube, Zenele
AU  - Mncube Z
AD  - HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University 
      of KwaZulu-Natal, Durban, South Africa.
FAU - Ismael, Nasreen
AU  - Ismael N
AD  - HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University 
      of KwaZulu-Natal, Durban, South Africa.
FAU - Goulder, Philip
AU  - Goulder P
AD  - HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University 
      of KwaZulu-Natal, Durban, South Africa.
AD  - Department of Paediatrics, University of Oxford, Oxford, UK.
FAU - Ndung'u, Thumbi
AU  - Ndung'u T
AD  - HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University 
      of KwaZulu-Natal, Durban, South Africa.
AD  - Ragon Institute of MGH, MIT and Harvard University, Cambridge, Massachusetts, 
      USA.
AD  - Africa Health Research Institute, Durban, South Africa.
AD  - Max Planck Institute for Infection Biology, Berlin, Germany.
AD  - Division of Infection and Immunity, University College London, London, UK.
FAU - Altfeld, Marcus
AU  - Altfeld M
AD  - Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for 
      Experimental Virology, Hamburg, Germany.
AD  - HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University 
      of KwaZulu-Natal, Durban, South Africa.
FAU - Thobakgale, Christina F
AU  - Thobakgale CF
AD  - HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University 
      of KwaZulu-Natal, Durban, South Africa.
AD  - Faculty of Health Sciences, Centre for HIV and STIs, National Institute for 
      Communicable Diseases, University of the Witwatersrand, Johannesburg, South 
      Africa.
LA  - eng
GR  - WT_/Wellcome Trust/United Kingdom
GR  - R01 AI067073/AI/NIAID NIH HHS/United States
GR  - R01 AI133673/AI/NIAID NIH HHS/United States
GR  - 102468/Z/13/Z/WT_/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - AIDS
JT  - AIDS (London, England)
JID - 8710219
RN  - 0 (HLA-C Antigens)
RN  - 0 (KIR2DL2 protein, human)
RN  - 0 (Receptors, KIR)
RN  - 0 (Receptors, KIR2DL2)
SB  - IM
MH  - Genes, gag
MH  - Genotype
MH  - *HIV Infections
MH  - *HIV-1/genetics
MH  - HLA-C Antigens/genetics
MH  - Humans
MH  - Killer Cells, Natural/immunology
MH  - Mutation
MH  - Receptors, KIR/genetics
MH  - Receptors, KIR2DL2/genetics
PMC - PMC7856308
MID - NIHMS1647971
COIS- Conflicts of interest The authors declare no conflicts of interest. The work was 
      supported by the Molecular Mechanisms of Viral Pathogenesis Program of the 
      Heinrich Pette Institute. CT was supported by the Wellcome Trust (102468/Z/13/Z). 
      The Sinikithemba cohort was funded by the NIH (Grant ROI-AI067073 Contract 
      NOI-AI-15422). This study was also supported in part through the South African 
      Research Chairs Initiative, International AIDS Vaccine Initiative (IAVI) (grant # 
      UKZNRSA1001) and the Victor Daitz Foundation. TN and MA are supported by the DFG 
      grant AL1043/BU3630. The views expressed in this publication are those of the 
      authors and not of the funders.
EDAT- 2020/12/05 06:00
MHDA- 2021/03/03 06:00
PMCR- 2022/01/01
CRDT- 2020/12/04 05:38
PHST- 2020/12/04 05:38 [entrez]
PHST- 2020/12/05 06:00 [pubmed]
PHST- 2021/03/03 06:00 [medline]
PHST- 2022/01/01 00:00 [pmc-release]
AID - 00002030-202101010-00017 [pii]
AID - 10.1097/QAD.0000000000002721 [doi]
PST - ppublish
SO  - AIDS. 2021 Jan 1;35(1):151-154. doi: 10.1097/QAD.0000000000002721.