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Molecular mechanism for selection and control of HIV-1 escape virus by T cells and KIR2DL2+ NK cells

ABSTRACT: NK cells and CD8+ T cells both contribute to HIV-1 control. These cells not only suppress HIV-1 replication, but also select HIV-1 escape mutant viruses. Most viruses bearing T cell escape mutations are expected to remain susceptible to NK cell suppression, but their control by NK cells is unclear. We investigated the role of HIV-1-specific CD8+ T cells and NK cells recognizing superimposed Pol peptides in selection and control of HIV-1 mutant virus. KIR2DL2+ NK cells had an enhanced ability to recognize HIV-1-infected cells after selection of Pol mutant virus by PolIY11-specific HLA-C*12:02-restricted T cells. Mass spectrometry-based immunopeptidome profiling of HIV-1-infected cells and analysis of crystal structures of TCR- and KIR2DL2-HLA-C*12:02-peptide complexes demonstrated the molecular basis for selection and recognition of the escape mutant epitope by TCR and KIR2DL2. The present study elucidates the mechanism for selection and control of an HIV-1 escape virus by T cells and NK cells.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human) Human Immunodeficiency Virus 1

TISSUE(S): Cell Suspension Culture, Permanent Cell Line Cell

SUBMITTER: Nicola Ternette

LAB HEAD: Nicola Ternette

PROVIDER: PXD058766 | Pride | 2025-08-29

REPOSITORIES: Pride

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			Action	DRS
	HFX0171_IPP272_C1202-NL43-EVEN.mgf	Mgf
	HFX0171_IPP272_C1202-NL43-ODD.mgf	Mgf
	HFX236_IPP364_NL43-V9A-Mut-Even.mgf	Mgf
	HFX236_IPP364_NL43-V9A-Mut-Odd.mgf	Mgf
	HFX255_IPP446_AK_C1202_NL43_V9A_even.mgf	Mgf

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Project description:Sanjuan2013 - Evolution of HIV T-cell epitope, immune activation model Model of cellular immune response against HIV. This model is described in the article: Immune activation promotes evolutionary conservation of T-cell epitopes in HIV-1. Sanjuán R, Nebot MR, Peris JB, Alcamí J. PLoS Biol. 2013 Apr;11(4):e1001523 Abstract: The immune system should constitute a strong selective pressure promoting viral genetic diversity and evolution. However, HIV shows lower sequence variability at T-cell epitopes than elsewhere in the genome, in contrast with other human RNA viruses. Here, we propose that epitope conservation is a consequence of the particular interactions established between HIV and the immune system. On one hand, epitope recognition triggers an anti-HIV response mediated by cytotoxic T-lymphocytes (CTLs), but on the other hand, activation of CD4(+) helper T lymphocytes (TH cells) promotes HIV replication. Mathematical modeling of these opposite selective forces revealed that selection at the intrapatient level can promote either T-cell epitope conservation or escape. We predict greater conservation for epitopes contributing significantly to total immune activation levels (immunodominance), and when TH cell infection is concomitant to epitope recognition (trans-infection). We suggest that HIV-driven immune activation in the lymph nodes during the chronic stage of the disease may offer a favorable scenario for epitope conservation. Our results also support the view that some pathogens draw benefits from the immune response and suggest that vaccination strategies based on conserved TH epitopes may be counterproductive. Note from the author: this version of the model is more general that the one described in the paper. This is because: (i) it can consider simultaneously Th-epitope escape mutants, CTL-epitope escape mutants and full T-cell (Th and CTL) escape mutants, by setting the mutation rate of Th and CTL escape mutants to zero. (ii) It allows for back mutations, which were ignored in all the simulations shown in the paper. (iii) It allows for a fitness cost of escape mutants, which was set to zero in the article. (iv) pAPCs can be infected and produce viruses (the rate of viral production for pAPCs was set to zero in the paper). This model is hosted on BioModels Database and identified by: MODEL1302180001 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Molecular mechanism for selection and control of HIV-1 escape virus by T cells and KIR2DL2+ NK cells

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