Selection of an HLA-C*03:04-Restricted HIV-1 p24 Gag Sequence Variant Is Associated with Viral Escape from KIR2DL3+ Natural Killer Cells: Data from an Observational Cohort in South Africa.

<h4>Background</h4>Viruses can evade immune surveillance, but the underlying mechanisms are insufficiently understood. Here, we sought to understand the mechanisms by which natural killer (NK) cells recognize HIV-1-infected cells and how this virus can evade NK-cell-mediated immune press...

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Main Authors: Angelique Hölzemer, Christina F Thobakgale, Camilo A Jimenez Cruz, Wilfredo F Garcia-Beltran, Jonathan M Carlson, Nienke H van Teijlingen, Jaclyn K Mann, Manjeetha Jaggernath, Seung-gu Kang, Christian Körner, Amy W Chung, Jamie L Schafer, David T Evans, Galit Alter, Bruce D Walker, Philip J Goulder, Mary Carrington, Pia Hartmann, Thomas Pertel, Ruhong Zhou, Thumbi Ndung'u, Marcus Altfeld
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2015-11-01
Series:PLoS Medicine
Online Access:https://doi.org/10.1371/journal.pmed.1001900
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author Angelique Hölzemer
Christina F Thobakgale
Camilo A Jimenez Cruz
Wilfredo F Garcia-Beltran
Jonathan M Carlson
Nienke H van Teijlingen
Jaclyn K Mann
Manjeetha Jaggernath
Seung-gu Kang
Christian Körner
Amy W Chung
Jamie L Schafer
David T Evans
Galit Alter
Bruce D Walker
Philip J Goulder
Mary Carrington
Pia Hartmann
Thomas Pertel
Ruhong Zhou
Thumbi Ndung'u
Marcus Altfeld
author_facet Angelique Hölzemer
Christina F Thobakgale
Camilo A Jimenez Cruz
Wilfredo F Garcia-Beltran
Jonathan M Carlson
Nienke H van Teijlingen
Jaclyn K Mann
Manjeetha Jaggernath
Seung-gu Kang
Christian Körner
Amy W Chung
Jamie L Schafer
David T Evans
Galit Alter
Bruce D Walker
Philip J Goulder
Mary Carrington
Pia Hartmann
Thomas Pertel
Ruhong Zhou
Thumbi Ndung'u
Marcus Altfeld
author_sort Angelique Hölzemer
collection DOAJ
description <h4>Background</h4>Viruses can evade immune surveillance, but the underlying mechanisms are insufficiently understood. Here, we sought to understand the mechanisms by which natural killer (NK) cells recognize HIV-1-infected cells and how this virus can evade NK-cell-mediated immune pressure.<h4>Methods and findings</h4>Two sequence mutations in p24 Gag associated with the presence of specific KIR/HLA combined genotypes were identified in HIV-1 clade C viruses from a large cohort of infected, untreated individuals in South Africa (n = 392), suggesting viral escape from KIR+ NK cells through sequence variations within HLA class I-presented epitopes. One sequence polymorphism at position 303 of p24 Gag (TGag303V), selected for in infected individuals with both KIR2DL3 and HLA-C*03:04, enabled significantly better binding of the inhibitory KIR2DL3 receptor to HLA-C*03:04-expressing cells presenting this variant epitope compared to the wild-type epitope (wild-type mean 18.01 ± 10.45 standard deviation [SD] and variant mean 44.67 ± 14.42 SD, p = 0.002). Furthermore, activation of primary KIR2DL3+ NK cells from healthy donors in response to HLA-C*03:04+ target cells presenting the variant epitope was significantly reduced in comparison to cells presenting the wild-type sequence (wild-type mean 0.78 ± 0.07 standard error of the mean [SEM] and variant mean 0.63 ± 0.07 SEM, p = 0.012). Structural modeling and surface plasmon resonance of KIR/peptide/HLA interactions in the context of the different viral sequence variants studied supported these results. Future studies will be needed to assess processing and antigen presentation of the investigated HIV-1 epitope in natural infection, and the consequences for viral control.<h4>Conclusions</h4>These data provide novel insights into how viruses can evade NK cell immunity through the selection of mutations in HLA-presented epitopes that enhance binding to inhibitory NK cell receptors. Better understanding of the mechanisms by which HIV-1 evades NK-cell-mediated immune pressure and the functional validation of a structural modeling approach will facilitate the development of novel targeted immune interventions to harness the antiviral activities of NK cells.
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institution Kabale University
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publishDate 2015-11-01
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spelling doaj-art-fa6dc56a9531426d9574a273ad87bc212025-08-20T03:25:16ZengPublic Library of Science (PLoS)PLoS Medicine1549-12771549-16762015-11-011211e1001900; discussion e100190010.1371/journal.pmed.1001900Selection of an HLA-C*03:04-Restricted HIV-1 p24 Gag Sequence Variant Is Associated with Viral Escape from KIR2DL3+ Natural Killer Cells: Data from an Observational Cohort in South Africa.Angelique HölzemerChristina F ThobakgaleCamilo A Jimenez CruzWilfredo F Garcia-BeltranJonathan M CarlsonNienke H van TeijlingenJaclyn K MannManjeetha JaggernathSeung-gu KangChristian KörnerAmy W ChungJamie L SchaferDavid T EvansGalit AlterBruce D WalkerPhilip J GoulderMary CarringtonPia HartmannThomas PertelRuhong ZhouThumbi Ndung'uMarcus Altfeld<h4>Background</h4>Viruses can evade immune surveillance, but the underlying mechanisms are insufficiently understood. Here, we sought to understand the mechanisms by which natural killer (NK) cells recognize HIV-1-infected cells and how this virus can evade NK-cell-mediated immune pressure.<h4>Methods and findings</h4>Two sequence mutations in p24 Gag associated with the presence of specific KIR/HLA combined genotypes were identified in HIV-1 clade C viruses from a large cohort of infected, untreated individuals in South Africa (n = 392), suggesting viral escape from KIR+ NK cells through sequence variations within HLA class I-presented epitopes. One sequence polymorphism at position 303 of p24 Gag (TGag303V), selected for in infected individuals with both KIR2DL3 and HLA-C*03:04, enabled significantly better binding of the inhibitory KIR2DL3 receptor to HLA-C*03:04-expressing cells presenting this variant epitope compared to the wild-type epitope (wild-type mean 18.01 ± 10.45 standard deviation [SD] and variant mean 44.67 ± 14.42 SD, p = 0.002). Furthermore, activation of primary KIR2DL3+ NK cells from healthy donors in response to HLA-C*03:04+ target cells presenting the variant epitope was significantly reduced in comparison to cells presenting the wild-type sequence (wild-type mean 0.78 ± 0.07 standard error of the mean [SEM] and variant mean 0.63 ± 0.07 SEM, p = 0.012). Structural modeling and surface plasmon resonance of KIR/peptide/HLA interactions in the context of the different viral sequence variants studied supported these results. Future studies will be needed to assess processing and antigen presentation of the investigated HIV-1 epitope in natural infection, and the consequences for viral control.<h4>Conclusions</h4>These data provide novel insights into how viruses can evade NK cell immunity through the selection of mutations in HLA-presented epitopes that enhance binding to inhibitory NK cell receptors. Better understanding of the mechanisms by which HIV-1 evades NK-cell-mediated immune pressure and the functional validation of a structural modeling approach will facilitate the development of novel targeted immune interventions to harness the antiviral activities of NK cells.https://doi.org/10.1371/journal.pmed.1001900
spellingShingle Angelique Hölzemer
Christina F Thobakgale
Camilo A Jimenez Cruz
Wilfredo F Garcia-Beltran
Jonathan M Carlson
Nienke H van Teijlingen
Jaclyn K Mann
Manjeetha Jaggernath
Seung-gu Kang
Christian Körner
Amy W Chung
Jamie L Schafer
David T Evans
Galit Alter
Bruce D Walker
Philip J Goulder
Mary Carrington
Pia Hartmann
Thomas Pertel
Ruhong Zhou
Thumbi Ndung'u
Marcus Altfeld
Selection of an HLA-C*03:04-Restricted HIV-1 p24 Gag Sequence Variant Is Associated with Viral Escape from KIR2DL3+ Natural Killer Cells: Data from an Observational Cohort in South Africa.
PLoS Medicine
title Selection of an HLA-C*03:04-Restricted HIV-1 p24 Gag Sequence Variant Is Associated with Viral Escape from KIR2DL3+ Natural Killer Cells: Data from an Observational Cohort in South Africa.
title_full Selection of an HLA-C*03:04-Restricted HIV-1 p24 Gag Sequence Variant Is Associated with Viral Escape from KIR2DL3+ Natural Killer Cells: Data from an Observational Cohort in South Africa.
title_fullStr Selection of an HLA-C*03:04-Restricted HIV-1 p24 Gag Sequence Variant Is Associated with Viral Escape from KIR2DL3+ Natural Killer Cells: Data from an Observational Cohort in South Africa.
title_full_unstemmed Selection of an HLA-C*03:04-Restricted HIV-1 p24 Gag Sequence Variant Is Associated with Viral Escape from KIR2DL3+ Natural Killer Cells: Data from an Observational Cohort in South Africa.
title_short Selection of an HLA-C*03:04-Restricted HIV-1 p24 Gag Sequence Variant Is Associated with Viral Escape from KIR2DL3+ Natural Killer Cells: Data from an Observational Cohort in South Africa.
title_sort selection of an hla c 03 04 restricted hiv 1 p24 gag sequence variant is associated with viral escape from kir2dl3 natural killer cells data from an observational cohort in south africa
url https://doi.org/10.1371/journal.pmed.1001900
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