Role of HLA adaptation in HIV evolution

Henrik N. Kløverpris; Alasdair Leslie; Philip Goulder

doi:10.3389/fimmu.2015.00665

Role of HLA adaptation in HIV evolution

Henrik N. Kløverpris, Alasdair Leslie, Philip Goulder^*

^*Corresponding author for this work

24 Citations (Scopus)

72 Downloads (Pure)

Abstract

Killing of HIV-infected cells by CD8⁺ T-cells imposes strong selection pressure on the virus toward escape. The HLA class I molecules that are successful in mediating some degree of control over the virus are those that tend to present epitopes in conserved regions of the proteome, such as in p24 Gag, in which escape also comes at a significant cost to viral replicative capacity (VRC). In some instances, compensatory mutations can fully correct for the fitness cost of such an escape variant; in others, correction is only partial. The consequences of these events within the HIV-infected host, and at the population level following transmission of escape variants, are discussed. The accumulation of escape mutants in populations over the course of the epidemic already shows instances of protective HLA molecules losing their impact, and in certain cases, a modest decline in HIV virulence in association with population-level increase in mutants that reduce VRC.

Original language	English
Article number	665
Journal	Frontiers in Immunology
Volume	6
Number of pages	15
ISSN	1664-3224
DOIs	https://doi.org/10.3389/fimmu.2015.00665
Publication status	Published - 2016

Keywords

CD8 T cells
HIV-1
HLA class I
Viral adaptation
Viral fitness
Viral replicative capacity

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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Role of HLA Adaptation in HIV EvolutionFinal published version, 843 KBLicence: CC BY

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title = "Role of HLA adaptation in HIV evolution",

abstract = "Killing of HIV-infected cells by CD8+ T-cells imposes strong selection pressure on the virus toward escape. The HLA class I molecules that are successful in mediating some degree of control over the virus are those that tend to present epitopes in conserved regions of the proteome, such as in p24 Gag, in which escape also comes at a significant cost to viral replicative capacity (VRC). In some instances, compensatory mutations can fully correct for the fitness cost of such an escape variant; in others, correction is only partial. The consequences of these events within the HIV-infected host, and at the population level following transmission of escape variants, are discussed. The accumulation of escape mutants in populations over the course of the epidemic already shows instances of protective HLA molecules losing their impact, and in certain cases, a modest decline in HIV virulence in association with population-level increase in mutants that reduce VRC.",

keywords = "CD8 T cells, HIV-1, HLA class I, Viral adaptation, Viral fitness, Viral replicative capacity",

author = "Kl{\o}verpris, {Henrik N.} and Alasdair Leslie and Philip Goulder",

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doi = "10.3389/fimmu.2015.00665",

language = "English",

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journal = "Frontiers in Immunology",

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T1 - Role of HLA adaptation in HIV evolution

AU - Kløverpris, Henrik N.

AU - Leslie, Alasdair

AU - Goulder, Philip

PY - 2016

Y1 - 2016

N2 - Killing of HIV-infected cells by CD8+ T-cells imposes strong selection pressure on the virus toward escape. The HLA class I molecules that are successful in mediating some degree of control over the virus are those that tend to present epitopes in conserved regions of the proteome, such as in p24 Gag, in which escape also comes at a significant cost to viral replicative capacity (VRC). In some instances, compensatory mutations can fully correct for the fitness cost of such an escape variant; in others, correction is only partial. The consequences of these events within the HIV-infected host, and at the population level following transmission of escape variants, are discussed. The accumulation of escape mutants in populations over the course of the epidemic already shows instances of protective HLA molecules losing their impact, and in certain cases, a modest decline in HIV virulence in association with population-level increase in mutants that reduce VRC.

AB - Killing of HIV-infected cells by CD8+ T-cells imposes strong selection pressure on the virus toward escape. The HLA class I molecules that are successful in mediating some degree of control over the virus are those that tend to present epitopes in conserved regions of the proteome, such as in p24 Gag, in which escape also comes at a significant cost to viral replicative capacity (VRC). In some instances, compensatory mutations can fully correct for the fitness cost of such an escape variant; in others, correction is only partial. The consequences of these events within the HIV-infected host, and at the population level following transmission of escape variants, are discussed. The accumulation of escape mutants in populations over the course of the epidemic already shows instances of protective HLA molecules losing their impact, and in certain cases, a modest decline in HIV virulence in association with population-level increase in mutants that reduce VRC.

KW - CD8 T cells

KW - HIV-1

KW - HLA class I

KW - Viral adaptation

KW - Viral fitness

KW - Viral replicative capacity

U2 - 10.3389/fimmu.2015.00665

DO - 10.3389/fimmu.2015.00665

M3 - Review

C2 - 26834742

AN - SCOPUS:84958231232

SN - 1664-3224

VL - 6

JO - Frontiers in Immunology

JF - Frontiers in Immunology

M1 - 665

ER -

Role of HLA adaptation in HIV evolution

Abstract

Keywords

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