HLA-A*7401-mediated control of HIV viremia is independent of its linkage disequilibrium with HLA-B*5703

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

  • Philippa C Matthews
  • Emily Adland
  • Jennifer Listgarten
  • Alasdair Leslie
  • Nompumelelo Mkhwanazi
  • Jonathan M Carlson
  • Mikkel Harndahl
  • Rebecca P Payne
  • Anthony Ogwu
  • Kuan-Hsiang Gary Huang
  • John Frater
  • Paolo Paioni
  • Henrik Kloverpris
  • Pieter Jooste
  • Dominique Goedhals
  • Cloete van Vuuren
  • Dewald Steyn
  • Lynn Riddell
  • Fabian Chen
  • Graz Luzzi
  • Thambiah Balachandran
  • Thumbi Ndung'u
  • Mary Carrington
  • Roger Shapiro
  • David Heckerman
  • Philip J R Goulder
The potential contribution of HLA-A alleles to viremic control in chronic HIV type 1 (HIV-1) infection has been relatively understudied compared with HLA-B. In these studies, we show that HLA-A*7401 is associated with favorable viremic control in extended southern African cohorts of >2100 C-clade-infected subjects. We present evidence that HLA-A*7401 operates an effect that is independent of HLA-B*5703, with which it is in linkage disequilibrium in some populations, to mediate lowered viremia. We describe a novel statistical approach to detecting additive effects between class I alleles in control of HIV-1 disease, highlighting improved viremic control in subjects with HLA-A*7401 combined with HLA-B*57. In common with HLA-B alleles that are associated with effective control of viremia, HLA-A*7401 presents highly targeted epitopes in several proteins, including Gag, Pol, Rev, and Nef, of which the Gag epitopes appear immunodominant. We identify eight novel putative HLA-A*7401-restricted epitopes, of which three have been defined to the optimal epitope. In common with HLA-B alleles linked with slow progression, viremic control through an HLA-A*7401-restricted response appears to be associated with the selection of escape mutants within Gag epitopes that reduce viral replicative capacity. These studies highlight the potentially important contribution of an HLA-A allele to immune control of HIV infection, which may have been concealed by a stronger effect mediated by an HLA-B allele with which it is in linkage disequilibrium. In addition, these studies identify a factor contributing to different HIV disease outcomes in individuals expressing HLA-B*5703.
OriginalsprogEngelsk
TidsskriftJournal of Immunology
Vol/bind186
Udgave nummer10
Sider (fra-til)5675-86
Antal sider12
ISSN1550-6606
DOI
StatusUdgivet - 2011

ID: 40354105