Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage.

One of the most important genetic factors known to affect the rate of disease progression in HIV-infected individuals is the genotype at the Class I Human Leukocyte Antigen (HLA) locus, which determines the HIV peptides targeted by cytotoxic T-lymphocytes (CTLs). Individuals with HLA-B*57 or B*5801...

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Autores principales: Denis R Chopera, Zenda Woodman, Koleka Mlisana, Mandla Mlotshwa, Darren P Martin, Cathal Seoighe, Florette Treurnicht, Debra Assis de Rosa, Winston Hide, Salim Abdool Karim, Clive M Gray, Carolyn Williamson, CAPRISA 002 Study Team
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Publicado: Public Library of Science (PLoS) 2008
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Acceso en línea:https://doaj.org/article/c930c4d75daf4947b374aacfb0fc4d67
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spelling oai:doaj.org-article:c930c4d75daf4947b374aacfb0fc4d672021-11-25T05:46:39ZTransmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage.1553-73661553-737410.1371/journal.ppat.1000033https://doaj.org/article/c930c4d75daf4947b374aacfb0fc4d672008-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18369479/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374One of the most important genetic factors known to affect the rate of disease progression in HIV-infected individuals is the genotype at the Class I Human Leukocyte Antigen (HLA) locus, which determines the HIV peptides targeted by cytotoxic T-lymphocytes (CTLs). Individuals with HLA-B*57 or B*5801 alleles, for example, target functionally important parts of the Gag protein. Mutants that escape these CTL responses may have lower fitness than the wild-type and can be associated with slower disease progression. Transmission of the escape variant to individuals without these HLA alleles is associated with rapid reversion to wild-type. However, the question of whether infection with an escape mutant offers an advantage to newly infected hosts has not been addressed. Here we investigate the relationship between the genotypes of transmitted viruses and prognostic markers of disease progression and show that infection with HLA-B*57/B*5801 escape mutants is associated with lower viral load and higher CD4+ counts.Denis R ChoperaZenda WoodmanKoleka MlisanaMandla MlotshwaDarren P MartinCathal SeoigheFlorette TreurnichtDebra Assis de RosaWinston HideSalim Abdool KarimClive M GrayCarolyn WilliamsonCAPRISA 002 Study TeamPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 4, Iss 3, p e1000033 (2008)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Denis R Chopera
Zenda Woodman
Koleka Mlisana
Mandla Mlotshwa
Darren P Martin
Cathal Seoighe
Florette Treurnicht
Debra Assis de Rosa
Winston Hide
Salim Abdool Karim
Clive M Gray
Carolyn Williamson
CAPRISA 002 Study Team
Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage.
description One of the most important genetic factors known to affect the rate of disease progression in HIV-infected individuals is the genotype at the Class I Human Leukocyte Antigen (HLA) locus, which determines the HIV peptides targeted by cytotoxic T-lymphocytes (CTLs). Individuals with HLA-B*57 or B*5801 alleles, for example, target functionally important parts of the Gag protein. Mutants that escape these CTL responses may have lower fitness than the wild-type and can be associated with slower disease progression. Transmission of the escape variant to individuals without these HLA alleles is associated with rapid reversion to wild-type. However, the question of whether infection with an escape mutant offers an advantage to newly infected hosts has not been addressed. Here we investigate the relationship between the genotypes of transmitted viruses and prognostic markers of disease progression and show that infection with HLA-B*57/B*5801 escape mutants is associated with lower viral load and higher CD4+ counts.
format article
author Denis R Chopera
Zenda Woodman
Koleka Mlisana
Mandla Mlotshwa
Darren P Martin
Cathal Seoighe
Florette Treurnicht
Debra Assis de Rosa
Winston Hide
Salim Abdool Karim
Clive M Gray
Carolyn Williamson
CAPRISA 002 Study Team
author_facet Denis R Chopera
Zenda Woodman
Koleka Mlisana
Mandla Mlotshwa
Darren P Martin
Cathal Seoighe
Florette Treurnicht
Debra Assis de Rosa
Winston Hide
Salim Abdool Karim
Clive M Gray
Carolyn Williamson
CAPRISA 002 Study Team
author_sort Denis R Chopera
title Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage.
title_short Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage.
title_full Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage.
title_fullStr Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage.
title_full_unstemmed Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage.
title_sort transmission of hiv-1 ctl escape variants provides hla-mismatched recipients with a survival advantage.
publisher Public Library of Science (PLoS)
publishDate 2008
url https://doaj.org/article/c930c4d75daf4947b374aacfb0fc4d67
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