Both HLA-B57 and Plasma HIV RNA Levels Contribute to the HIV-Specific CD8+ T Cell Response in HIV Controllers

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Published inJournal of Virology Vol. 88; no. 1; pp. 176 - 187
Main Authors Lécuroux, Camille, Sáez-Cirión, Asier, Girault, Isabelle, Versmisse, Pierre, Boufassa, Faroudy, Avettand-Fenoël, Véronique, Rouzioux, Christine, Meyer, Laurence, Pancino, Gianfranco, Lambotte, Olivier, Sinet, Martine, Venet, Alain
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.01.2014
Subjects
CD8-Positive T-Lymphocytes - immunology
Disease Progression
Enzyme-Linked Immunosorbent Assay
Female
HIV - genetics
HIV - physiology
HIV Infections - immunology
HIV Infections - virology
HLA-B Antigens - blood
Human immunodeficiency virus
Humans
Immunology
Life Sciences
Male
Pathogenesis and Immunity
RNA, Viral - blood
Virus Replication
HIV Infections
CD8-Positive T-Lymphocytes
Virus Replication
HIV
Enzyme-Linked Immunosorbent Assay
RNA
HLA-B Antigens
Humans
Viral
Female
Male
Disease Progression
Online AccessGet full text
ISSN0022-538X
1098-5514
1070-6321
1098-5514
DOI10.1128/JVI.02098-13

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Abstract Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to JVI .asm.org, visit: JVI       
AbstractList CD8+ T cell responses are thought to play an important role during HIV infection, particularly in HIV controllers (HIC) in whom viral replication is spontaneously controlled without any treatment. We have demonstrated that CD8+ T cells from these subjects are able to suppress viral replication in vitro. In parallel, HIV-specific CD8+ responses were shown to be strong and of high quality, with proliferative abilities and cytotoxic capacities, in HIC. The HLA-B*57 allele, which is associated with a better clinical outcome in HIV infection, is overrepresented in HIC. However, we showed that these patients constitute a heterogeneous group that includes subjects who present weak suppression of viral replication in vitro and HIV-specific responses. We performed an extensive study of 101 HIC (49 HLA-B*57+ and 52 HLA-B*57−) to determine the impact of HLA-B*57 on the HIV-specific CD8+ response. The HLA-B*57-restricted response displayed better qualitative features, such as higher functional avidity, higher proliferation capacity, and a higher level of cytokine production, than responses not restricted by HLA-B*57. However, the highest frequencies of HIV-specific CD8+ T cells were observed only in a subset of HLA-B*57+ subjects. They were tightly associated with the ability to suppress viral replication in vitro. In contrast, the subset of HLA-B*57+ subjects with a weak ability to suppress viral replication had significantly lower ultrasensitive viral loads than all the other groups of controllers. In conclusion, both HLA-B*57 and the amount of ultrasensitive viral load seem to play a role in HIV-specific CD8+ T cell responses in HIC.
CD8+ T cell responses are thought to play an important role during HIV infection, particularly in HIV controllers (HIC) in whom viral replication is spontaneously controlled without any treatment. We have demonstrated that CD8+ T cells from these subjects are able to suppress viral replication in vitro. In parallel, HIV-specific CD8+ responses were shown to be strong and of high quality, with proliferative abilities and cytotoxic capacities, in HIC. The HLA-B*57 allele, which is associated with a better clinical outcome in HIV infection, is overrepresented in HIC. However, we showed that these patients constitute a heterogeneous group that includes subjects who present weak suppression of viral replication in vitro and HIV-specific responses. We performed an extensive study of 101 HIC (49 HLA-B*57+ and 52 HLA-B*57-) to determine the impact of HLA-B*57 on the HIV-specific CD8+ response. The HLA-B*57-restricted response displayed better qualitative features, such as higher functional avidity, higher proliferation capacity, and a higher level of cytokine production, than responses not restricted by HLA-B*57. However, the highest frequencies of HIV-specific CD8+ T cells were observed only in a subset of HLA-B*57+ subjects. They were tightly associated with the ability to suppress viral replication in vitro. In contrast, the subset of HLA-B*57+ subjects with a weak ability to suppress viral replication had significantly lower ultrasensitive viral loads than all the other groups of controllers. In conclusion, both HLA-B*57 and the amount of ultrasensitive viral load seem to play a role in HIV-specific CD8+ T cell responses in HIC.
CD8 + T cell responses are thought to play an important role during HIV infection, particularly in HIV controllers (HIC) in whom viral replication is spontaneously controlled without any treatment. We have demonstrated that CD8 + T cells from these subjects are able to suppress viral replication in vitro . In parallel, HIV-specific CD8 + responses were shown to be strong and of high quality, with proliferative abilities and cytotoxic capacities, in HIC. The HLA-B*57 allele, which is associated with a better clinical outcome in HIV infection, is overrepresented in HIC. However, we showed that these patients constitute a heterogeneous group that includes subjects who present weak suppression of viral replication in vitro and HIV-specific responses. We performed an extensive study of 101 HIC (49 HLA-B*57 + and 52 HLA-B*57 − ) to determine the impact of HLA-B*57 on the HIV-specific CD8 + response. The HLA-B*57-restricted response displayed better qualitative features, such as higher functional avidity, higher proliferation capacity, and a higher level of cytokine production, than responses not restricted by HLA-B*57. However, the highest frequencies of HIV-specific CD8 + T cells were observed only in a subset of HLA-B*57 + subjects. They were tightly associated with the ability to suppress viral replication in vitro . In contrast, the subset of HLA-B*57 + subjects with a weak ability to suppress viral replication had significantly lower ultrasensitive viral loads than all the other groups of controllers. In conclusion, both HLA-B*57 and the amount of ultrasensitive viral load seem to play a role in HIV-specific CD8 + T cell responses in HIC.
Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to JVI .asm.org, visit: JVI       
CD8(+) T cell responses are thought to play an important role during HIV infection, particularly in HIV controllers (HIC) in whom viral replication is spontaneously controlled without any treatment. We have demonstrated that CD8(+) T cells from these subjects are able to suppress viral replication in vitro. In parallel, HIV-specific CD8(+) responses were shown to be strong and of high quality, with proliferative abilities and cytotoxic capacities, in HIC. The HLA-B*57 allele, which is associated with a better clinical outcome in HIV infection, is overrepresented in HIC. However, we showed that these patients constitute a heterogeneous group that includes subjects who present weak suppression of viral replication in vitro and HIV-specific responses. We performed an extensive study of 101 HIC (49 HLA-B*57(+) and 52 HLA-B*57(-)) to determine the impact of HLA-B*57 on the HIV-specific CD8(+) response. The HLA-B*57-restricted response displayed better qualitative features, such as higher functional avidity, higher proliferation capacity, and a higher level of cytokine production, than responses not restricted by HLA-B*57. However, the highest frequencies of HIV-specific CD8(+) T cells were observed only in a subset of HLA-B*57(+) subjects. They were tightly associated with the ability to suppress viral replication in vitro. In contrast, the subset of HLA-B*57(+) subjects with a weak ability to suppress viral replication had significantly lower ultrasensitive viral loads than all the other groups of controllers. In conclusion, both HLA-B*57 and the amount of ultrasensitive viral load seem to play a role in HIV-specific CD8(+) T cell responses in HIC.CD8(+) T cell responses are thought to play an important role during HIV infection, particularly in HIV controllers (HIC) in whom viral replication is spontaneously controlled without any treatment. We have demonstrated that CD8(+) T cells from these subjects are able to suppress viral replication in vitro. In parallel, HIV-specific CD8(+) responses were shown to be strong and of high quality, with proliferative abilities and cytotoxic capacities, in HIC. The HLA-B*57 allele, which is associated with a better clinical outcome in HIV infection, is overrepresented in HIC. However, we showed that these patients constitute a heterogeneous group that includes subjects who present weak suppression of viral replication in vitro and HIV-specific responses. We performed an extensive study of 101 HIC (49 HLA-B*57(+) and 52 HLA-B*57(-)) to determine the impact of HLA-B*57 on the HIV-specific CD8(+) response. The HLA-B*57-restricted response displayed better qualitative features, such as higher functional avidity, higher proliferation capacity, and a higher level of cytokine production, than responses not restricted by HLA-B*57. However, the highest frequencies of HIV-specific CD8(+) T cells were observed only in a subset of HLA-B*57(+) subjects. They were tightly associated with the ability to suppress viral replication in vitro. In contrast, the subset of HLA-B*57(+) subjects with a weak ability to suppress viral replication had significantly lower ultrasensitive viral loads than all the other groups of controllers. In conclusion, both HLA-B*57 and the amount of ultrasensitive viral load seem to play a role in HIV-specific CD8(+) T cell responses in HIC.
Author Alain Venet
Laurence Meyer
Asier Sáez-Cirión
Pierre Versmisse
Véronique Avettand-Fenoël
Camille Lécuroux
Christine Rouzioux
Faroudy Boufassa
Martine Sinet
Olivier Lambotte
Isabelle Girault
Gianfranco Pancino
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Issue 1
Keywords HIV Infections
CD8-Positive T-Lymphocytes
Virus Replication
HIV
Enzyme-Linked Immunosorbent Assay
RNA
HLA-B Antigens
Humans
Viral
Female
Male
Disease Progression
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Snippet Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
CD8 + T cell responses are thought to play an important role during HIV infection, particularly in HIV controllers (HIC) in whom viral replication is...
CD8(+) T cell responses are thought to play an important role during HIV infection, particularly in HIV controllers (HIC) in whom viral replication is...
CD8+ T cell responses are thought to play an important role during HIV infection, particularly in HIV controllers (HIC) in whom viral replication is...
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StartPage 176
SubjectTerms CD8-Positive T-Lymphocytes - immunology
Disease Progression
Enzyme-Linked Immunosorbent Assay
Female
HIV - genetics
HIV - physiology
HIV Infections - immunology
HIV Infections - virology
HLA-B Antigens - blood
Human immunodeficiency virus
Humans
Immunology
Life Sciences
Male
Pathogenesis and Immunity
RNA, Viral - blood
Virus Replication
Title Both HLA-B57 and Plasma HIV RNA Levels Contribute to the HIV-Specific CD8+ T Cell Response in HIV Controllers
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https://www.ncbi.nlm.nih.gov/pubmed/24131719
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https://pubmed.ncbi.nlm.nih.gov/PMC3911721
https://jvi.asm.org/content/jvi/88/1/176.full.pdf
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