Natural Suppression of Human Immunodeficiency Virus Type 1 Replication Is Mediated by Transitional Memory CD8+ T Cells

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Published inJournal of Virology Vol. 85; no. 4; pp. 1696 - 1705
Main Authors Killian, M. Scott, Johnson, Carl, Teque, Fernando, Fujimura, Sue, Levy, Jay A.
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.02.2011
American Society for Microbiology (ASM)
Subjects
Adult
Antigens, CD - metabolism
Apoptosis Regulatory Proteins - metabolism
Biological and medical sciences
CD8-Positive T-Lymphocytes - immunology
Female
Fundamental and applied biological sciences. Psychology
HIV Infections - immunology
HIV Infections - virology
HIV-1 - immunology
HIV-1 - physiology
Human immunodeficiency virus 1
Humans
Immunologic Memory - immunology
Lymphocyte Activation
Male
Microbiology
Middle Aged
Miscellaneous
Pathogenesis and Immunity
Programmed Cell Death 1 Receptor
T-Lymphocyte Subsets - immunology
Viral Load
Virology
Virus Replication - immunology
Virus
HIV-1 virus
Suppression
Retroviridae
Replication
Human immunodeficiency virus
Lentivirus
CD8 T lymphocyte
Online AccessGet full text
ISSN0022-538X
1098-5514
1098-5514
DOI10.1128/JVI.01120-10

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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 HIV replication is suppressed in vitro by a CD8(+) cell noncytotoxic antiviral response (CNAR). This activity directly correlates with an asymptomatic clinical state. The objective of this study was to identify the phenotype of CD8(+) cell subsets having strong CNAR activity. CD8(+) cell subset frequencies and CNAR levels were measured for human immunodeficiency virus (HIV)-uninfected individuals and three groups of HIV type 1 (HIV-1)-infected individuals: asymptomatic individuals with low-level viremia (vHIV), antiretroviral-drug-treated subjects with undetectable virus levels (TxHIV), and therapy-naïve aviremic elite controllers (EC). CD8(+) cells from the vHIV individuals exhibited the highest HIV-suppressing activity and had elevated frequencies of CD45RA(-) CD27(+) and PD-1(+) (CD279(+)) cells. Functional assessments of CD8(+) cells sorted into distinct subsets established that maximal CNAR activity was mediated by CD45RA(-) CCR7(-) CD27(+) and PD-1(+) CD8(+) cells. T cell receptor (TCR) repertoire profiles of CD8(+) cell subsets having strong CNAR activity exhibited increased perturbations in comparison to those of inactive subsets. Together, these studies suggest that CNAR is driven by HIV replication and that this antiviral activity is associated with oligoclonally expanded activated CD8(+) cells expressing PD-1 and having a transitional memory cell phenotype. The findings better describe the identity of CD8(+) cells showing CNAR and should facilitate the evaluation of this important immune response in studies of HIV pathogenesis, resistance to infection, and vaccine development.
HIV replication is suppressed in vitro by a CD8+ cell noncytotoxic antiviral response (CNAR). This activity directly correlates with an asymptomatic clinical state. The objective of this study was to identify the phenotype of CD8+ cell subsets having strong CNAR activity. CD8+ cell subset frequencies and CNAR levels were measured for human immunodeficiency virus (HIV)-uninfected individuals and three groups of HIV type 1 (HIV-1)-infected individuals: asymptomatic individuals with low-level viremia (vHIV), antiretroviral-drug-treated subjects with undetectable virus levels (TxHIV), and therapy-naieve aviremic elite controllers (EC). CD8+ cells from the vHIV individuals exhibited the highest HIV-suppressing activity and had elevated frequencies of CD45RA- CD27+ and PD-1+ (CD279+) cells. Functional assessments of CD8+ cells sorted into distinct subsets established that maximal CNAR activity was mediated by CD45RA- CCR7- CD27+ and PD-1+ CD8+ cells. T cell receptor (TCR) repertoire profiles of CD8+ cell subsets having strong CNAR activity exhibited increased perturbations in comparison to those of inactive subsets. Together, these studies suggest that CNAR is driven by HIV replication and that this antiviral activity is associated with oligoclonally expanded activated CD8+ cells expressing PD-1 and having a transitional memory cell phenotype. The findings better describe the identity of CD8+ cells showing CNAR and should facilitate the evaluation of this important immune response in studies of HIV pathogenesis, resistance to infection, and vaccine development.
HIV replication is suppressed in vitro by a CD8 + cell noncytotoxic antiviral response (CNAR). This activity directly correlates with an asymptomatic clinical state. The objective of this study was to identify the phenotype of CD8 + cell subsets having strong CNAR activity. CD8 + cell subset frequencies and CNAR levels were measured for human immunodeficiency virus (HIV)-uninfected individuals and three groups of HIV type 1 (HIV-1)-infected individuals: asymptomatic individuals with low-level viremia (vHIV), antiretroviral-drug-treated subjects with undetectable virus levels (TxHIV), and therapy-naïve aviremic elite controllers (EC). CD8 + cells from the vHIV individuals exhibited the highest HIV-suppressing activity and had elevated frequencies of CD45RA − CD27 + and PD-1 + (CD279 + ) cells. Functional assessments of CD8 + cells sorted into distinct subsets established that maximal CNAR activity was mediated by CD45RA − CCR7 − CD27 + and PD-1 + CD8 + cells. T cell receptor (TCR) repertoire profiles of CD8 + cell subsets having strong CNAR activity exhibited increased perturbations in comparison to those of inactive subsets. Together, these studies suggest that CNAR is driven by HIV replication and that this antiviral activity is associated with oligoclonally expanded activated CD8 + cells expressing PD-1 and having a transitional memory cell phenotype. The findings better describe the identity of CD8 + cells showing CNAR and should facilitate the evaluation of this important immune response in studies of HIV pathogenesis, resistance to infection, and vaccine development.
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       
HIV replication is suppressed in vitro by a CD8(+) cell noncytotoxic antiviral response (CNAR). This activity directly correlates with an asymptomatic clinical state. The objective of this study was to identify the phenotype of CD8(+) cell subsets having strong CNAR activity. CD8(+) cell subset frequencies and CNAR levels were measured for human immunodeficiency virus (HIV)-uninfected individuals and three groups of HIV type 1 (HIV-1)-infected individuals: asymptomatic individuals with low-level viremia (vHIV), antiretroviral-drug-treated subjects with undetectable virus levels (TxHIV), and therapy-naïve aviremic elite controllers (EC). CD8(+) cells from the vHIV individuals exhibited the highest HIV-suppressing activity and had elevated frequencies of CD45RA(-) CD27(+) and PD-1(+) (CD279(+)) cells. Functional assessments of CD8(+) cells sorted into distinct subsets established that maximal CNAR activity was mediated by CD45RA(-) CCR7(-) CD27(+) and PD-1(+) CD8(+) cells. T cell receptor (TCR) repertoire profiles of CD8(+) cell subsets having strong CNAR activity exhibited increased perturbations in comparison to those of inactive subsets. Together, these studies suggest that CNAR is driven by HIV replication and that this antiviral activity is associated with oligoclonally expanded activated CD8(+) cells expressing PD-1 and having a transitional memory cell phenotype. The findings better describe the identity of CD8(+) cells showing CNAR and should facilitate the evaluation of this important immune response in studies of HIV pathogenesis, resistance to infection, and vaccine development.HIV replication is suppressed in vitro by a CD8(+) cell noncytotoxic antiviral response (CNAR). This activity directly correlates with an asymptomatic clinical state. The objective of this study was to identify the phenotype of CD8(+) cell subsets having strong CNAR activity. CD8(+) cell subset frequencies and CNAR levels were measured for human immunodeficiency virus (HIV)-uninfected individuals and three groups of HIV type 1 (HIV-1)-infected individuals: asymptomatic individuals with low-level viremia (vHIV), antiretroviral-drug-treated subjects with undetectable virus levels (TxHIV), and therapy-naïve aviremic elite controllers (EC). CD8(+) cells from the vHIV individuals exhibited the highest HIV-suppressing activity and had elevated frequencies of CD45RA(-) CD27(+) and PD-1(+) (CD279(+)) cells. Functional assessments of CD8(+) cells sorted into distinct subsets established that maximal CNAR activity was mediated by CD45RA(-) CCR7(-) CD27(+) and PD-1(+) CD8(+) cells. T cell receptor (TCR) repertoire profiles of CD8(+) cell subsets having strong CNAR activity exhibited increased perturbations in comparison to those of inactive subsets. Together, these studies suggest that CNAR is driven by HIV replication and that this antiviral activity is associated with oligoclonally expanded activated CD8(+) cells expressing PD-1 and having a transitional memory cell phenotype. The findings better describe the identity of CD8(+) cells showing CNAR and should facilitate the evaluation of this important immune response in studies of HIV pathogenesis, resistance to infection, and vaccine development.
HIV replication is suppressed in vitro by a CD8 + cell noncytotoxic antiviral response (CNAR). This activity directly correlates with an asymptomatic clinical state. The objective of this study was to identify the phenotype of CD8 + cell subsets having strong CNAR activity. CD8 + cell subset frequencies and CNAR levels were measured for human immunodeficiency virus (HIV)-uninfected individuals and three groups of HIV type 1 (HIV-1)-infected individuals: asymptomatic individuals with low-level viremia (vHIV), antiretroviral-drug-treated subjects with undetectable virus levels (TxHIV), and therapy-naïve aviremic elite controllers (EC). CD8 + cells from the vHIV individuals exhibited the highest HIV-suppressing activity and had elevated frequencies of CD45RA − CD27 + and PD-1 + (CD279 + ) cells. Functional assessments of CD8 + cells sorted into distinct subsets established that maximal CNAR activity was mediated by CD45RA − CCR7 − CD27 + and PD-1 + CD8 + cells. T cell receptor (TCR) repertoire profiles of CD8 + cell subsets having strong CNAR activity exhibited increased perturbations in comparison to those of inactive subsets. Together, these studies suggest that CNAR is driven by HIV replication and that this antiviral activity is associated with oligoclonally expanded activated CD8 + cells expressing PD-1 and having a transitional memory cell phenotype. The findings better describe the identity of CD8 + cells showing CNAR and should facilitate the evaluation of this important immune response in studies of HIV pathogenesis, resistance to infection, and vaccine development.
Author M. Scott Killian
Jay A. Levy
Carl Johnson
Fernando Teque
Sue Fujimura
AuthorAffiliation Department of Medicine, University of California San Francisco, San Francisco, California 94143
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Issue 4
Keywords Virus
HIV-1 virus
Suppression
Retroviridae
Replication
Human immunodeficiency virus
Lentivirus
CD8 T lymphocyte
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SSID ssj0014464
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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...
HIV replication is suppressed in vitro by a CD8 + cell noncytotoxic antiviral response (CNAR). This activity directly correlates with an asymptomatic clinical...
HIV replication is suppressed in vitro by a CD8(+) cell noncytotoxic antiviral response (CNAR). This activity directly correlates with an asymptomatic clinical...
HIV replication is suppressed in vitro by a CD8+ cell noncytotoxic antiviral response (CNAR). This activity directly correlates with an asymptomatic clinical...
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StartPage 1696
SubjectTerms Adult
Antigens, CD - metabolism
Apoptosis Regulatory Proteins - metabolism
Biological and medical sciences
CD8-Positive T-Lymphocytes - immunology
Female
Fundamental and applied biological sciences. Psychology
HIV Infections - immunology
HIV Infections - virology
HIV-1 - immunology
HIV-1 - physiology
Human immunodeficiency virus 1
Humans
Immunologic Memory - immunology
Lymphocyte Activation
Male
Microbiology
Middle Aged
Miscellaneous
Pathogenesis and Immunity
Programmed Cell Death 1 Receptor
T-Lymphocyte Subsets - immunology
Viral Load
Virology
Virus Replication - immunology
Title Natural Suppression of Human Immunodeficiency Virus Type 1 Replication Is Mediated by Transitional Memory CD8+ T Cells
URI http://jvi.asm.org/content/85/4/1696.abstract
https://www.ncbi.nlm.nih.gov/pubmed/21147929
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https://www.proquest.com/docview/904467471
https://pubmed.ncbi.nlm.nih.gov/PMC3028886
Volume 85
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