Immune Escape Precedes Breakthrough Human Immunodeficiency Virus Type 1 Viremia and Broadening of the Cytotoxic T-Lymphocyte Response in an HLA-B27-Positive Long-Term-Nonprogressing Child

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Published inJournal of Virology Vol. 78; no. 16; pp. 8927 - 8930
Main Authors FEENEY, M. E, TANG, Y, ROOSEVELT, K. A, LESLIE, A. J, MCINTOSH, K, KARTHAS, N, WALKER, B. D, GOULDER, P. J. R
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.08.2004
Subjects
Amino Acid Sequence
Biological and medical sciences
Child
Disease Progression
Epitopes, T-Lymphocyte - chemistry
Epitopes, T-Lymphocyte - genetics
Fundamental and applied biological sciences. Psychology
HIV Infections - immunology
HIV Infections - virology
HIV Long-Term Survivors
HIV-1 - genetics
HIV-1 - immunology
HLA-B27 Antigen - metabolism
Human immunodeficiency virus 1
Human viral diseases
Humans
Immunodominant Epitopes - chemistry
Immunodominant Epitopes - genetics
Infectious diseases
Medical sciences
Microbiology
Miscellaneous
Molecular Sequence Data
Mutation
Pathogenesis and Immunity
T-Lymphocytes, Cytotoxic - immunology
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
Viremia - immunology
Viremia - virology
Virology
Human
Immunopathology
HLA-System
Microbiology
HIV-1 virus
Viremia
Retroviridae
Cytotoxicity
AIDS
Lentivirus
Immune deficiency
Long term
Virology
Infection
Virus
Viral disease
T-Lymphocyte
Human immunodeficiency virus
Child
Cytotoxic T lymphocyte
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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 The emergence of cytotoxic T-lymphocyte (CTL) escape mutations in human immunodeficiency virus type 1 (HIV-1) proteins has been anecdotally associated with progression to AIDS, but it has been difficult to determine whether viral mutation is the cause or the result of increased viral replication. Here we describe a perinatally HIV-infected child who maintained a plasma viral load of <400 copies/ml for almost a decade until a nonbinding escape mutation emerged within the immunodominant CTL epitope. The child subsequently experienced a reemergence of HIV-1 viremia accompanied by a marked increase in the number of CTL epitopes targeted. This temporal pattern suggests that CD8 escape can play a causal role in the loss of immune control.
ABSTRACT The emergence of cytotoxic T-lymphocyte (CTL) escape mutations in human immunodeficiency virus type 1 (HIV-1) proteins has been anecdotally associated with progression to AIDS, but it has been difficult to determine whether viral mutation is the cause or the result of increased viral replication. Here we describe a perinatally HIV-infected child who maintained a plasma viral load of <400 copies/ml for almost a decade until a nonbinding escape mutation emerged within the immunodominant CTL epitope. The child subsequently experienced a reemergence of HIV-1 viremia accompanied by a marked increase in the number of CTL epitopes targeted. This temporal pattern suggests that CD8 escape can play a causal role in the loss of immune control.
The emergence of cytotoxic T-lymphocyte (CTL) escape mutations in human immunodeficiency virus type 1 (HIV-1) proteins has been anecdotally associated with progression to AIDS, but it has been difficult to determine whether viral mutation is the cause or the result of increased viral replication. Here we describe a perinatally HIV-infected child who maintained a plasma viral load of <400 copies/ml for almost a decade until a nonbinding escape mutation emerged within the immunodominant CTL epitope. The child subsequently experienced a reemergence of HIV-1 viremia accompanied by a marked increase in the number of CTL epitopes targeted. This temporal pattern suggests that CD8 escape can play a causal role in the loss of immune control.
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       
Author M. E. Feeney
K. McIntosh
B. D. Walker
Y. Tang
P. J. R. Goulder
N. Karthas
A. J. Leslie
K. A. Roosevelt
AuthorAffiliation Partners AIDS Research Center and Infectious Disease Division, Massachusetts General Hospital and Harvard Medical School, 1 Children's Hospital, Boston, Massachusetts, 2 Department of Paediatrics, Nuffield Department of Medicine, University of Oxford, Oxford, United Kingdom, 3 Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 4
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Issue 16
Keywords Human
Immunopathology
HLA-System
Microbiology
HIV-1 virus
Viremia
Retroviridae
Cytotoxicity
AIDS
Lentivirus
Immune deficiency
Long term
Virology
Infection
Virus
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Human immunodeficiency virus
Child
Cytotoxic T lymphocyte
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Corresponding author. Mailing address: Partners AIDS Research Center, 5th Floor, 149 13th St., Charlestown, MA 02129. Phone: (617) 726-6126. Fax: (617) 726-5411. E-mail: mfeeney@partners.org.
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PublicationTitle Journal of Virology
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PublicationYear 2004
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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...
The emergence of cytotoxic T-lymphocyte (CTL) escape mutations in human immunodeficiency virus type 1 (HIV-1) proteins has been anecdotally associated with...
ABSTRACT The emergence of cytotoxic T-lymphocyte (CTL) escape mutations in human immunodeficiency virus type 1 (HIV-1) proteins has been anecdotally associated...
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SubjectTerms Amino Acid Sequence
Biological and medical sciences
Child
Disease Progression
Epitopes, T-Lymphocyte - chemistry
Epitopes, T-Lymphocyte - genetics
Fundamental and applied biological sciences. Psychology
HIV Infections - immunology
HIV Infections - virology
HIV Long-Term Survivors
HIV-1 - genetics
HIV-1 - immunology
HLA-B27 Antigen - metabolism
Human immunodeficiency virus 1
Human viral diseases
Humans
Immunodominant Epitopes - chemistry
Immunodominant Epitopes - genetics
Infectious diseases
Medical sciences
Microbiology
Miscellaneous
Molecular Sequence Data
Mutation
Pathogenesis and Immunity
T-Lymphocytes, Cytotoxic - immunology
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
Viremia - immunology
Viremia - virology
Virology
Title Immune Escape Precedes Breakthrough Human Immunodeficiency Virus Type 1 Viremia and Broadening of the Cytotoxic T-Lymphocyte Response in an HLA-B27-Positive Long-Term-Nonprogressing Child
URI http://jvi.asm.org/content/78/16/8927.abstract
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