In Vivo Emergence of Vicriviroc Resistance in a Human Immunodeficiency Virus Type 1 Subtype C-Infected Subject

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Published inJournal of Virology Vol. 82; no. 16; pp. 8210 - 8214
Main Authors Tsibris, Athe M. N., Sagar, Manish, Gulick, Roy M., Su, Zhaohui, Hughes, Michael, Greaves, Wayne, Subramanian, Mani, Flexner, Charles, Giguel, Françoise, Leopold, Kay E., Coakley, Eoin, Kuritzkes, Daniel R.
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.08.2008
American Society for Microbiology (ASM)
Subjects
Amino Acid Sequence
Anti-HIV Agents - pharmacology
Antibodies, Monoclonal - chemistry
Biological and medical sciences
CCR5 Receptor Antagonists
DNA Primers - chemistry
Drug Resistance, Viral
Fundamental and applied biological sciences. Psychology
HIV Infections - drug therapy
HIV Infections - pathology
HIV-1 - metabolism
Humans
Microbiology
Miscellaneous
Molecular Sequence Data
Piperazines - pharmacology
Pyrimidines - pharmacology
Receptors, CCR5 - metabolism
Recombination, Genetic
Sequence Homology, Amino Acid
Time Factors
Vaccines and Antiviral Agents
Viral Envelope Proteins - chemistry
Virology
Human
Immunopathology
Antiretroviral agent
HIV-1 virus
Retroviridae
AIDS
Immune deficiency
Lentivirus
Virology
Infection
Virus
Resistance
In vivo
Viral disease
Antiviral
Vicriviroc
Human immunodeficiency virus
Subtype
Online AccessGet full text
ISSN0022-538X
1098-5514
1070-6321
1098-5514
DOI10.1128/JVI.00444-08

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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 Little is known about the in vivo development of resistance to human immunodeficiency virus type 1 (HIV-1) CCR5 antagonists. We studied 29 subjects with virologic failure from a phase IIb study of the CCR5 antagonist vicriviroc (VCV) and identified one individual with HIV-1 subtype C who developed VCV resistance. Studies with chimeric envelopes demonstrated that changes within the V3 loop were sufficient to confer VCV resistance. Resistant virus showed VCV-enhanced replication, cross-resistance to another CCR5 antagonist, TAK779, and increased sensitivity to aminooxypentane-RANTES and the CCR5 monoclonal antibody HGS004. Pretreatment V3 loop sequences reemerged following VCV discontinuation, implying that VCV resistance has associated fitness costs.
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       
Little is known about the in vivo development of resistance to human immunodeficiency virus type 1 (HIV-1) CCR5 antagonists. We studied 29 subjects with virologic failure from a phase IIb study of the CCR5 antagonist vicriviroc (VCV) and identified one individual with HIV-1 subtype C who developed VCV resistance. Studies with chimeric envelopes demonstrated that changes within the V3 loop were sufficient to confer VCV resistance. Resistant virus showed VCV-enhanced replication, cross-resistance to another CCR5 antagonist, TAK779, and increased sensitivity to aminooxypentane-RANTES and the CCR5 monoclonal antibody HGS004. Pretreatment V3 loop sequences reemerged following VCV discontinuation, implying that VCV resistance has associated fitness costs.Little is known about the in vivo development of resistance to human immunodeficiency virus type 1 (HIV-1) CCR5 antagonists. We studied 29 subjects with virologic failure from a phase IIb study of the CCR5 antagonist vicriviroc (VCV) and identified one individual with HIV-1 subtype C who developed VCV resistance. Studies with chimeric envelopes demonstrated that changes within the V3 loop were sufficient to confer VCV resistance. Resistant virus showed VCV-enhanced replication, cross-resistance to another CCR5 antagonist, TAK779, and increased sensitivity to aminooxypentane-RANTES and the CCR5 monoclonal antibody HGS004. Pretreatment V3 loop sequences reemerged following VCV discontinuation, implying that VCV resistance has associated fitness costs.
Author Daniel R. Kuritzkes
Wayne Greaves
Charles Flexner
Françoise Giguel
Mani Subramanian
Michael Hughes
Eoin Coakley
Athe M. N. Tsibris
Roy M. Gulick
Kay E. Leopold
Manish Sagar
Zhaohui Su
AuthorAffiliation Massachusetts General Hospital, Boston, Massachusetts, 1 Harvard Medical School, Boston, Massachusetts, 2 Brigham and Women's Hospital, Boston, Massachusetts, 3 Weill Medical College, Cornell University, New York, New York, 4 Harvard School of Public Health, Boston, Massachusetts, 5 Schering-Plough Research Institute, Kenilworth, New Jersey, 6 Human Genome Sciences, Rockville, Maryland, 7 Johns Hopkins University, Baltimore, Maryland, 8 Harvard University, Cambridge, Massachusetts, 9 Monogram Biosciences, South San Francisco, California 10
AuthorAffiliation_xml – name: Massachusetts General Hospital, Boston, Massachusetts, 1 Harvard Medical School, Boston, Massachusetts, 2 Brigham and Women's Hospital, Boston, Massachusetts, 3 Weill Medical College, Cornell University, New York, New York, 4 Harvard School of Public Health, Boston, Massachusetts, 5 Schering-Plough Research Institute, Kenilworth, New Jersey, 6 Human Genome Sciences, Rockville, Maryland, 7 Johns Hopkins University, Baltimore, Maryland, 8 Harvard University, Cambridge, Massachusetts, 9 Monogram Biosciences, South San Francisco, California 10
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Issue 16
Keywords Human
Immunopathology
Antiretroviral agent
HIV-1 virus
Retroviridae
AIDS
Immune deficiency
Lentivirus
Virology
Infection
Virus
Resistance
In vivo
Viral disease
Antiviral
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Corresponding author. Mailing address: Section of Retroviral Therapeutics, Brigham and Women's Hospital, 65 Landsdowne St., Room 435, Cambridge, MA 02139. Phone: (617) 768-8371. Fax: (617) 768-8738. E-mail: dkuritzkes@partners.org
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Little is known about the in vivo development of resistance to human immunodeficiency virus type 1 (HIV-1) CCR5 antagonists. We studied 29 subjects with...
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SubjectTerms Amino Acid Sequence
Anti-HIV Agents - pharmacology
Antibodies, Monoclonal - chemistry
Biological and medical sciences
CCR5 Receptor Antagonists
DNA Primers - chemistry
Drug Resistance, Viral
Fundamental and applied biological sciences. Psychology
HIV Infections - drug therapy
HIV Infections - pathology
HIV-1 - metabolism
Humans
Microbiology
Miscellaneous
Molecular Sequence Data
Piperazines - pharmacology
Pyrimidines - pharmacology
Receptors, CCR5 - metabolism
Recombination, Genetic
Sequence Homology, Amino Acid
Time Factors
Vaccines and Antiviral Agents
Viral Envelope Proteins - chemistry
Virology
Title In Vivo Emergence of Vicriviroc Resistance in a Human Immunodeficiency Virus Type 1 Subtype C-Infected Subject
URI http://jvi.asm.org/content/82/16/8210.abstract
https://www.ncbi.nlm.nih.gov/pubmed/18495779
https://www.proquest.com/docview/69367032
https://pubmed.ncbi.nlm.nih.gov/PMC2519584
https://www.ncbi.nlm.nih.gov/pmc/articles/2519584
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