Blinded, Multicenter Comparison of Methods To Detect a Drug-Resistant Mutant of Human Immunodeficiency Virus Type 1 at Low Frequency | Zendy

Elias K. Halvas | Zendy; Grace M. Aldrovandi | Zendy; Peter Balfe | Zendy; Ingrid A. Beck | Zendy; Valerie F. Boltz | Zendy; John M. Coffin | Zendy; Lisa M. Frenkel | Zendy; J. Darren Hazelwood | Zendy; Victoria A. Johnson | Zendy; Mary F. Kearney | Zendy; Andrea Kovács | Zendy; Daniel R. Kuritzkes | Zendy; Karin J. Metzner | Zendy; Dwight V. Nissley | Zendy; Marek Nowicki | Zendy; Sarah Palmer | Zendy; Rainer Ziermann | Zendy; Yuqi Zhao | Zendy; Cheryl Jennings | Zendy; James W. Bremer | Zendy; Donald Brambilla | Zendy; John W. Mellors | Zendy

Open Access

Blinded, Multicenter Comparison of Methods To Detect a Drug-Resistant Mutant of Human Immunodeficiency Virus Type 1 at Low Frequency

Author(s) -

Elias K. Halvas,

Grace M. Aldrovandi,

Peter Balfe,

Ingrid A. Beck,

Valerie F. Boltz,

John M. Coffin,

Lisa M. Frenkel,

J. Darren Hazelwood,

Victoria A. Johnson,

Mary F. Kearney,

Andrea Kovács,

Daniel R. Kuritzkes,

Karin J. Metzner,

Dwight V. Nissley,

Marek Nowicki,

Sarah Palmer,

Rainer Ziermann,

Yuqi Zhao,

Cheryl Jennings,

James W. Bremer,

Donald Brambilla,

John W. Mellors

Publication year - 2006

Publication title -

journal of clinical microbiology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.349

H-Index - 255

eISSN - 1070-633X

pISSN - 0095-1137

DOI - 10.1128/jcm.00449-06

Subject(s) - reverse transcriptase , mutant , biology , virology , virus , wild type , asparagine , genetics , polymerase chain reaction , gene , amino acid

We determined the abilities of 10 technologies to detect and quantify a common drug-resistant mutant of human immunodeficiency virus type 1 (lysine to asparagine at codon 103 of the reverse transcriptase) using a blinded test panel containing mutant-wild-type mixtures ranging from 0.01% to 100% mutant. Two technologies, allele-specific reverse transcriptase PCR and a Ty1HRT yeast system, could quantify the mutant down to 0.1 to 0.4%. These technologies should help define the impact of low-frequency drug-resistant mutants on response to antiretroviral therapy.

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