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Title: Discordances between interpretation algorithms for genotypic resistance to protease and reverse transcriptase inhibitors of human immunodeficiency virus are subtype dependent
Authors: Snoeck, Joke ×
Kantor, Rami
Shafer, Robert W
Van Laethem, Kristel
Deforche, Koen
Carvalho, Ana Patricia
Wynhoven, Brian
Soares, Marcelo A
Cane, Patricia
Clarke, John
Pillay, Candice
Sirivichayakul, Sunee
Ariyoshi, Koya
Holguin, Africa
Rudich, Hagit
Rodrigues, Rosangela
Bouzas, Maria Belen
Brun-Vézinet, Françoise
Reid, Caroline
Cahn, Pedro
Brigido, Luis Fernando
Grossman, Zehava
Soriano, Vincent
Sugiura, Wataru
Phanuphak, Praphan
Morris, Lynn
Weber, Jonathan
Pillay, Deenan
Tanuri, Amilcar
Harrigan, Richard P
Camacho, Ricardo
Schapiro, Jonathan M
Katzenstein, David
Vandamme, Anne-Mieke #
Issue Date: Feb-2006
Publisher: American Society for Microbiology (ASM)
Series Title: Antimicrobial Agents and Chemotherapy vol:50 issue:2 pages:694-701
Abstract: The major limitation of drug resistance genotyping for human immunodeficiency virus remains the interpretation of the results. We evaluated the concordance in predicting therapy response between four different interpretation algorithms (Rega 6.3, HIVDB-08/04, ANRS [07/04], and VGI 8.0). Sequences were gathered through a worldwide effort to establish a database of non-B subtype sequences, and demographic and clinical information about the patients was gathered. The most concordant results were found for nonnucleoside reverse transcriptase (RT) inhibitors (93%), followed by protease inhibitors (84%) and nucleoside RT inhibitor (NRTIs) (76%). For therapy-naive patients, for nelfinavir, especially for subtypes C and G, the discordances were driven mainly by the protease (PRO) mutational pattern 82I/V + 63P + 36I/V for subtype C and 82I + 63P + 36I + 20I for subtype G. Subtype F displayed more discordances for ritonavir in untreated patients due to the combined presence of PRO 20R and 10I/V. In therapy-experienced patients, subtype G displayed a lot of discordances for saquinavir and indinavir due to mutational patterns involving PRO 90 M and 82I. Subtype F had more discordance for nelfinavir attributable to the presence of PRO 88S and 82A + 54V. For the NRTIs lamivudine and emtricitabine, CRF01_AE had more discordances than subtype B due to the presence of RT mutational patterns 65R + 115 M and 118I + 215Y, respectively. Overall, the different algorithms agreed well on the level of resistance scored, but some of the discordances could be attributed to specific (subtype-dependent) combinations of mutations. It is not yet known whether therapy response is subtype dependent, but the advice given to clinicians based on a genotypic interpretation algorithm differs according to the subtype.
URI: 
ISSN: 0066-4804
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Clinical and Epidemiological Virology (Rega Institute)
× corresponding author
# (joint) last author

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