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dc.creatorManasa, J
dc.creatorVarghese, V
dc.creatorPond, SLK
dc.creatorRhee, SY
dc.creatorTzou, PL
dc.creatorFessel, WJ
dc.creatorJang, KS
dc.creatorWhite, E
dc.creatorRögnvaldsson, T
dc.creatorKatzenstein, DA
dc.creatorShafer, RW
dc.date.accessioned2021-01-28T21:39:35Z
dc.date.available2021-01-28T21:39:35Z
dc.date.issued2017-12-01
dc.identifier.issn2045-2322
dc.identifier.issn2045-2322
dc.identifier.doihttp://dx.doi.org/10.34944/dspace/5091
dc.identifier.other28912582 (pubmed)
dc.identifier.urihttp://hdl.handle.net/20.500.12613/5109
dc.description.abstract© 2017 The Author(s). Several groups have proposed that genotypic determinants in gag and the gp41 cytoplasmic domain (gp41-CD) reduce protease inhibitor (PI) susceptibility without PI-resistance mutations in protease. However, no gag and gp41-CD mutations definitively responsible for reduced PI susceptibility have been identified in individuals with virological failure (VF) while receiving a boosted PI (PI/r)-containing regimen. To identify gag and gp41 mutations under selective PI pressure, we sequenced gag and/or gp41 in 61 individuals with VF on a PI/r (n = 40) or NNRTI (n = 20) containing regimen. We quantified nonsynonymous and synonymous changes in both genes and identified sites exhibiting signal for directional or diversifying selection. We also used published gag and gp41 polymorphism data to highlight mutations displaying a high selection index, defined as changing from a conserved to an uncommon amino acid. Many amino acid mutations developed in gag and in gp41-CD in both the PI-A nd NNRTI-treated groups. However, in neither gene, were there discernable differences between the two groups in overall numbers of mutations, mutations displaying evidence of diversifying or directional selection, or mutations with a high selection index. If gag and/or gp41 encode PI-resistance mutations, they may not be confined to consistent mutations at a few sites.
dc.format.extent11559-
dc.language.isoen
dc.relation.haspartScientific Reports
dc.relation.isreferencedbySpringer Science and Business Media LLC
dc.rightsCC BY
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectAdult
dc.subjectEvolution, Molecular
dc.subjectFemale
dc.subjectGenotype
dc.subjectHIV Envelope Protein gp41
dc.subjectHIV Infections
dc.subjectHIV Protease Inhibitors
dc.subjectHIV-1
dc.subjectHumans
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectMutation
dc.subjectRitonavir
dc.subjectSelection, Genetic
dc.subjectSequence Analysis, DNA
dc.subjectYoung Adult
dc.subjectgag Gene Products, Human Immunodeficiency Virus
dc.titleEvolution of gag and gp41 in Patients Receiving Ritonavir-Boosted Protease Inhibitors
dc.typeArticle
dc.type.genreJournal Article
dc.relation.doi10.1038/s41598-017-11893-8
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.creator.orcidPond, Sergei L. Kosakovsky|0000-0003-4817-4029
dc.date.updated2021-01-28T21:39:31Z
refterms.dateFOA2021-01-28T21:39:35Z


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