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Basic Characteristics of Mutations
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Mutation Site
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M230I |
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Mutation Site Sentence
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Table 2.Prevalence of NNRTI-Associated DRMs among PLWH receiving RPV as their only NNRTI. |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
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RT |
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Standardized Encoding Gene
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gag-pol:155348
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Genotype/Subtype
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HIV-1 |
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Viral Reference
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-
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Functional Impact and Mechanisms
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Disease
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HIV Infections
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Immune
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- |
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Target Gene
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-
|
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Clinical and Epidemiological Correlations
|
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Clinical Information
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Y |
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Treatment
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NNRTIs |
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Location
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Italy;United States;Portugal;Germany;Russia;Sweden;Netherlands;Luxembourg;Poland;Sweden |
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Literature Information
|
|
PMID
|
39599830
|
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Title
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Spectrum of Non-Nucleoside Reverse Transcriptase Inhibitor-Associated Drug Resistance Mutations in Persons Living with HIV-1 Receiving Rilpivirine
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Author
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Nagarajan P,Zhou J,Di Teodoro G,Incardona F,Seguin-Devaux C,Kaiser R,Abecasis AB,Gomes P,Tao K,Zazzi M,Shafer RW
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Journal
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Viruses
|
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Journal Info
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2024 Oct 31;16(11):1715
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Abstract
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INTRODUCTION: Few data are currently available on the nonnucleoside reverse transcriptase (RT) inhibitors (NNRTI) resistance mutations selected in persons living with HIV-1 (PLWH) who develop virological failure while receiving rilpivirine (RPV). METHODS: We analyzed pooled HIV-1 RT genotypic data from 280 PLWH in the multicenter EuResist database and 115 PLWH in the Stanford HIV Drug Resistance Database (HIVDB) who received RPV as their only NNRTI. RESULTS: Among the 395 PLWH receiving RPV, 180 (45.6%) had one or more NNRTI-associated DRMs. Overall, 44 NNRTI-associated DRMs were identified, including 26 that occurred in two or more PLWHs. Seven mutations had a prevalence >/=10% among the 180 PLWH with one or more NNRTI-associated DRM: E138K (32.2%), V90I (25.0%), K101E (17.8%), Y181C (17.2%), E138A (13.9%), H221Y (12.2%), and K103N (10.6%). Y181C was significantly more likely to co-occur with K101E, V179F, H221Y, and M230L. Ten novel non-polymorphic mutations at known NNRTI-associated mutation positions were also identified, usually in just one PLWH: L100F, V108A, T139I, P225S, M230V, Y232C, and T240A/I/M/S. CONCLUSIONS: Our analysis extends the spectrum of mutations emerging in PLWH receiving RPV. Additional phenotypic characterization of RPV-selected mutations is necessary to better understand their biological and possible clinical significance.
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Sequence Data
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-
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