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Basic Characteristics of Mutations
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Mutation Site
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K20T |
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Mutation Site Sentence
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For NNRTI, the most common drug resistance-associated mutations were K103N (35.9%), V179D (33.3%), Y181C (12.8%), and L100I (12.8%), while for PI, they were K20T (7.7%) and L90M (5.1%). One of the three patients (33.3%) who failed Triumeq treatment had E138K, G140S, and Q148H INSTI mutations (Figure 4) |
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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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PR |
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Standardized Encoding Gene
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gag-pol
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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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PIs |
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Location
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Taiwan(China) |
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Literature Information
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PMID
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30122963
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Title
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HIV-1 genotypic drug resistance in patients with virological failure to single-tablet antiretroviral regimens in southern Taiwan
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Author
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Tsai HC,Chen IT,Lee SS,Chen YS
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Journal
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Infection and drug resistance
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Journal Info
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2018 Aug 3;11:1061-1071
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Abstract
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PURPOSE: Sparse data are available on the prevalence of resistance among HIV-1-infected patients with virological failure to a single-tablet regimen (STR). This study aimed to evaluate the prevalence of HIV genotypic drug resistance in HIV-1-infected patients with virological failure to STRs in southern Taiwan. PATIENTS AND METHODS: This retrospective study investigated drug resistance in patients with virological failure to STR from January 2016 to September 2017. Antiretroviral resistance mutations were defined using the 2017 International AIDS Society-USA HIV drug resistance algorithm, and drug resistance was compared using the HIVdb program of the Stanford University HIV Drug Resistance Database. Variables between resistance and non-resistance groups were compared. RESULTS: Thirty-nine HIV-1-infected patients with treatment failure were tested for resistance, of whom 89% were infected by men who have sex with men. Subtype B HIV-1 strains were found in 90% of the patients. Eight patients were treatment naive and initiated STRs, while 31 patients experienced treatment failure after switching to STRs. Eighty-seven percent of the patients harbored any of four classes of resistance (nucleoside reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors (PIs), and integrase strand transfer inhibitors). The prevalence rates of nucleoside reverse transcriptase inhibitor, non-nucleoside reverse transcriptase inhibitor, PI, and integrase strand transfer inhibitor resistance were 72%, 82%, 10%, and 3%, respectively. Patients with PI resistance were more likely to respond to treatment with a non-tenofovir disoproxil fumarate/emtricitabine/efavirenz-based STR (.=0.004) and a longer duration of antiretroviral therapy (101 months [72.0-123.3] vs 11 months [7-44], P=0.007). There were no associations between different STRs and transmission risk factors, HIV subtype, duration of antiretroviral therapy, and resistance to tenofovir disoproxil fumarate. CONCLUSION: A high rate of antiretroviral drug resistance was found in the patients who failed STR treatment. The presence of PI resistance in these patients represented an inappropriate switch from a multiple tablet regimen to an STR. These findings should remind clinicians that detailed drug resistance history and close monitoring are mandatory after switching to an STR.
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Sequence Data
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-
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