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Basic Characteristics of Mutations
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Mutation Site
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I161X |
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Mutation Site Sentence
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Table 2. Primary and secondary resistance mutations in the Integrase by Sanger population sequencing |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsense mutation |
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Gene/Protein/Region
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IN |
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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 B |
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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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Raltegravir |
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Location
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Spain |
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Literature Information
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PMID
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27177767
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Title
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Usefulness of Integrase resistance testing in proviral HIV-1 DNA in patients with Raltegravir prior failure
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Author
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Fernandez-Caballero JA,Chueca N,Alvarez M,Merida MD,Lopez J,Sanchez JA,Vinuesa D,Martinez MA,Hernandez J,Garcia F
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Journal
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BMC infectious diseases
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Journal Info
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2016 May 13;16:197
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Abstract
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BACKGROUND: In our study, we have hypothesized that proviral DNA may show the history of mutations that emerged at previous failures to a Raltegravir containing regimen, in patients who are currently undetectable and candidates to simplification to a Dolutegravir containing regimen, in order to decide on once a day or twice a day dosing. METHODS: We have performed a pilot, observational, retrospective, non interventional study, including 7 patients infected by HIV-1, all with a history of previous failure to a RAL containing regimen, that were successfully salvaged and had reached viral suppression. A genotypic viral Integrase region study was available for each patient at the moment of RAL failure. After an average (IQR) time of 48 months (29-53) Integrase resistance mutations in proviral DNA were studied. RESULTS: All the patients were infected by HIV-1 B subtypes, with a mean age of 55 (range 43 to 56), originating from Spain, and 4 were women. Median viral load (log) and CD4 count at the moment of the study on proviral DNA was of 1.3 log cp/ml (range 0-1.47) and 765.5 cells/muL (range; 436.75-1023.75). The median time (IQR) between previous failure to RAL and the study on proviral DNA was 48 (29-53) months. At Raltegravir failure, N155H was detected in four patients, and other secondary mutations were detected in five patients (71.4 %). In proviral DNA, N155H was detected by population sequencing in three patients (42.8 %), and UDS demonstrated a 9.77 % relative abundance of N155H in the remaining patient. Sanger sequencing correctly identified all the secondary mutations. CONCLUSION: This is a pilot study that demonstrates the possibility of properly identifying N155H and some secondary mutations 29-53 months after failure.
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Sequence Data
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-
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