Примери за използване на Genotypic resistance на Английски и техните преводи на Български
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Genotypic resistance.
Analyses based on genotypic resistance testing.
Five subjects had virologic failure through theend of the study; no phenotypic or genotypic resistance to Genvoya was detected.
Successful genotype, n Genotypic resistance to DOR or control(DRV or EFV) 2(DOR).
Conversions at position 80, 180 and polymorphic positions 91, 229 were always detected in sequences that harboured the M204I mutation that confers genotypic resistance.
Genotypic resistance analyses were conducted on samples with plasma HIV-1 RNA> 1000 copies/ml.
The VIKING-4 study examined dolutegravir(plus optimized background therapy)in subjects with primary genotypic resistance to INIs at Screening in 30 subjects.
Genotypic resistance testing should guide the use of EDURANT(see sections 4.4 and 5.1).
At 48-weeks, a higher proportion of patients receiving APTIVUS/ ritonavir achieved a treatment response in comparison to the comparator protease inhibitor/ ritonavir for nearly all of the possible combinations of genotypic resistance mutations(see table below).
Genotypic resistance: The genetic code of HIV has mutations that are linked to drug resistance. .
Subjects were excluded from the efficacy analysis due to data integrity at one study site*The Genotypic Susceptibility Score(GSS)was defined as the total number of ARTs in BR to which a subject's viral isolate showed susceptibility at baseline based upon genotypic resistance tests.
During Year 2, genotypic resistance to ETV was detected in 2 patients(1.1% cumulative probability of resistance through Year 2).
In the week 96 pooled resistance analysis for patients receiving emtricitabine/tenofovir disoproxil+ rilpivirine hydrochloride in the Phase III clinical studies C209 andC215, there were 78 virologic failure patients with genotypic resistance information available for 71 of those patients.
In the double blind, placebo controlled VIKING-4 study(ING116529), 30 HIV-1 infected,ART-experienced adults with primary genotypic resistance to INIs at Screening, were randomised to receive either dolutegravir 50 mg twice daily or placebo with the current failing regimen for 7 days followed by an open label phase with all subjects receiving dolutegravir.
Genotypic resistance test was performed in study NV-02B-007(GLOBE; n= 680) in patients with virological rebound(confirmed increase of≥ 1 log10 copies/ml HBV DNA from nadir).
RESIST-1 and RESIST-2 are ongoing, randomised, open-label, multicentre studies in HIV-positive, triple-class experienced patients, evaluating treatment with APTIVUS co-administered with low dose ritonavir(500 mg/ 200 mg twice daily) plus an optimised background regimen(OBR)individually defined for each patient based on genotypic resistance testing and patient history.
Some genotypic resistance data indicate that in most patients failing NNRTI, viral strains express cross-resistance to the other NNRTIs.
Patients were required to have a baseline HIV-1 RNA concentration of at least 1500 copies/ml, were stratified by age(2 to< 6 years, 6 to< 12 years and 12 to 18 years) and randomized to receive one of two tipranavir with ritonavir dose regimens: 375 mg/m2/150 mg/m dose, compared to the 290 mg/m2/115 mg/m2 dose, plus background therapy of at least two nonprotease inhibitor antiretroviral medicinal products,optimized using baseline genotypic resistance testing.
Through Week 96, genotypic resistance testing results were available from 25 patients in the QD group and 26 patients in the BID group who had incomplete virologic response.
Through Week 48, genotypic resistance testing results were available from 75 patients in the QD group and 75 patients in the BID group who had incomplete virologic response.
Cumulative genotypic resistance rates were also assessed by applying a mathematical model where only patients with undetectable HBV DNA at the beginning of the respective year are considered.
Genotypic resistance to efavirenz, predominantly the K103N mutation, developed in virus from 13/19(68%) patients in the emtricitabine/tenofovir disoproxil/efavirenz group and in virus from 21/29(72%) patients in the comparative group.
A documented absence of genotypic resistance(prior to starting first therapy) to doravirine, lamivudine, and tenofovir was part of the inclusion criteria for patients who switched from a PI- or INI-based regimen.
Genotypic resistance to efavirenz, predominantly the K103N mutation, developed in virus from 13/19(68%) patients in the efavirenz+ emtricitabine+ tenofovir disoproxil group and in virus from 21/29(72%) patients in the efavirenz+ lamivudine/zidovudine group.
Protease inhibitor resistance was defined as genotypic resistance to atazanavir or either component of the local NRTI backbone based on the criteria of 1 any major mutations: I50L, I84V, N88S and 2≥ 2 of the following minor or cross resistant mutations: M46I/L, G48V, I54L/V/M/T/A, V82A/T/FI, L90M, V32I.
Genotypic Entecavir Resistance Through Year 5, Lamivudine-Refractory Studies Year 1 Year 2 Year 3a.
OSS: combined genotypic and phenotypic resistance(Monogram Biosciences Net Assessment).
The BR was selected by the investigator based on genotypic/phenotypic resistance testing and prior antiretroviral treatment history.