コーパス検索結果 (left1)
通し番号をクリックするとPubMedの該当ページを表示します
1 NNRTI concentrations were measured by sensitive high-per
2 NNRTI regimen choice and preexisting NNRTI-resistant min
3 NNRTI resistance was particularly high in children expos
4 NNRTIs are noncompetitive inhibitors that bind in a hydr
5 NNRTIs are recommended components of highly active antir
6 NNRTIs modestly affect liver stage Plasmodium parasites,
7 9%] of 597 patients without TAMs; p<0.0001), NNRTI resistance (107 [93%] vs 462 [77%]; p<0.0001), and
8 ruption, 22/131 (16.8%) patients showed >/=1 NNRTI-RAM, including eight patients with NNRTI-RAMs dete
11 children randomised to WHO-recommended 2NRTI+NNRTI long-term ART, 308/378 (81%) monitored with CD4 co
13 MTCT), a substantial proportion will acquire NNRTI-resistant HIV, potentially compromising response t
14 s) were continued for median nine days after NNRTI interruption, did not prevent NNRTI-RAMs, but incr
18 NNRTI strategy"), all individuals who had an NNRTI-resistance mutation identified by ultra-deep seque
22 be a suitable alternative for patients on an NNRTI with emtricitabine and tenofovir regimen consideri
25 drug resistance, primarily due to M184V and NNRTI mutations, has been identified in 60%-72%, althoug
26 z-containing therapy in both NNRTI-naive and NNRTI-experienced patients and to determine their associ
27 vity against multidrug (IC(50) = 5.9 nM) and NNRTI (IC(50) = 12.9 nM) resistant viruses than parent n
35 Resistance-associated mutations (RAMs) and NNRTI concentrations were studied in plasma from 132 pat
37 hinge points for this essential motion, and NNRTIs therefore act as "molecular wedges," sterically b
40 ecular mechanisms of resistance to NRTIs and NNRTIs, and their complex relationships, may help in des
46 At week 48, the overall difference between NNRTI- and PI-based regimens in selection of any major N
47 difference in prevalence of M184V/I between NNRTI and PI (crude unweighted prevalence 3.2% vs 1.4%);
48 To explore potential interactions between NNRTI and INSTI resistance mutations, we investigated th
49 nalysis to evaluate the relationship between NNRTI-resistant minority variants and the likelihood and
50 ltidrug efavirenz-containing therapy in both NNRTI-naive and NNRTI-experienced patients and to determ
51 f sub-Saharan Africa; this rise is driven by NNRTI resistance in studies from east and southern Afric
54 the observation that mutant viruses carrying NNRTI plus INSTI resistance mutations had reduced amount
56 ference in prevalence of K65R when comparing NNRTI (1.3%) with PI (0.67%); absolute weighted differen
58 TI) and a TMC-derivative (a diarylpyrimidine NNRTI) linked via a poly(ethylene glycol) (PEG) linker.
59 tance is dependent upon the affinity of each NNRTI to the RT and further influenced by the presence o
60 hus, the development of novel more effective NNRTIs as anti-HIV-1 agents with fewer long-term liabili
61 ce, also reduce RNase H cleavage and enhance NNRTI resistance in the context of the patient RT pol do
64 DR-associated mutations were more common for NNRTIs (5.4%), followed by nucleoside reverse transcript
67 guided design to develop two next-generation NNRTI drug candidates, compounds I and II, which are mem
68 o examine the prevalence of 1(st)-generation NNRTI resistance in Europe, the United States (US), and
70 ome a barrier to the use of 1(st)-generation NNRTIs and the increased costs associated with regimen f
73 everse-transcriptase inhibitors (hereafter, "NNRTI strategy"), all individuals who had an NNRTI-resis
74 ariable logistic regression analysis, higher NNRTI minority variant copy numbers, non-white race, and
75 of an RT-DNA-nevirapine complex revealed how NNRTI binding forbids RT from forming a polymerase compe
76 scence anisotropy approaches to discover how NNRTIs modulate the intra-molecular conformational chang
77 e were detected more often at study entry in NNRTI-experienced patients than NNRTI-naive patients by
79 TI-resistant variants were more prevalent in NNRTI-experienced patients and were associated with redu
80 tant with NNRTI BP mutants further increases NNRTI resistance from 3- to 30-fold, supporting the role
81 eoside reverse-transcriptase (RT) inhibitor (NNRTI) resistance mutations (from 0.3% to 7.1%), particu
82 eoside reverse transcriptase (RT) inhibitor (NNRTI) that efficiently inhibits HIV-1 resistant to firs
83 nnucleoside reverse transcriptase inhibitor (NNRTI) and a common component of clinically approved ant
84 -nucleoside reverse transcriptase inhibitor (NNRTI) based FDC of rilpivirine plus tenofovir disoproxi
86 -nucleoside reverse transcriptase inhibitor (NNRTI) efavirenz (EFV) showed subunit-specific perturbat
87 nnucleoside reverse transcriptase inhibitor (NNRTI) MIV-150 in carrageenan reduced vaginal infection
88 nnucleoside reverse transcriptase inhibitor (NNRTI) mutations (2.9%) and protease inhibitor mutations
89 nnucleoside reverse-transcriptase inhibitor (NNRTI) mutations (hazard ratio, 77.5; 95% confidence int
91 -nucleoside reverse transcriptase inhibitor (NNRTI) or who are on a multitablet NNRTI-containing regi
92 nnucleoside reverse-transcriptase inhibitor (NNRTI) regimen in Africa and Asia, comparing the genotyp
93 -nucleoside reverse-transcriptase inhibitor (NNRTI) resistance in people initiating antiretroviral th
94 nnucleoside reverse transcriptase inhibitor (NNRTI) resistance mutations are associated with an incre
95 nnucleoside reverse-transcriptase inhibitor (NNRTI) resistance, and 4.2% had protease inhibitor (PI)
98 -nucleoside reverse transcriptase inhibitor (NNRTI), rilpivirine (TMC278; Tibotec Pharmaceuticals, Co
99 nnucleoside reverse transcriptase inhibitor (NNRTI)- or lopinavir/ritonavir (LPV/r)-based regimen wer
100 nnucleoside reverse-transcriptase inhibitor (NNRTI)-based (hazard ratio, 7.10; 95% confidence interva
102 -nucleoside reverse transcriptase inhibitor (NNRTI)-based highly active antiretroviral therapy (HAART
103 -nucleoside reverse-transcriptase inhibitor (NNRTI)-based regimen to one including a protease inhibit
104 nnucleoside reverse transcriptase inhibitor (NNRTI)-based regimens with a backbone of tenofovir/emtri
106 nnucleoside reverse-transcriptase inhibitor (NNRTI)-based therapy suggest that 76%-90% of living pati
107 -nucleoside reverse transcriptase inhibitor (NNRTI)-resistant mutants have been shown to emerge after
108 nnucleoside reverse-transcriptase inhibitor (NNRTI)-resistant variants at the initiation of multidrug
109 nnucleoside reverse-transcriptase inhibitor (NNRTI)-resistant variants on the risk of virologic failu
112 -nucleoside reverse transcriptase inhibitor (NNRTI; nevirapine or efavirenz) in sub-Saharan Africa.
113 is pocket binds nonnucleoside RT inhibitors (NNRTI); therefore, NNRTI sensitivity was used to probe e
114 oside reverse transcriptase (RT) inhibitors (NNRTI) and integrase (IN) strand transfer inhibitors (IN
115 nucleoside reverse transcriptase inhibitors (NNRTI) 3 and 4 with HIV-1 reverse transcriptase (RT).
116 nucleoside reverse transcriptase inhibitors (NNRTI) efavirenz (EFV) and nevirapine (NVP) in first-lin
117 nucleoside reverse transcriptase inhibitors (NNRTI) in east Africa (36% per year [21 to 52]; p<0.0001
118 nucleoside reverse transcriptase inhibitors (NNRTI), which are similar in structure to earlier descri
119 nucleoside reverse transcriptase inhibitors (NNRTI; Efavirenz, Etravirine, Rilpivirine and Nevirapine
121 elopment of novel non-nucleoside inhibitors (NNRTIs) with activity against variants of HIV reverse tr
122 sms compared to nonnucleoside RT inhibitors (NNRTIs) and nucleoside/nucleotide RT inhibitors (NRTIs).
125 nucleoside and non-nucleoside RT inhibitors (NNRTIs) by mechanisms that are not well understood.
128 s resistant to non-nucleoside RT inhibitors (NNRTIs), suggesting the involvement of binding site(s) o
130 oside reverse transcriptase (RT) inhibitors (NNRTIs) are hindered by their unsatisfactory pharmacokin
131 oside reverse transcriptase (RT) inhibitors (NNRTIs) are important components of multidrug therapy fo
132 oside reverse transcriptase (RT) inhibitors (NNRTIs) are routinely used to treat HIV-1 infection, yet
134 nucleoside reverse transcriptase inhibitors (NNRTIs) are potent and commonly prescribed antiviral age
135 nucleoside reverse transcriptase inhibitors (NNRTIs) are usually part of first-line treatment regimen
136 nucleoside reverse transcriptase inhibitors (NNRTIs) efavirenz and nevirapine are commonly used in fi
137 nucleoside reverse transcriptase inhibitors (NNRTIs) has been associated with baseline human immunode
138 nucleoside reverse transcriptase inhibitors (NNRTIs) have been observed among previously untreated in
139 nucleoside reverse transcriptase inhibitors (NNRTIs) have inherent flexibility, helping to maintain a
140 nucleoside reverse transcriptase inhibitors (NNRTIs) in pregnant and breastfeeding women will result
142 nucleoside reverse transcriptase inhibitors (NNRTIs) might compromise HIV control in low-income and m
143 nucleoside reverse transcriptase inhibitors (NNRTIs) play a central role in the treatment of AIDS, bu
144 nucleoside reverse transcriptase inhibitors (NNRTIs) reached 45% (95% CI: 27-64%) in 2015, all based
145 nucleoside reverse transcriptase inhibitors (NNRTIs) that target the viral polymerase have been a key
146 nucleoside reverse-transcriptase inhibitors (NNRTIs) was observed among VCT clients aged 18-21 years.
147 nucleoside reverse transcriptase inhibitors (NNRTIs) with a novel aryl-phospho-indole (APhI) scaffold
148 nucleoside reverse transcriptase inhibitors (NNRTIs), and protease inhibitors (PIs) among primigravid
149 nucleoside reverse transcriptase inhibitors (NNRTIs), and their biological activity was evaluated.
150 nucleoside reverse transcriptase inhibitors (NNRTIs), nucleotide substrates, Mg ions, temperature, an
153 nucleoside reverse transcriptase inhibitors [NNRTIs]), integrase strand transfer inhibitors, and viru
154 nucleoside reverse transcriptase inhibitors [NNRTIs], and 60.3% [P = 0.94] in patients receiving NNRT
155 dictive of reduced susceptibility to initial NNRTI-based regimens: 4.5% and 6.5% of patient isolates
157 up O lineage resulted in a loss of intrinsic NNRTI resistance and was accompanied by fitness loss.
158 resistance mutations, particularly involving NNRTI resistance, were significantly associated with a d
159 ons in both groups, suggesting that isolated NNRTI-associated transmitted drug resistance may not be
160 r individuals to whom variants with isolated NNRTI-associated drug resistance were transmitted are at
161 ce mutations in 33 individuals with isolated NNRTI-associated transmitted drug resistance and 49 matc
162 alogue mutations (T215F, D67N, K70R, K219Q), NNRTIs (L100I, Y181C, K103N, V108I, Y188L), and PIs (V82
163 g the Incoming Nucleotide Binding, Knuckles, NNRTI Adjacent, and 399 sites, located in the polymerase
165 regimen compared with zidovudine/lamivudine/NNRTI, PI resistance at switch (6.69; 2.49-17.98; P < .0
166 al failure of the WHO-recommended first-line NNRTI-based regimen was higher in the presence of K103N.
167 inst RT variants carrying one of three major NNRTI resistance mutations: K103N, Y181C, or G190A.
170 3.0% and 8.8% having resistance to 1 or more NNRTI or nucleoside reverse transcriptase inhibitors, re
171 nhibitor (NNRTI) or who are on a multitablet NNRTI-containing regimen and want a regimen simplificati
173 ong potential for further development as new NNRTIs for the potential treatment of HIV infection.
174 ent results highlight the chiral IASs as new NNRTIs with improved resistance profile against the muta
177 ological failure during treatment with a non-NNRTI-containing regimen, we identified minority variant
179 The short and practical synthesis of novel NNRTI relies on two sequential Pd-catalyzed aminations a
180 tor (NRTI) mutations; 33 (73%) had non-NRTI (NNRTI) mutations; and 30 (66.7%) had both NRTI and NNRTI
189 se data are promising for the development of NNRTI-containing gels to prevent rectal HIV transmission
190 RTI resistance and also offset the effect of NNRTI resistance mutations thereby restoring NNRTI bindi
193 e detailed understanding of the mechanism of NNRTI inhibition and the effect of binding upon domain m
201 men became cost effective at a prevalence of NNRTI resistance higher than 15%, for cost-effectiveness
204 activity (EC50<1 nM) against a wide range of NNRTI-resistant viruses and a favorable pharmacokinetic
208 l structure data suggest that the binding of NNRTIs forces RT into a wide-open conformation in which
211 fect of the reduction in RNase H cleavage on NNRTI resistance is dependent upon the affinity of each
214 d to either lopinavir-ritonavir-based ART or NNRTI-based ART and were followed for 6 months to 2 year
215 nitiated antiretroviral therapy with a PI or NNRTI and a backbone containing either TDF/FTC or ABC/3T
218 mong studied drugs, Efavirenz, but not other NNRTIs, altered claudin-5 expression, increased endothel
220 these results confirm key predictions of our NNRTI resistance model and provide support for a unifyin
222 ing supports the use of EFV as the preferred NNRTI in first-line treatment regimen for HIV treatment,
225 her, and with the prevalence of pretreatment NNRTI resistance greater than 10%, a policy to measure v
227 In 2016, the prevalence of pretreatment NNRTI resistance was near WHO's 10% threshold for changi
228 respective of the prevalence of pretreatment NNRTI resistance, because of the increased cost of the p
230 ys after NNRTI interruption, did not prevent NNRTI-RAMs, but increased detection of NRTI-RAMs (OR 4.2
231 170 received the study regimen: 86 received NNRTI-based ART, and 84 lopinavir-ritonavir-based ART.
232 lts (55% female) were enrolled: 20 receiving NNRTI-based and 20 receiving LPV/r-based treatment.
233 eligible for ART or were currently receiving NNRTI-based ART were randomly assigned to either lopinav
236 o observed that K103N, a clinically relevant NNRTI resistance mutation, does not prevent binding betw
239 rm high-affinity dead-end complexes, both RT/NNRTI/DNA complexes being unable to bind the incoming nu
247 to emerge after interruption of suppressive NNRTI-based antiretroviral therapy (ART) using routine t
248 udy entry in NNRTI-experienced patients than NNRTI-naive patients by both single-genome sequencing (8
250 e most recent time-based trends suggest that NNRTI-resistance prevalence may be stable or decreasing.
254 e design of more effective inhibitors at the NNRTI site and also drive the identification of novel al
255 and tenofovir (switch group) or continue the NNRTI plus emtricitabine and tenofovir regimen (no-switc
257 ase H cleavage and provide more time for the NNRTI to dissociate from the RT, resulting in the resump
258 We demonstrate that changes distant from the NNRTI binding pocket decrease inhibitor binding (increas
260 cooperative unfolding of a beta-sheet in the NNRTI binding pocket, which was previously observed in u
266 (R))) and an extended release version of the NNRTI nevirapine, (Viramune XR((R))) were recent additio
267 based regimen than among those receiving the NNRTI-based regimen (1.32 vs. 2.25 episodes per person-y
270 th WT RT suggested an optimal binding to the NNRTI binding pocket favoring the high anti-viral potenc
272 ly 600 ns), we have captured RT bound to the NNRTI efavirenz in a closed conformation similar to that
276 everse transcriptase (RT) genotypes with the NNRTI resistance mutations K101E+G190S are highly resist
277 articipants who initiated treatment with the NNRTI strategy, the risk of VF was significantly greater
279 nucleoside RT inhibitors (NNRTI); therefore, NNRTI sensitivity was used to probe enzyme differences i
284 ich CN and RH mutations confer resistance to NNRTIs, we hypothesized that these mutations reduce RNas
288 orable resistance implications of PI- versus NNRTI-based first line therapy, widespread use of PI-bas
289 st likely occurs through a mechanism whereby NNRTIs stimulate priming or elongation of the tRNA.
290 rates <400 copies/ml were 8/13 (61.5%) with NNRTI-RAMs, 7/11 (63.6%) with NRTI-RAMs only, and 51/59
292 ndomized clinical trials comparing bPI- with NNRTI-based first-line antiretroviral therapy regimens u
293 pinavir-ritonavir-based ART as compared with NNRTI-based ART reduced the incidence of malaria by 41%,
296 d 0.17 (95% CI 0.03, 1.15) for patients with NNRTI-RAMs or NRTI-RAMs only respectively vs. those with
297 d correlate the detection of resistance with NNRTI concentrations after treatment interruption and vi
298 215F/Y) were found to be highly stable, with NNRTI and PI mutations being relatively less persistent.
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。