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1                                              NNRTI concentrations were measured by sensitive high-per
2                                              NNRTI PDR would continue to increase if DTG-based ART wa
3                                              NNRTI regimen choice and preexisting NNRTI-resistant min
4                                              NNRTI resistance prior to treatment is associated with l
5                                              NNRTI resistance was particularly high in children expos
6                                              NNRTIs are recommended components of highly active antir
7                                              NNRTIs modestly affect liver stage Plasmodium parasites,
8 icipants, the prevalence of SDRMs was 11.0%, NNRTI mutations 8.2%, NRTI mutations 4.5%, and PI mutati
9 9%] of 597 patients without TAMs; p<0.0001), NNRTI resistance (107 [93%] vs 462 [77%]; p<0.0001), and
10 ruption, 22/131 (16.8%) patients showed >/=1 NNRTI-RAM, including eight patients with NNRTI-RAMs dete
11 tions, compared to the use of 2 NRTIs plus 1 NNRTI.
12 hiral indolyarylsulfones (IASs) as new HIV-1 NNRTIs.
13 children randomised to WHO-recommended 2NRTI+NNRTI long-term ART, 308/378 (81%) monitored with CD4 co
14 MTCT), a substantial proportion will acquire NNRTI-resistant HIV, potentially compromising response t
15 s) were continued for median nine days after NNRTI interruption, did not prevent NNRTI-RAMs, but incr
16                             Four weeks after NNRTI interruption, 19/31 (61.3%) and 34/39 (87.2%) pati
17 d in cellulo antiretroviral activity against NNRTI-resistant strains.
18 nt with a first-line treatment containing an NNRTI and two NRTIs, had virological failure (confirmed
19 m the polymerase site; however, unlike in an NNRTI-bound state in which structural elements of RT res
20 ch a switch compared with continuation of an NNRTI-containing regimen.
21 50 copies per mL for at least 6 months on an NNRTI plus emtricitabine and tenofovir regimen.
22 apy after first-line virologic failure on an NNRTI regimen.
23 be a suitable alternative for patients on an NNRTI with emtricitabine and tenofovir regimen consideri
24 08.2; P<.0001), while protease inhibitor and NNRTI replacement rates were similar.
25  drug resistance, primarily due to M184V and NNRTI mutations, has been identified in 60%-72%, althoug
26 vity against multidrug (IC(50) = 5.9 nM) and NNRTI (IC(50) = 12.9 nM) resistant viruses than parent n
27              Prior exposure to both NRTI and NNRTI and confirmed virologic failure on a PI-containing
28 DR to PI and NRTI was seen in 1.6%, NRTI and NNRTI in 3.4%, and triple class TDR in 0.9%.
29  mutations; and 30 (66.7%) had both NRTI and NNRTI mutations.
30 ptase (RT) mutation associated with NRTI and NNRTI resistance, respectively.
31 in drug-resistance patterns in both NRTI and NNRTI were observed by site.
32                                  Both PI and NNRTI use was associated with increases in APRI over tim
33 ed in gag and in gp41-CD in both the PI- and NNRTI-treated groups.
34   Resistance-associated mutations (RAMs) and NNRTI concentrations were studied in plasma from 132 pat
35 individuals received boosted ARVs (-24%) and NNRTIs (-13%) but the use of comedications was higher.
36 mplexes is hindered by a kinetic barrier and NNRTIs mostly interact with free RT.
37  reverse transcriptase inhibitors (NRTIs and NNRTIs).
38 ecular mechanisms of resistance to NRTIs and NNRTIs, and their complex relationships, may help in des
39  rilpivirine, the most recently FDA-approved NNRTI, bear a cyanovinylphenyl (CVP) group.
40 nd have lower cytotoxicity than the approved NNRTI drugs efavirenz and rilpivirine.
41 defined mutation, of which 98% (120/122) are NNRTI mutations.
42 -Saharan Africa at any prevalence of pre-ART NNRTI resistance.
43 are started on or switched to DTG-based ART, NNRTI PDR would reach 25.9% in 2040.
44 the risk of viral failure at week 48 between NNRTI and bPI (P = .19).
45   At week 48, the overall difference between NNRTI- and PI-based regimens in selection of any major N
46  difference in prevalence of M184V/I between NNRTI and PI (crude unweighted prevalence 3.2% vs 1.4%);
47    To explore potential interactions between NNRTI and INSTI resistance mutations, we investigated th
48 nalysis to evaluate the relationship between NNRTI-resistant minority variants and the likelihood and
49 f sub-Saharan Africa; this rise is driven by NNRTI resistance in studies from east and southern Afric
50 tance to nevirapine or efavirenz imparted by NNRTI mutations.
51 mpound I and efavirenz, the standard of care NNRTI.
52 the observation that mutant viruses carrying NNRTI plus INSTI resistance mutations had reduced amount
53                             We characterized NNRTI and TMP-SMX effects on Plasmodium liver stages in
54 deficiency Virus (HIV)-1 and the most common NNRTI-resistant variants, and has a favorable and unique
55 ference in prevalence of K65R when comparing NNRTI (1.3%) with PI (0.67%); absolute weighted differen
56 TI) and a TMC-derivative (a diarylpyrimidine NNRTI) linked via a poly(ethylene glycol) (PEG) linker.
57 hus, the development of novel more effective NNRTIs as anti-HIV-1 agents with fewer long-term liabili
58 etween RT and IN mutations are important for NNRTI and INSTI resistance and viral fitness.
59 pecific rates ranged from 10.0% to 12.8% for NNRTIs, 4.1% to 8.1% for nucleoside RT inhibitors (NRTIs
60 DR-associated mutations were more common for NNRTIs (5.4%), followed by nucleoside reverse transcript
61 gravir gained 6.0 kg, compared to 2.6 kg for NNRTIs (P < .05), and 0.5 kg for elvitegravir (P < .05).
62 e patterns on susceptibility was largest for NNRTIs.
63                                         Four NNRTI SDRMs-K101E, K103N, Y181C, and G190A-accounted for
64 guided design to develop two next-generation NNRTI drug candidates, compounds I and II, which are mem
65 o examine the prevalence of 1(st)-generation NNRTI resistance in Europe, the United States (US), and
66 inhibits HIV-1 resistant to first generation NNRTIs.
67 ome a barrier to the use of 1(st)-generation NNRTIs and the increased costs associated with regimen f
68               Resistance to 1(st)-generation NNRTIs is found among treated and untreated HIV-infected
69 ighly efficient DABOs as "second generation" NNRTIs.
70 n which more than 10% of ART initiators have NNRTI resistance.
71 ariable logistic regression analysis, higher NNRTI minority variant copy numbers, non-white race, and
72 of an RT-DNA-nevirapine complex revealed how NNRTI binding forbids RT from forming a polymerase compe
73 scence anisotropy approaches to discover how NNRTIs modulate the intra-molecular conformational chang
74 ugh 2013, driven primarily by an increase in NNRTI resistance.
75 introducing DTG would lead to a reduction in NNRTI PDR in all scenarios if ART initiators are started
76 of RT bound to a nonnucleoside RT inhibitor (NNRTI) and dsDNA; a hyperextended thumb conformation hel
77 ]; P < .001) and nonnucleoside RT inhibitor (NNRTI)-associated TDR (OR, 1.11 per year [95% CI, 1.08-1
78 n a TDF/XTC plus nonnucleoside RT inhibitor (NNRTI)-containing regimen.
79 eoside reverse-transcriptase (RT) inhibitor (NNRTI) resistance mutations (from 0.3% to 7.1%), particu
80 eoside reverse transcriptase (RT) inhibitor (NNRTI) that efficiently inhibits HIV-1 resistant to firs
81 -nucleoside reverse transcriptase inhibitor (NNRTI) at codons Lys103Asn, Tyr181Cys, Gly190Ala, and to
82 -nucleoside reverse transcriptase inhibitor (NNRTI) based FDC of rilpivirine plus tenofovir disoproxi
83 -nucleoside reverse transcriptase inhibitor (NNRTI) binding site.
84 -nucleoside reverse transcriptase inhibitor (NNRTI) efavirenz (EFV) showed subunit-specific perturbat
85 nnucleoside reverse transcriptase inhibitor (NNRTI) mutations (2.9%) and protease inhibitor mutations
86 nnucleoside reverse-transcriptase inhibitor (NNRTI) mutations (hazard ratio, 77.5; 95% confidence int
87 -nucleoside reverse transcriptase inhibitor (NNRTI) or 3 NRTIs as long-term ART.
88 -nucleoside reverse transcriptase inhibitor (NNRTI) or who are on a multitablet NNRTI-containing regi
89 -nucleoside reverse transcriptase inhibitor (NNRTI) plus two NRTIs has failed.
90 nnucleoside reverse-transcriptase inhibitor (NNRTI) regimen in Africa and Asia, comparing the genotyp
91 -nucleoside reverse-transcriptase inhibitor (NNRTI) resistance in people initiating antiretroviral th
92 nnucleoside reverse transcriptase inhibitor (NNRTI) resistance mutations are associated with an incre
93 nnucleoside reverse-transcriptase inhibitor (NNRTI) resistance, and 4.2% had protease inhibitor (PI)
94 -nucleoside reverse transcriptase inhibitor (NNRTI) resistance.
95 nnucleoside reverse transcriptase inhibitor (NNRTI) resistance.
96 -nucleoside reverse-transcriptase inhibitor (NNRTI), is active against wild-type Human Immunodeficien
97 rus (HIV)-1 reverse transcriptase inhibitor (NNRTI), was safe and effective in preventing HIV-1 infec
98 nnucleoside reverse transcriptase inhibitor (NNRTI)- or lopinavir/ritonavir (LPV/r)-based regimen wer
99 nnucleoside reverse-transcriptase inhibitor (NNRTI)-based (hazard ratio, 7.10; 95% confidence interva
100 nnucleoside reverse transcriptase inhibitor (NNRTI)-based ART between January 2007 and June 2016 were
101 nnucleoside reverse-transcriptase inhibitor (NNRTI)-based ART.
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
105 nnucleoside reverse transcriptase inhibitor (NNRTI)-based regimens.
106 nnucleoside reverse-transcriptase inhibitor (NNRTI)-based therapy suggest that 76%-90% of living pati
107 nnucleoside reverse-transcriptase inhibitor (NNRTI)-containing regimen.
108 -nucleoside reverse transcriptase inhibitor (NNRTI)-resistant mutants have been shown to emerge after
109 -nucleoside reverse transcriptase inhibitor (NNRTI).
110 nnucleoside reverse transcriptase inhibitor (NNRTI).
111 nnucleoside reverse transcriptase inhibitor (NNRTI)/nucleoside reverse transcriptase inhibitor PDR vs
112 nnucleoside reverse transcriptase inhibitor (NNRTI; N = 52) or protease inhibitor (PI; N = 42).
113 -nucleoside reverse transcriptase inhibitor (NNRTI; nevirapine or efavirenz) in sub-Saharan Africa.
114 oside reverse transcriptase (RT) inhibitors (NNRTI) and integrase (IN) strand transfer inhibitors (IN
115 nucleoside reverse transcriptase inhibitors (NNRTI) and transitioning to dolutegravir as part of a mo
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 nnucleosidereverse transcriptase inhibitors (NNRTI) SDRMs (1 K101E, 2 K103N) and 1 protease inhibitor
119 nucleoside reverse transcriptase inhibitors (NNRTI), which are similar in structure to earlier descri
120 nucleoside reverse transcriptase inhibitors (NNRTI), with dolutegravir and bictegravir associated wit
121 nucleoside reverse transcriptase inhibitors (NNRTI; Efavirenz, Etravirine, Rilpivirine and Nevirapine
122  (NRTIs) and five non-nucleoside inhibitors (NNRTIs) are approved HIV-1 drugs.
123 elopment of novel non-nucleoside inhibitors (NNRTIs) with activity against variants of HIV reverse tr
124 sms compared to nonnucleoside RT inhibitors (NNRTIs) and nucleoside/nucleotide RT inhibitors (NRTIs).
125                Non-nucleoside RT inhibitors (NNRTIs) are a class of highly specific drugs which bind
126 n of RT and of non-nucleoside RT inhibitors (NNRTIs) by isothermal titration calorimetry (ITC).
127 de (NRTIs) and non-nucleoside RT inhibitors (NNRTIs) when combined with certain mutations.
128 s resistant to non-nucleoside RT inhibitors (NNRTIs), suggesting the involvement of binding site(s) o
129 he discovery of nonnucleoside RT inhibitors (NNRTIs).
130 oside reverse transcriptase (RT) inhibitors (NNRTIs) are hindered by their unsatisfactory pharmacokin
131 oside reverse transcriptase (RT) inhibitors (NNRTIs) are routinely used to treat HIV-1 infection, yet
132 nucleoside reverse transcriptase inhibitors (NNRTIs) (32%) based regimens.
133 nucleoside reverse transcriptase inhibitors (NNRTIs) and 2 protease inhibitors (PIs).
134 nucleoside reverse transcriptase inhibitors (NNRTIs) are usually part of first-line treatment regimen
135 nucleoside reverse transcriptase inhibitors (NNRTIs) efavirenz and nevirapine are commonly used in fi
136 nucleoside reverse transcriptase inhibitors (NNRTIs) has been associated with baseline human immunode
137 nucleoside reverse transcriptase inhibitors (NNRTIs) have been observed among previously untreated in
138 nucleoside reverse transcriptase inhibitors (NNRTIs) in pregnant and breastfeeding women will result
139 nucleoside reverse transcriptase inhibitors (NNRTIs) measured in the population starting ART.
140 nucleoside reverse transcriptase inhibitors (NNRTIs) might compromise HIV control in low-income and m
141 nucleoside reverse transcriptase inhibitors (NNRTIs) play a central role in the treatment of AIDS, bu
142 nucleoside reverse transcriptase inhibitors (NNRTIs) reached 45% (95% CI: 27-64%) in 2015, all based
143 nucleoside reverse transcriptase inhibitors (NNRTIs) that target the viral polymerase have been a key
144 nucleoside reverse transcriptase inhibitors (NNRTIs) threatens the success of the global scale-up of
145 nucleoside reverse-transcriptase inhibitors (NNRTIs) was observed among VCT clients aged 18-21 years.
146 nucleoside reverse transcriptase inhibitors (NNRTIs) with a novel aryl-phospho-indole (APhI) scaffold
147 nucleoside reverse transcriptase inhibitors (NNRTIs), and protease inhibitors (PIs) among primigravid
148 nucleoside reverse transcriptase inhibitors (NNRTIs), and their biological activity was evaluated.
149 nucleoside reverse transcriptase inhibitors (NNRTIs), nucleoside reverse transcriptase inhibitors (NR
150 nucleoside reverse transcriptase inhibitors (NNRTIs), nucleoside reverse transcriptase inhibitors (NR
151 nucleoside reverse transcriptase inhibitors (NNRTIs), with dolutegravir and bictegravir associated wi
152 nucleoside reverse transcriptase inhibitors (NNRTIs).
153 nucleoside reverse transcriptase inhibitors (NNRTIs).
154 nucleoside reverse transcriptase inhibitors [NNRTIs]), integrase strand transfer inhibitors, and viru
155 dictive of reduced susceptibility to initial NNRTI-based regimens: 4.5% and 6.5% of patient isolates
156 low-up, 100/158 (63%) participants initiated NNRTI-containing ART (dapivirine: 39/65; placebo: 61/93)
157 ons in both groups, suggesting that isolated NNRTI-associated transmitted drug resistance may not be
158 r individuals to whom variants with isolated NNRTI-associated drug resistance were transmitted are at
159 ce mutations in 33 individuals with isolated NNRTI-associated transmitted drug resistance and 49 matc
160 alogue mutations (T215F, D67N, K70R, K219Q), NNRTIs (L100I, Y181C, K103N, V108I, Y188L), and PIs (V82
161 g the Incoming Nucleotide Binding, Knuckles, NNRTI Adjacent, and 399 sites, located in the polymerase
162              Three of these sites (Knuckles, NNRTI Adjacent, and Incoming Nucleotide Binding) are inh
163  regimen compared with zidovudine/lamivudine/NNRTI, PI resistance at switch (6.69; 2.49-17.98; P < .0
164 al failure of the WHO-recommended first-line NNRTI-based regimen was higher in the presence of K103N.
165 inst RT variants carrying one of three major NNRTI resistance mutations: K103N, Y181C, or G190A.
166 3.0% and 8.8% having resistance to 1 or more NNRTI or nucleoside reverse transcriptase inhibitors, re
167 nhibitor (NNRTI) or who are on a multitablet NNRTI-containing regimen and want a regimen simplificati
168 re 1.3, 1.9, and 2.2 years in the ART-naive, NNRTI, and PI groups, respectively (P = .01).
169 ong potential for further development as new NNRTIs for the potential treatment of HIV infection.
170 ent results highlight the chiral IASs as new NNRTIs with improved resistance profile against the muta
171 ce in untreated patients and impact on newer NNRTIs.
172 ological failure during treatment with a non-NNRTI-containing regimen, we identified minority variant
173 ological failure during treatment with a non-NNRTI-containing regimen.
174   The short and practical synthesis of novel NNRTI relies on two sequential Pd-catalyzed aminations a
175 tor (NRTI) mutations; 33 (73%) had non-NRTI (NNRTI) mutations; and 30 (66.7%) had both NRTI and NNRTI
176 ingly, two subjects had major DRMs to NRTIs, NNRTIs, and 4 mutations in the Gag P2/NC CS.
177 lass TDR was 10.0%, 5.1%, and 1.6% to NRTIs, NNRTIs, and PIs.
178            Triple-class resistance to NRTIs, NNRTIs, and PR inhibitors was observed in 24 (53%) patie
179 nucleotide analog (NRTI) and non-nucleoside (NNRTI) drugs used in treating HIV-1 infections.
180 C was received by 67% of PI users and 69% of NNRTI users.
181 103N, Y181C, and G190A-accounted for >80% of NNRTI-associated TDR in all regions and subtypes.
182                      In SSA and SSEA, 89% of NNRTI SDRMs were associated with high-level resistance t
183 s show that, compared to the continuation of NNRTI-based ART, introducing DTG would lead to a reducti
184                                The degree of NNRTI and NRTI resistance after first-line virologic fai
185 RTI resistance and also offset the effect of NNRTI resistance mutations thereby restoring NNRTI bindi
186 reased risk of resistance-related failure of NNRTI/NRTI second-line regimens.
187              However, there was no impact of NNRTI PDR alone.
188                      After the initiation of NNRTI-containing ART, dapivirine and placebo participant
189 men, DTG-based ART could reduce the level of NNRTI PDR from 52.4% (without DTG) to 10.4% (with univer
190                               High levels of NNRTI and NRTI DRMs among CLHIV receiving ABC/3TC/LPV/r
191 uld only slow down the increase in levels of NNRTI PDR.
192 e detailed understanding of the mechanism of NNRTI inhibition and the effect of binding upon domain m
193                            A small number of NNRTI-resistance mutations were responsible for most cas
194                                  The odds of NNRTI-associated TDR also increased in Latin America/Car
195              The adjusted odds ratio (OR) of NNRTI-RAM detection was 7.62 (95% confidence interval [C
196 men became cost effective at a prevalence of NNRTI resistance higher than 15%, for cost-effectiveness
197                   The reported prevalence of NNRTI resistance was generally higher in US/Canada than
198 argely on the country-specific prevalence of NNRTI resistance.
199 activity (EC50<1 nM) against a wide range of NNRTI-resistant viruses and a favorable pharmacokinetic
200 p DTG-based regimens for halting the rise of NNRTI resistance.
201 an region could face an unidentified rise of NNRTI-resistant HIV.
202 ne use were associated with a higher risk of NNRTI resistance at virologic failure.
203 epidemiological model of the transmission of NNRTI resistance in South Africa.
204 l structure data suggest that the binding of NNRTIs forces RT into a wide-open conformation in which
205                                   Binding of NNRTIs to preformed RT/DNA complexes is hindered by a ki
206 rpretation of the mechanism of inhibition of NNRTIs.
207 e impact of the scale-up of DTG-based ART on NNRTI pretreatment drug resistance (PDR) in South Africa
208 started on a DTG-based regimen, and those on NNRTI-based regimens are rapidly switched to DTG.
209 re was no difference between those with only NNRTI PDR vs no PDR (aHR, 1.05; 95% CI, 0.82-1.34) at th
210  users (8% per 5 years, 95% CI, -3%, 19%) or NNRTI users (3% per 5 years, 95% CI, -7%, 12%).
211 61 individuals with VF on a PI/r (n = 40) or NNRTI (n = 20) containing regimen.
212 d to either lopinavir-ritonavir-based ART or NNRTI-based ART and were followed for 6 months to 2 year
213 nitiated antiretroviral therapy with a PI or NNRTI and a backbone containing either TDF/FTC or ABC/3T
214 ults (>=18 years) initiating INSTI-, PI-, or NNRTI-based regimens from 01/2007-12/2017 who had weight
215 sistance to tenofovir, cytosine analogue, or NNRTIs.
216 mong studied drugs, Efavirenz, but not other NNRTIs, altered claudin-5 expression, increased endothel
217 ng 171 viremic ART-experienced participants, NNRTI mutation prevalence was 83.6%, NRTI 67.8%, and PI
218         NNRTI regimen choice and preexisting NNRTI-resistant minority variants were both associated w
219 ing supports the use of EFV as the preferred NNRTI in first-line treatment regimen for HIV treatment,
220                       Among those prescribed NNRTI-based ART, participants given efavirenz were less
221 e were substantial increases in pretreatment NNRTI resistance per year in all regions.
222 nd considered the prevalence of pretreatment NNRTI drug resistance in 2017.
223 her, and with the prevalence of pretreatment NNRTI resistance greater than 10%, a policy to measure v
224         Prevalence estimates of pretreatment NNRTI resistance in 2016 were 11.0% (7.5-15.9) in southe
225      In 2016, the prevalence of pretreatment NNRTI resistance was near WHO's 10% threshold for changi
226 respective of the prevalence of pretreatment NNRTI resistance, because of the increased cost of the p
227 ys after NNRTI interruption, did not prevent NNRTI-RAMs, but increased detection of NRTI-RAMs (OR 4.2
228  170 received the study regimen: 86 received NNRTI-based ART, and 84 lopinavir-ritonavir-based ART.
229 were randomised to standard of care received NNRTI-based first-line ART.
230 lts (55% female) were enrolled: 20 receiving NNRTI-based and 20 receiving LPV/r-based treatment.
231 eligible for ART or were currently receiving NNRTI-based ART were randomly assigned to either lopinav
232 00 (90% CI, .92-1.09) for patients receiving NNRTI- and LPV/r-based treatment, respectively.
233 o observed that K103N, a clinically relevant NNRTI resistance mutation, does not prevent binding betw
234                             After restarting NNRTI-based ART (n = 90), virologic suppression rates <4
235 NNRTI resistance mutations thereby restoring NNRTI binding.
236 ansition could decrease the effect of rising NNRTI resistance and yield improved ART outcomes, it als
237 rm high-affinity dead-end complexes, both RT/NNRTI/DNA complexes being unable to bind the incoming nu
238                              Once formed, RT/NNRTI complexes bind DNA either in a seemingly polymeras
239           HIV-1-specific nonnucleoside RTIs (NNRTIs), protease inhibitors (PIs), and integrase inhibi
240                              Our data showed NNRTI treatment modestly reduced P. yoelii liver stage p
241 (IC50) of EFV than viruses carrying a single NNRTI mutation.
242 ong 22,884 eligible individuals, 47% started NNRTI-, 30% PI-, and 23% INSTI-based cART with median fo
243 more weight at 18 months than those starting NNRTI-based and elvitegravir-based regimens.
244                                     STRATEGY-NNRTI is a 96 week, international, multicentre, randomis
245  to emerge after interruption of suppressive NNRTI-based antiretroviral therapy (ART) using routine t
246  patients, including patients on suppressive NNRTI-based ART.
247                                We found that NNRTI binding to RT induces opening of the fingers and t
248       These results provide reassurance that NNRTI-based ART regimens are effective among women who a
249 tegrase; a comparative analysis reveals that NNRTI-induced mutations behave differently from the othe
250 e most recent time-based trends suggest that NNRTI-resistance prevalence may be stable or decreasing.
251                   It is widely believed that NNRTIs function as "molecular wedges", disrupting the re
252                                          The NNRTI resistance mutations had no effect on RAL suscepti
253 a9-strand that involve the YMDD loop and the NNRTI binding pocket.
254 and tenofovir (switch group) or continue the NNRTI plus emtricitabine and tenofovir regimen (no-switc
255 ors (IIs) did not affect HK2, except for the NNRTI etravirine (ETV).
256 in the lopinavir-ritonavir group than in the NNRTI group (5.6% vs. 2.3%, P=0.16).
257  levels significantly more frequently in the NNRTI group.
258 in the lopinavir-ritonavir group than in the NNRTI group.
259 iviral activity against HIV-1, including the NNRTI-resistant Y188L mutated virus.
260                       The interaction of the NNRTI nevirapine (NVP) with HIV-1 reverse transcriptase
261 (R))) and an extended release version of the NNRTI nevirapine, (Viramune XR((R))) were recent additio
262 based regimen than among those receiving the NNRTI-based regimen (1.32 vs. 2.25 episodes per person-y
263 nvolvement of binding site(s) other than the NNRTI binding pocket.
264 th WT RT suggested an optimal binding to the NNRTI binding pocket favoring the high anti-viral potenc
265 ly 600 ns), we have captured RT bound to the NNRTI efavirenz in a closed conformation similar to that
266 in addition to several interactions with the NNRTI binding pocket.
267 everse transcriptase (RT) genotypes with the NNRTI resistance mutations K101E+G190S are highly resist
268                                          The NNRTIs bind in an allosteric pocket in RT approximately
269                                    Among the NNRTIs, rilpivirine was associated with more weight gain
270  higher prevalence of HIV drug resistance to NNRTI in ART initiators.
271 nt HIV, potentially compromising response to NNRTI-based antiretroviral therapy (ART).
272 t HIV-1 disease progression and responses to NNRTI-containing antiretroviral therapy (ART).
273 re only for people with DTG AEs switching to NNRTI-based regimens.
274 structures of RT(172R) and RT(172K) bound to NNRTIs or DNA/dNTP.
275                                      DRMs to NNRTIs and NRTIs were found among 65% and 51% of all CLH
276 revalence of pretreatment drug resistance to NNRTIs is high.
277 lone caused a reduction in susceptibility to NNRTIs, while G112D alone did not.
278 /M230I double mutant was less susceptible to NNRTIs than was M230I alone.
279 TDR to NRTIs and PIs was <5%, whereas TDR to NNRTIs was 5%-15%.
280 tance mutations that differ from traditional NNRTI resistance mutations.
281 e inhibitors of HIV-1 reverse transcriptase (NNRTIs).
282                Among people with transmitted NNRTI resistance (7.2%), baseline genotype influences ca
283 orable resistance implications of PI- versus NNRTI-based first line therapy, widespread use of PI-bas
284 d for raltegravir- (HR=1.42 [1.06-1.91]) vs. NNRTI-initiators.
285 isk (HR=1.17 [0.92-1.48]) similar to PI- vs. NNRTI-initiators (HR=1.27 [1.07-1.51]).
286 tion was attenuated (HR=1.03 [0.71-1.49] vs. NNRTIs) when accounting for 12-month weight.
287                  Persons starting INSTIs vs. NNRTIs had incident DM risk (HR=1.17 [0.92-1.48]) simila
288 g first cART regimens with INSTIs or PIs vs. NNRTIs may confer greater risk of DM, likely mediated th
289 is located near the hydrophobic region where NNRTIs bind.
290 st likely occurs through a mechanism whereby NNRTIs stimulate priming or elongation of the tRNA.
291  rates <400 copies/ml were 8/13 (61.5%) with NNRTI-RAMs, 7/11 (63.6%) with NRTI-RAMs only, and 51/59
292        Since a major problem associated with NNRTI treatment is the emergence of drug resistant virus
293 ndomized clinical trials comparing bPI- with NNRTI-based first-line antiretroviral therapy regimens u
294 pinavir-ritonavir-based ART as compared with NNRTI-based ART reduced the incidence of malaria by 41%,
295    Thus, M230I could directly interfere with NNRTI binding but G112D could not.
296 /=1 NNRTI-RAM, including eight patients with NNRTI-RAMs detected only by sensitive testing.
297 d 0.17 (95% CI 0.03, 1.15) for patients with NNRTI-RAMs or NRTI-RAMs only respectively vs. those with
298 d correlate the detection of resistance with NNRTI concentrations after treatment interruption and vi
299 215F/Y) were found to be highly stable, with NNRTI and PI mutations being relatively less persistent.
300 of virological failure during treatment with NNRTI-containing regimens.
301 h and without M184V/I during VF on a TDF/XTC/NNRTI-containing regimen.

 
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