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1 patients who withdrew for reasons other than virologic failure).
2 an independent risk factor for clinical and virologic failure.
3 higher probability of Y181C detection after virologic failure.
4 ed with a higher risk of NNRTI resistance at virologic failure.
5 d during 1998-2006 with a primary outcome of virologic failure.
6 s; 2) for treatment changes, and 3) for each virologic failure.
7 type of resistance mutations detected after virologic failure.
8 nd types of resistance mutations detected at virologic failure.
9 after 5 months of treatment, in a context of virologic failure.
10 ications were associated with higher odds of virologic failure.
11 mL were associated with an increased risk of virologic failure.
12 alf (19 of 32) had resistance at the time of virologic failure.
13 tricitabine resistance in most patients with virologic failure.
14 27 of the remaining subjects who experienced virologic failure.
15 iscontinued treatment for reasons other than virologic failure.
16 patients who withdrew for reasons other than virologic failure.
17 was not detected among subjects experiencing virologic failure.
18 but did increase 4-12 weeks before confirmed virologic failure.
19 pies/mL were at increased risk of subsequent virologic failure.
20 subjects in the random cohort, 57 (26%) had virologic failure.
21 cts plus unselected subjects who experienced virologic failure.
22 was associated with decreased likelihood of virologic failure.
23 evirapine were independently associated with virologic failure.
24 sed before study treatment (baseline) and at virologic failure.
25 oviral therapy (baseline) and at the time of virologic failure.
26 tly at baseline but were not associated with virologic failure.
27 drug concentrations and increase the risk of virologic failure.
28 times to virologic suppression and risks of virologic failure.
29 antiretroviral therapy (ART), predict future virologic failure.
30 e performed for participants identified with virologic failure.
31 s were found in 20 of 47 patients (43%) with virologic failure.
32 ion of antiretroviral therapy and to prevent virologic failure.
33 l, Mozambique, were previously evaluated for virologic failure.
34 No patient had virologic failure.
35 pleted treatment in either study experienced virologic failure.
36 .15; 95% CI, 1.03-1.28) were associated with virologic failure.
37 in a subset of patients treated with SOF at virologic failure.
38 reappeared at relapse in all 3 patients with virologic failure.
39 0.98; 95% CI, .97-.99) decreased the risk of virologic failure.
40 ce of L159F or V321A to 2% (1 of 50 each) at virologic failure.
41 1 subtype were independently associated with virologic failure.
42 Relapse accounted for all cases of virologic failure.
43 ths, 15 (19%) follow-up losses, and 31 (38%) virologic failures.
44 virologic suppression (88%-93%), subsequent virologic failure (0.1%-0.6%/month), and Medicaid-discou
45 rologic failures (hazard ratio for the first virologic failure, 0.39; hazard ratio for the second vir
46 c failure, 0.39; hazard ratio for the second virologic failure, 0.47), as well as the failure of the
50 ce interval, 1.46 to 3.72; P<0.001), with 57 virologic failures (14%) in the abacavir-lamivudine grou
51 rom the randomly selected subcohort (51 with virologic failure, 144 without virologic failure), plus
54 d lopinavir group), and 5 died without prior virologic failure (4 in the nevirapine group and 1 in th
55 t LLV (GSS <3) had a 2.1-fold higher risk of virologic failure (95% confidence interval, 1.2- to 3.7-
57 were maintained on their study regimen after virologic failure accumulated additional Nvp and 3TC mut
59 fected with hepatitis C virus who experience virologic failure after treatment with direct-acting ant
67 was associated with decreased likelihood of virologic failure and decreased emergence of efavirenz-r
70 Associations between selected covariates and virologic failure and resistance were evaluated using ge
71 copies per milliliter or more, the times to virologic failure and the first adverse event were both
72 tical or behavioral interventions to prevent virologic failure and to stimulate complete recovery of
73 avirenz and nelfinavir, and they may predict virologic failure and/or emergence of drug-resistant vir
75 f patients with genotype 1b infection, 1 had virologic failure, and 2 did not have data available at
76 nd 3TC mutations were detected frequently at virologic failure, and Nvp mutations were more common am
78 0% of the women who had received placebo had virologic failure, as compared with 18.4% of those who h
80 ase in CD4 cell count, and a smaller risk of virologic failure at 12 months for atazanavir compared w
82 s associated with 2.5 to 3 times the risk of virologic failure at either 95% or greater or less than
83 level data were used to estimate the risk of virologic failure based on a Prentice weighted case-coho
84 ter NRTI discontinuation among those without virologic failure but did increase 4-12 weeks before con
87 rimary end point for mothers and infants was virologic failure by the 6-month visit after initiation
89 ew DM diagnosis plus DM-related medication), virologic failure, cART regimen switch, administrative c
91 HLA class I alleles subsequently experienced virologic failure compared to those without protective a
92 ith detectable minority variants experienced virologic failure compared with 15% of those without min
93 with HIV-1 infection had increased rates of virologic failure, compared with efavirenz plus dual NRT
95 use of CCR5 antagonists even in the face of virologic failure could provide a relative degree of pro
96 HIV-1 RNA <50 and >=50 copies/mL, confirmed virologic failure (CVF; 2 consecutive HIV-1 RNA >=200 co
97 mL and <50 copies/mL, incidence of confirmed virologic failure (CVF; 2 consecutive measurements >=200
98 of post-ART follow-up, 19 (24%) experienced virologic failure (dapivirine: 6/32, 19%; placebo: 13/39
100 end point was the time from randomization to virologic failure (defined as a confirmed HIV-1 RNA leve
101 pared the cumulative incidence of subsequent virologic failure (defined as an HIV RNA viral load of >
103 remained; however, VL monitoring and earlier virologic failure detection may result in lower NRTI res
104 une activation, indicating that a history of virologic failure does not inexorably lead to increased
106 tly associated with higher-level resistance; virologic failure during the peginterferon/ribavirin-tre
113 confirmed nonadherence as the major cause of virologic failure for 9 (45%) of 20 highly treatment-exp
115 IV-1) minority variants increase the risk of virologic failure for first-line nonnucleoside reverse t
119 Among the nevirapine-treated children with virologic failure for whom data on resistance were avail
123 ng among ART experienced Ugandan adults with virologic failure (>=1,000 copies/mL) using leftover pla
124 ng among ART-experienced Ugandan adults with virologic failure (>=1000 copies/mL) using leftover plas
125 ns were associated with an increased risk of virologic failure (hazard ratio (HR], 2.3 [95% confidenc
126 ignificantly associated with shorter time to virologic failure (hazard ratio [HR], 2.03; P = .035), a
127 to whites, blacks had an increased hazard of virologic failure (hazard ratio [HR]; 1.7; 95% confidenc
129 .48 to 1.06), as well as to delay the second virologic failure (hazard ratio, 0.56; 95 percent confid
130 9 copies/mL for 6 months doubled the risk of virologic failure (hazard ratio, 2.22; 95% CI, 1.60-3.09
131 cantly delayed both the first and the second virologic failures (hazard ratio for the first virologic
133 /m2 has been identified as a risk factor for virologic failure; however, data are limited due to smal
134 A testing of virus from the first episode of virologic failure identified protease resistance mutatio
135 of persistent LLV on the subsequent risk of virologic failure in a cohort of people living with HIV
136 (baseline) drug resistance and subtype with virologic failure in a multinational, randomized clinica
137 ignificantly less likely than NVP to lead to virologic failure in both trials (RR 0.85 [0.73-0.99] I(
138 RNA levels from 330 subjects who experienced virologic failure in clinical trials of direct-acting an
139 nd levels of susceptibility after first-line virologic failure in individuals from Thailand, South Af
140 on with nevirapine was a strong predictor of virologic failure in our cohort, which was not explained
141 ion (Merck 035), but was not associated with virologic failure in patients receiving initial combinat
142 (1%) and was only associated with increased virologic failure in patients treated for short duration
145 d in two of these four animals, resulting in virologic failure in the animal with the highest level o
147 ent adherence estimated the relative risk of virologic failure in the presence of NNRTI-resistant min
148 nts was associated with an increased risk of virologic failure in the setting of recent treatment adh
150 dy was stopped because of increased rates of virologic failure in the VCV 25 mg/day arm (relative haz
151 to identify a significantly earlier time to virologic failure in women randomized to ATV/r compared
156 or >=1 year in 2005-2015 were followed until virologic failure, loss to follow-up, death, or study en
157 identify high-risk individuals and to detect virologic failure may limit the effectiveness of antiret
158 high rates of sustained virologic response, virologic failure may still occur, potentially leading t
170 iciency virus-infected patients experiencing virologic failure of an indinavir- or ritonavir-containi
171 iation between detected minority DRM and the virologic failure of first-line antiretroviral therapy (
173 Y181C mutants more than tripled the risk of virologic failure of first-line efavirenz-based antiretr
176 ces in plasma obtained before therapy and at virologic failure of initial ART among 63 participants w
177 frequent occurrence of E138K/M184I after the virologic failure of rilpivirine-, lamivudine-, and emtr
178 ress viral replication even after short-term virologic failure of three-drug HAART and despite ongoin
179 xposure to both NRTI and NNRTI and confirmed virologic failure on a PI-containing regimen were requir
180 hibitors (NRTIs) and non-NRTIs and confirmed virologic failure on a protease inhibitor-containing reg
181 erall, one-third of patients who experienced virologic failure on an indinavir-containing regimen sup
183 emerged frequently in patients experiencing virologic failure on antiretroviral combinations that do
184 odeficiency virus (HIV) have higher rates of virologic failure on antiretroviral therapy (ART) and of
185 -type HIV, and the proportion of people with virologic failure on dolutegravir-based antiretroviral t
186 source-limited settings, genotype testing at virologic failure on first-line antiretroviral therapy (
188 n treatment-naive noncirrhotic patients with virologic failure on MK-5172 (100-800 mg/day) plus pegyl
189 eatment-experienced patients who experienced virologic failure on treatment regimens containing the C
192 iated with decreased adherence, but not with virologic failure or development of drug resistance in t
195 n vs a TAF-based regimen at week 48, with no virologic failure or emergent resistance reported with D
196 e until initiation of ART and the time until virologic failure or initiation of ART were similar in t
200 l-determined change in regimen due to either virologic failure or treatment-related toxic effects.
204 ts, all pairwise comparisons of incidence of virologic failure over 96 weeks showed equivalence withi
209 200 copies/mL doubled the risk of developing virologic failure (pLLV 200-499: HR, 1.81 [95% CI, 1.08-
210 hort (51 with virologic failure, 144 without virologic failure), plus 127 of the remaining subjects w
216 linded treatment in the high stratum, higher virologic failure rates were seen with ABC/3TC with EFV
217 t frequently observed resistance mutation at virologic failure regardless of the baseline minority va
220 45 patients without intermittent viremia had virologic failure (relative risk, 0.76; 95% confidence i
221 he outcome of treatment-which contributes to virologic failure, resistance generation and viral trans
224 In this analysis, blacks had a 40% higher virologic failure risk than whites that was not explaine
225 ex with 3 primary study endpoints of time to virologic failure, safety, and tolerability events were
226 given HIV RNA level measured 12 weeks after virologic failure, subsequent CD4+ T cell decline was sl
228 ntiretroviral therapy show a shorter time to virologic failure than patients infected with wild-type
229 ation therapy were more likely to experience virologic failure than those who had taken amprenavir mo
230 e combined efavirenz groups (11 percent) had virologic failure; the time to virologic failure was sig
232 as performed at baseline and periodically in virologic failures throughout the 24-week posttherapy fo
233 mens, respectively, reached protocol-defined virologic failure; time to virologic failure was not sig
235 ith the detection of R155K/D168A in NS3 from virologic failures treated with simeprevir but not grazo
239 rs (INSTIs) have been reported to experience virologic failure (VF) in the absence of resistance muta
241 resistant variants have been associated with virologic failure (VF) of initial NVP-based combination
243 avir/ritonavir (LPV/r) monotherapy following virologic failure (VF) on first-line human immunodeficie
248 ime from randomization to death or confirmed virologic failure ([VF]) (plasma HIV RNA<1 log(10) below
250 Participants in the POC arm with confirmed virologic failure vs those in the SOC arm were switched
253 significantly increased independent risk of virologic failure was associated with continuing a 3TC-c
254 f NNRTI and NRTI resistance after first-line virologic failure was associated with higher VL at study
255 finavir recipients, a trend toward decreased virologic failure was associated with the polymorphism C
263 ents with genotype 1a infection, the rate of virologic failure was higher in the ribavirin-free group
265 a median follow-up of 112 weeks, the time to virologic failure was longer in the efavirenz group than
269 protocol-defined virologic failure; time to virologic failure was not significantly different (hazar
271 Cox proportional hazards model, the risk for virologic failure was not significantly greater in the A
273 Antiretroviral resistance at the time of virologic failure was rare but more frequent with ralteg
274 lanned subgroup analyses, increased risk for virologic failure was seen in non-Hispanic black patient
276 0 copies per milliliter or more, the time to virologic failure was significantly shorter in the abaca
277 percent) had virologic failure; the time to virologic failure was significantly shorter in the tripl
280 or (NNRTI)-resistant variants on the risk of virologic failure, we reanalyzed a case-cohort substudy
281 Independent predictors of higher rates of virologic failure were <95% adherence, receiving the 4-d
283 +) T-cell counts obtained after triple-class virologic failure were analyzed using generalized estima
284 RT sequences from participants with N348I at virologic failure were assayed for drug susceptibility.
285 IV-1 amino acid changes from pretreatment to virologic failure were evaluated in protease and reverse
289 load (VL) <50 copies ml(-1) and without past virologic failure were randomized (1:1) to continue oral
290 with HIV-1 RNA <50 copies/mL and no previous virologic failure were randomized (1:1, stratified by ba
291 y virus (HIV)-infected subjects experiencing virologic failure while receiving a ritonavir-containing
292 PI-naive patients designated as experiencing virologic failure while receiving ATV-containing regimen
295 Women assigned to ATV/r had a higher risk of virologic failure with either nucleoside reverse transcr
297 Fifteen percent of patients experienced virologic failure with no known resistance mutations, wh
298 al transmission of HIV-1 had higher rates of virologic failure with subsequent nevirapine-based antir
299 s) or 24 weeks (41 patients who had previous virologic failure with telaprevir or boceprevir plus peg
300 telaprevir-treated patients had on-treatment virologic failure, with no significant difference with o