ライフサイエンスコーパス: DAA

1 DAA therapy increased patients' numbers of T-regulatory

2 DAA therapy induces a high LDR rate in HCV-associated in

3 DAA treatment in concomitance with chemotherapy was show

4 DAA trial results may have limited generalizability, sin

5 DAA-resistant HCV is generally dominant at virological f

6 DAA-resistant mutants were less frequently observed in c

7 DAA-treated and untreated patients were similar for sex

8 DAAs for HCV are likely to be heralded as one of medicin

9 DAAs remain a safe and highly effective treatment for th

10 for HCV genotype 3 infection are limited (2 DAA regimens).

11 on-free HCV regimen that included at least 2 DAAs.

12 ce-daily, 2-direct-acting-antiviral-agent (2-DAA) combination of simeprevir + TMC647055/ritonavir +/-

13 pe with DAA failure with sequences from 2322 DAA-naive patients, infected with HCV genotypes 1 to 4.

14 From the 23rd DAA, it was observed the beginning of loss of firmness,

15 The 2- and 3-DAA combinations were well tolerated.

16 C647055/ritonavir +/- ribavirin and of the 3-DAA combination of simeprevir + TMC647055/ritonavir + JN

17 mbination treatments with anti-miR-122 and a DAA had additive or synergistic antiviral effects.

18 ve sustained virological response (SVR) on a DAA-based regimen were randomized to receive treatment w

19 or 3 infection who had previously received a DAA regimen but not an NS5A inhibitor were randomly assi

20 Treatment with a DAA during therapeutic vaccination provided transient co

21 cross HCV genotypes in whom treatment with a DAA regimen had previously failed.

22 ients who had been previously treated with a DAA-containing regimen.

23 ment-naive or were treated previously with a DAA.

24 ler ultrasound (DUS) arterial abnormalities (DAA) after orthotopic liver transplantation (OLT) often

25 hacrylate (AMA), and N,N-diallyl acrylamide (DAA) by Cs-ligated zirconocenium ester enolate catalysts

26 el activation (direct allosteric activation (DAA)) by operating at two distinct sites in the absence

27 ective in C3bBb decay-accelerating activity (DAA) and factor I cofactor activity (CA).

28 all possible 3-mer sequences: AAA, AAD, ADA, DAA, ADD, DAD, DDA, and DDD.

29 s from patients with HCV-CV before and after DAA therapy to determine mechanisms of these drugs and t

30 llected from these patients before and after DAA therapy, and also from 12 healthy donors and 12 indi

31 f immune mediators before, during, and after DAA treatment of HCV infection.

32 ells increased in patients with HCV-CV after DAA-based therapy (mean fluorescence units, 37 +/- 2.4 b

33 ansferases did not normalize during or after DAA therapy, or they normalized transiently but then inc

34 ive and innate immune cell populations after DAA therapy in patients with chronic hepatitis C virus i

35 ort on a case of late HBV reactivation after DAA-based treatment of recurrent hepatitis C in an antib

36 transiently but then increased sharply after DAA therapy.

37 ts who fail directly-acting antiviral agent (DAA)-based treatment is unknown.

38 is C virus (HCV) using direct-acting agents (DAA) has been associated with a financial burden to heal

39 Direct acting antiviral agents (DAA) are highly effective yet expensive.

40 pulation but direct acting antiviral agents (DAA) provide an effective cure of HCV infection without

41 Direct-acting antiviral agents (DAAs) are highly effective and well tolerated in patient

42 Direct-acting antiviral agents (DAAs) are used increasingly to treat hepatitis C virus (

43 s containing direct-acting antiviral agents (DAAs) have limited retreatment options.

44 rugs and HCV direct-acting antiviral agents (DAAs) must be carefully considered.

45 Direct-acting antiviral agents (DAAs) represent the standard of care for patients with h

46 new interferon-free direct antiviral agents (DAAs) showed high efficacy and safety, and preliminary d

47 d use of new direct-acting antiviral agents (DAAs) to eliminate circulating HCV before or after trans

48 pies, called direct-acting antiviral agents (DAAs), are available that achieve cure rates of >90% in

49 Among DAA-experienced patients treated for 12 weeks, 100% with

50 so decreased in the PI (-17%; P = 0.002) and DAA eras (-24%; P < 0.001).

51 laboratory presentations, complications, and DAA therapy.

52 tween the regular outpatient medications and DAA therapies in a large real-world cohort.

53 ASH populations increased in both the PI and DAA eras (P < 0.001 for all) whereas HCC WL in HBV remai

54 iral response by 12 weeks after therapy, and DAA regimens were well tolerated.

55 herapy (SVR12) with direct-acting antiviral (DAA) agents for recurrent HCV infection after liver tran

56 N)-based therapy to direct-acting antiviral (DAA) agents, yet some safety concerns have arisen involv

57 data with all-oral direct-acting antiviral (DAA) combinations in these patients are scarce.

58 f the VA to deliver direct-acting antiviral (DAA) HCV therapy, supported by an infrastructure to effe

59 , interferon-free directly acting antiviral (DAA) medications, treatment of hepatitis C virus (HCV) i

60 usly treated with a direct-acting antiviral (DAA) regimen.

61 Highly effective direct-acting antiviral (DAA) regimens (90% efficacy) are becoming available for

62 al of multiple oral direct-acting antiviral (DAA) regimens by the U.S. Food and Drug Administration (

63 Direct-acting antiviral (DAA) regimens without IFN are now being used to treat HC

64 of interferon-free direct-acting antiviral (DAA) regimens, including combinations of DAAs and fixed-

65 ng treatment with a direct-acting antiviral (DAA) targeting the HCV NS5b polymerase protein.

66 MS: Interferon-free direct-acting antiviral (DAA) therapies are effective in patients with hepatitis

67 Although direct-acting antiviral (DAA) therapies for chronic hepatitis C virus (HCV) infec

68 ifs in the era of directly acting antiviral (DAA) therapies.

69 Direct-acting antiviral (DAA) therapy for hepatitis C virus (HCV) infection has r

70 safety of all-oral direct-acting antiviral (DAA) therapy in HCV-associated MCS (HCV-MCS) is largely

71 Direct-acting antiviral (DAA) therapy, recently approved for patients with decomp

72 dividuals receiving direct-acting antiviral (DAA) therapy.

73 duction of all-oral direct-acting antiviral (DAA) treatment has revolutionized care of patients with

74 of two alternative direct-acting antiviral (DAA) treatment policies in a real-life cohort of hepatit

75 of interferon-free, direct-acting antiviral (DAA)-based combination therapies.

76 d patients who fail direct-acting antiviral (DAA)-based regimens remains unknown.

77 PI; 2011-2013), and direct-acting antiviral (DAA; 2014-2015).

78 with combination directly acting antivirals (DAA) for 8-24 weeks is associated with high rates of sus

79 of interferon-free direct-acting antivirals (DAA) in treating chronic hepatitis C virus (HCV) is limi

80 esponse (SVR) with direct-acting antivirals (DAA) is unclear.

81 patients involves direct-acting antivirals (DAA).

82 Direct-acting antivirals (DAAs) against hepatitis C virus (HCV) have been describe

83 Direct-acting antivirals (DAAs) against Hepatitis C virus (HCV) show effective ant

84 ination with other direct acting antivirals (DAAs) and the antiarrhythmic drug, amiodarone (AMIO).

85 do not respond to direct-acting antivirals (DAAs) and the feasibility of further shortening regimens

86 Direct-acting antivirals (DAAs) effectively eradicate chronic hepatitis C virus (H

87 CV) infection with direct-acting antivirals (DAAs) for 6 weeks achieves sustained virologic response

88 nt approval of HCV direct-acting antivirals (DAAs) has renewed discussions as to whether these therap

89 safe and effective direct-acting antivirals (DAAs) have become the standard-of-care treatment.

90 All-oral direct acting antivirals (DAAs) have been shown to have high safety and efficacy i

91 Direct-acting antivirals (DAAs) have changed the landscape of hepatitis C virus (H

92 Direct-acting antivirals (DAAs) have led to a high cure rate in treated patients w

93 load decline with direct-acting antivirals (DAAs) in blood.

94 regimens combining direct-acting antivirals (DAAs) in HCV-associated lymphoproliferative disorders ar

95 ectiveness of oral direct-acting antivirals (DAAs) in predominantly minority HIV/HCV coinfected popul

96 oduced the first directly acting antivirals (DAAs) into Egypt through the government funded National

97 bility of all-oral direct-acting antivirals (DAAs) is delayed because of differing regulatory require

98 treatment with HCV direct-acting antivirals (DAAs) leads to substantial cost reductions.

99 C clearance with directly acting antivirals (DAAs) may be associated with acute decreases in hemoglob

100 Oral direct-acting antivirals (DAAs) represent a major advance in hepatitis C virus (HC

101 ng need to develop direct-acting antivirals (DAAs) to combat such deadly viruses.

102 s C virus (HCV) to direct-acting antivirals (DAAs), due to the small number of patients with treatmen

103 In the era of direct-acting antivirals (DAAs), it is unclear whether the efficacy of treatment a

104 f highly effective direct-acting antivirals (DAAs), many questions pertaining to HCV remain, but they

105 avirin and the new direct-acting antivirals (DAAs), such as NS3 protease and NS5B polymerase inhibito

106 th the approval of direct-acting antivirals (DAAs), the management of drug-drug interactions (DDIs) h

107 f new HCV-specific direct-acting antivirals (DAAs), which have an unprecedented efficacy to clear the

108 logic responses to direct-acting antivirals (DAAs), which lack immunomodulatory properties.

109 for resistance to direct-acting antivirals (DAAs).

110 hout scaled-up HCV direct-acting antivirals (DAAs).

111 ction treated with direct-acting antivirals (DAAs).

112 erferon (IFN)-free direct-acting antivirals (DAAs; 8-12 weeks, 95% sustained virological response, po

113 r DDIs if treated with the recently approved DAA regimens.

114 al of causing DDIs for the recently approved DAAs has not been systematically investigated.

115 he patients' age and fibrosis stage, assumed DAA treatment cost of euro15,000/patient, and the Italia

116 In the context of the available DAA therapies, we used a dynamic individual-based model

117 SVR12 rates for sofosbuvir-based DAA regimens in HCV-MCS were 83%, significantly higher t

118 ion without CV, patients with HCV-CV, before DAA therapy, had a lower percentage of CD4+CD25hiFoxP3+

119 ls were significantly higher in serum before DAA treatment of patients who eventually developed de no

120 NS3, NS5A, and NS5B among patients failed by DAA therapy.

121 nslocation of Nrf2, whereas HCV clearance by DAAs combination does neither.

122 luate the guideline-based treatment costs by DAAs from the perspective of the Brazilian Ministry of H

123 tural protein [NS]3, NS5A, NS5B) targeted by DAAs.

124 ociated with increased SVR rates for certain DAA regimens and patient groups.

125 o previously failed short-course combination DAA therapy, we demonstrate a high SVR rate in response

126 hlight the greatest successes of combination DAA therapies, discuss the ongoing challenges, and ident

127 Combining DAAs with different mechanisms may allow for shorter tre

128 ion without inducing RAVs and may complement DAAs to reduce the emergence of RAVs.

129 Complementing DAAs, viral entry inhibitors have been shown to prevent

130 Conversely, DAA single treatment with simeprevir or daclatasvir redu

131 Of the 145 596 patients seen in the current DAA era, 17 791 (10.2%) received treatment during the fi

132 ic response, the optimal approach to current DAA failures, the impact of targeting people who inject

133 tive clinical trial of patients with HCV-CV, DAA-based therapy restored disturbances in peripheral B-

134 The ICERs decrease with decreasing DAA prices, becoming cost-saving for the base price (eur

135 Under base case conditions, the deferred DAA treatment strategy was found to be the "dominant" st

136 pretransplant DAA treatment versus deferred DAA treatment using a cost-effectiveness decision analys

137 and 2015, 91 of 514 OLT recipients developed DAA (defined by HA resistive index [HARI] <0.5) and rece

138 renal transplant recipients with 4 different DAA regimens.

139 e 3 trials of direct acting antiviral drugs (DAAs) for hepatitis C virus (HCV) excluded patients coin

140 All-oral direct-acting antiviral drugs (DAAs) for hepatitis C virus, which have response rates o

141 ediment to achieving SVR with short-duration DAA therapy.

142 s in levels of inflammatory cytokines during DAA treatment also provides important information about

143 e HCV NS3-NS5b nonstructural proteins during DAA treatment resulted in a multifunctional CD8(+) T-cel

144 itis C-Salvage Study for Patients who Failed DAA/PR Therapy) demonstrated a 96.2% sustained virologic

145 ological response at week 12 after finishing DAAs was obtained in 45 patients (98%); the overall LDR

146 t CA on self-surfaces but less important for DAA.

147 monoinfected patients who were selected for DAA therapy at 2 intervals between 2011 and 2014 were as

148 effectiveness and safety of interferon-free DAA regimens in patients with advanced liver disease, in

149 the broad implementation of interferon-free DAA regimens.

150 , and national criteria for, interferon-free DAA reimbursement among countries in the European Union

151 o be cost-effective if short-course IFN-free DAAs are used and could be highly cost-effective if PWID

152 HCV case-finding and IFN-free DAAs could be highly cost-effective if DAA cost is 10% l

153 Switching to 8-week to 12-week IFN-free DAAs in prisons could increase cost-effectiveness (ICER

154 Interferon-free DAAs are projected to achieve marked reductions in HCV-a

155 screening and treatment with interferon-free DAAs that are required to control HCV incidence and HCV-

156 d were heterogeneous regarding HCV genotype, DAAs received, and baseline HBV characteristics.

157 patients with prior virologic failure to HCV DAA-containing therapy.

158 cost-effectiveness ratio associated with HCV DAA treatment before transplant less than US $150 000/qu

159 more, these studies suggest that not all HCV DAAs and, in particular, not all HCV nonstructural prote

160 Clinical trials of HCV DAAs were reviewed to identify combinations with consist

161 29 patients with HBV-R receiving HCV DAAs.

162 s a safety concern in patients receiving HCV DAAs.

163 All patients started on treatment with HCV DAAs since January 2014 were included.

164 -free DAAs could be highly cost-effective if DAA cost is 10% lower or with 8 weeks' duration.

165 reduced CA on ES but was less compromised in DAA.

166 y observed in combination treatments than in DAA single treatments.

167 ICER was sensitive to variations in DAA costs, in the utility value of patients in fibrosis

168 among 255 HCV coinfected patients initiating DAAs between February 2014 and March 2016 in an urban cl

169 because of high discounts over international DAA prices due to negotiation between BMoH and pharmaceu

170 V population subgroups in the receipt of new DAA treatment.

171 investigation into the effects of these new DAAs therapies on patient reported outcomes (PROs).

172 ine as a consequence of treatment with novel DAAs in chronic HCV patients reduces serum levels of NK

173 ferent classes of competitive antagonists of DAA.

174 ent or prior HBV infection in the context of DAA treatment is unknown.

175 w availability of HCV(+) organs, low cost of DAA treatment, high cost of HCV recurrence) was the incr

176 th, quasispecies diversity, and detection of DAA resistance-associated variants (RAVs), mixed HCV gen

177 The median duration of DAA therapy was 12 weeks (range, 6-24 weeks).

178 uppress HCV replication and the emergence of DAA-resistant mutants.

179 y DC has decreased by over 30% in the era of DAA therapy.

180 CV genotype 1 infection and prior failure of DAA-containing therapy; RBV coadministration did not imp

181 Generalizability of DAA trials was assessed by applying the eligibility crit

182 emic vasodilators (SVD) to the management of DAA after OLT.

183 The standard management of DAA involves computed tomographic angiography (CTA) foll

184 ived treatment during the first 16 months of DAA approval.

185 ls did not prevent persistent replication of DAA-resistant HCV variants that emerged during treatment

186 However, the selection of DAA-resistance mutants is a growing problem that needs t

187 Premature stop of DAA was reported for 8 patients.

188 , highlight current and future strategies of DAA treatment timing, and discuss the potential role of

189 Preliminary studies of DAA combination therapies suggest improved response rate

190 ting an adequately powered clinical trial of DAA use for PEP and the low cost-effectiveness of such a

191 e quantified the impact of administration of DAAs at current and at enhanced screening and treatment

192 the compatibility of a novel combination of DAAs (the 3D regimen) with commonly prescribed HIV-1 pro

193 al (DAA) regimens, including combinations of DAAs and fixed-dose combination pills.

194 The effects of DAAs in mitigating the HCV-related complications of live

195 CV-induced carcinogenesis and the effects of DAAs.

196 and (3) identify the predictors of HRQoL of DAAs therapy users cross the three different time period

197 essing this question, but the prescribing of DAAs for PEP has been reported.

198 However, the high list price of DAAs has led many governments to restrict their reimburs

199 Ongoing surveillance of DAAs for cardiotoxicities may be beneficial, especially

200 ission could be achieved through scale-up of DAAs and moderately effective behavioral interventions.

201 entification of the ideal regimen and use of DAAs reveals new ways to treat this specific population

202 rease in liver cancer recurrence upon use of DAAs.

203 e evaluated the effect of race and gender on DAA receipt after adjusting for socioeconomic status, li

204 d in clinical trials, which had an impact on DAA development and subsequent approvals.

205 e aminotransferase results obtained while on DAA treatment or 7 days after.

206 dence of HBV reactivation occurring while on DAA treatment.

207 This review will focus on DAAs that have received regulatory approval in the Unite

208 our center with HCV who have been started on DAAs.

209 l studies are needed to identify the optimal DAA regimen for kidney transplant recipients, accounting

210 LT versus post-LT treatment with an all-oral DAA regimen among HCV patients with hepatocellular carci

211 treatment with a highly effective, all-oral DAA regimen provides the best health outcomes and is the

212 ) CO13 HEPAVIH cohort initiating an all-oral DAA regimen were consecutively included.

213 luded 189 patients who initiated an all-oral DAA regimen with the following characteristics: median a

214 LT versus post-LT treatment with an all-oral DAA regimen.

215 this prospective real-life cohort, all-oral DAA regimens were well tolerated and associated with a h

216 is C virus-infected veterans completing oral DAA treatment.

217 Multiple oral DAA regimens show high rates of safety, tolerability, an

218 Even in the oral DAA era, 320,000 patients will die, 157,000 will develop

219 eactivation among veterans treated with oral DAA therapy.

220 92 000 HCV-infected veterans since all-oral DAAs became available in January 2014, with cure rates e

221 iterature on the efficacy and safety of oral DAAs for treatment of persons with chronic HCV infection

222 eceive HCV treatment from the launch of oral DAAs in 2014 until 2030.

223 associated disease burden in the era of oral DAAs.

224 still remain substantial in the era of oral DAAs.

225 )-based therapies as well as the recent oral DAAs, risk-based and birth-cohort HCV screening, and the

226 -based regimen and 7 patients received other DAAs.

227 ients with HCV genotype 1 infection and past DAA treatment experience.

228 ficiency virus [HIV] positive) pre- and post-DAA therapy (median follow-up 28 months).

229 ng the genotype and information on potential DAA resistance.

230 We compared pretransplant DAA treatment versus deferred DAA treatment using a cost

231 for favorable outcomes in the pretransplant DAA treatment arm (low availability of HCV(+) organs, lo

232 The pretransplant DAA treatment strategy trended towards cost-effectivenes

233 t cost savings compared to the pretransplant DAA treatment strategy.

234 ent options for patients who failed previous DAA-containing regimens, particularly those with nonstru

235 Twelve patients received DAA therapy between December 2013 and September 2014.

236 ack patients had 21% lower odds of receiving DAA than whites (odds ratio [OR] = 0.79; 95% confidence

237 require clinical monitoring while receiving DAA therapy.

238 ients with decompensated cirrhosis receiving DAAs present lower response rates and experience more SA

239 However, the odds of receiving DAAs were 29% lower for younger women compared with youn

240 nique reports of HBV-R in patients receiving DAAs from 22 November 2013 to 15 October 2016.

241 ed social support) of HCV patients receiving DAAs therapy prior, during and at the end of therapy; (2

242 tions included, the most commonly reimbursed DAA was ombitasvir, paritaprevir, and ritonavir, with da

243 f-like) sheep erythrocytes (ES) but retained DAA.

244 The efficacy of selected DAAs was determined in dose-response assays, in which th

245 Six DAA regimens showed high sustained virologic response (S

246 ith different concentrations of the specific DAA.

247 Data were collected on pretreatment status, DAA regimen, the treatment initiation date and duration,

248 Our preliminary data demonstrate that DAAs can be used safely and effectively in patients afte

249 We did not find any evidence to suggest that DAAs promote HCC.

250 s in this family that are able to act at the DAA site through variation at the aryl ring substituent

251 allow us to propose a binding model for the DAA site, featuring a largely non-polar pocket accessed

252 PspCN did not improve the DAA of any CFH variant on ES Conversely, PspCN boosted t

253 5% in the PI era (P = 0.004) and 32% in the DAA era (P < 0.001) compared to the IFN era.

254 41% in the PI era (P < 0.001) and 81% in the DAA era (P < 0.001).

255 Overall, the DAA offers a new approach to systemizing ageing resource

256 Similar to the DAA cohort, black patients had significantly lower odds

257 cology and drug interaction potential of the DAAs, review the interaction data with DAAs and antiretr

258 Adding a third DAA to LDV/SOF may result in a moderate SVR rate, lower

259 previously demonstrated that adding a third DAA to ledipasvir and sofosbuvir (LDV/SOF) can result in

260 e for sofosbuvir, whereas resistance to this DAA can be induced in genotype 3a.

261 In the present study, we evaluated three DAAs (simeprevir, daclatasvir, and sofosbuvir) in combin

262 ased testing, linkage to care, and access to DAA therapy.

263 mmary, the addition of miR-122 antagonism to DAA single treatments had additive or synergistic antivi

264 %) had a complete clinical response of CV to DAA therapy at week 24, defined by improvement of all th

265 Specifically, 8,125 patients naive to DAA treatment, without clinical, sociodemographic, or in

266 from HBV laboratory data performed prior to DAA initiation.

267 of HARI normalization after SVD and time to DAA longer than 30 days were associated with clinically

268 with a HCV+ donor responded equally well to DAA therapy those transplanted with a kidney from an HCV

269 achieve virological cure, HCV resistance to DAAs has an important role in the failure of interferon-

270 of serum aminotransferases, despite SVR12 to DAAs for HCV infection after liver transplantation.

271 cians (PCPs), or specialist physicians using DAA therapy.

272 ing treatment with direct-acting anti-viral (DAA) agents that lower the risk of posttransplant HCV re

273 t conserved epitopes may not be averted when DAA therapy fails prematurely due to emergence of resist

274 observational study was to evaluate whether DAA antiviral treatment of DLBCL/HCV-infected patients i

275 With DAA scale-up to 80% within 1 year of diagnosis (regardle

276 to be relevant if they were associated with DAA failure in patients or conferred a greater than twof

277 tion treatment in HCV-replicating cells with DAA and anti-miR-122 sharply reduced HCV RNA amounts.

278 ce and occurrence after viral clearance with DAA agents.

279 patients received rituximab concurrent with DAA therapy.

280 d determinants of HCC in patients cured with DAA.

281 B sequences from 626 patients in Europe with DAA failure with sequences from 2322 DAA-naive patients,

282 increase to 11% by 2025, but stabilize with DAA introduction in 2015.

283 Among 22,500 patients treated with DAA (19,518 with SVR; 2982 without SVR), the mean (stand

284 titis C virus patients who were treated with DAA in any of the 129 Veterans Health Administration hos

285 with HCV-CV (median age, 59 y) treated with DAA therapy (21 patients received sofosbuvir plus ribavi

286 Among patients treated with DAA, SVR was associated with a considerable reduction in

287 eporting is voluntary, HBV-R associated with DAAs likely is underreported.

288 f the DAAs, review the interaction data with DAAs and antiretroviral agents, and identify the knowled

289 ct of targeting people who inject drugs with DAAs, vaccine prospects, and application of neutralizing

290 Treatment of HCV(+) MC with DAAs provides a valuable tool for untangling the molecul

291 The choice of regimens with DAAs should be individualized after thorough assessment

292 tors that might be used synergistically with DAAs to prevent or treat graft infection.

293 In all, 9 of 62,290 patients treated with DAAs had evidence of HBV reactivation occurring while on

294 liver transplantation who were treated with DAAs, with or without ribavirin, from 2014 through 2016

295 ients with HBV-HCV co-infection treated with DAAs.

296 ffective in patients previously treated with DAAs.

297 (CLL) and chronic HCV infection treated with DAAs.

298 in HBV-HCV-coinfected patients treated with DAAs.

299 in the United States through treatment with DAAs would require nearly universal screening of PWIDs,

300 strong rationale for prospective trials with DAAs in this setting.