ライフサイエンスコーパス: RBV

1 RBV and IFN alfa were effective against CHIKV as monothe

2 RBV dose reduction occurred in 25% without any treatment

3 RBV enhances the pSTAT4 and IFN-gamma response of NK cel

4 RBV levels were associated with on-treatment Hb decline

5 Total costs were TVR (61%), IFN (24%), RBV (4%), adverse event management (8%), professional fe

6 eficiency have been shown to protect against RBV-induced anemia.

7 ITPase deficiency protects against RBV-induced anemia, but is not associated with SVR.

8 an impaired antiviral response to IFN-alpha+RBV combination treatment, whereas IFN-lambda treatment

9 and induced viral clearance by the IFN-alpha+RBV combination treatment.

10 f the autophagy response overcomes IFN-alpha+RBV resistance mechanisms associated with HCV infection.

11 e data suggest that treatment with IFN-alpha/RBV can moderately reduce the reservoir of HIV-1-infecte

12 Here, we show that treatment with IFN-alpha/RBV led to a moderate but significant and sustained decl

13 s the established association with IFN-alpha/RBV therapy treatment outcome of another IFNL4 variant,

14 ed interferon-alpha and ribavirin (IFN-alpha/RBV) treatment for chronic hepatitis C virus (HCV) infec

15 (100%) of those receiving SOF, GS-9669, and RBV.

16 5 (92%) of those receiving SOF, GS-9669, and RBV.

17 ed VDV 200 mg QD, TGV 30 mg twice-daily, and RBV 1,000-1,200 mg/day.

18 sponse (SVR) over treatment with Peg-IFN and RBV alone.

19 and 3 (n=29/18/1) were treated with IFN and RBV combination for 4 (range, 1-9) weeks.

20 e findings suggest that SOF plus Peg-IFN and RBV for 12 weeks is effective and safe in patients who h

21 d previously failed DCV-ASV plus Peg-IFN and RBV).

22 or 36 weeks of dual therapy with PEG-IFN and RBV.

23 egimens of one or more DAAs plus Peg-IFN and RBV.

24 Patients were treated with TVR, PEG-IFN, and RBV for 12 weeks, followed by 12 or 36 weeks of dual the

25 Patient experience with IFN- and RBV-free anti-HCV (hepatitis C virus) regimens has not b

26 dipasvir/sofosbuvir), the first Peg-IFN- and RBV-free regimen for CHC GT1 patients, on work productiv

27 IFN- and RBV-free regimens with LDV/SOF result in early HCV suppr

28 of 9 (100%) of those receiving SOF, LDV, and RBV and 10 of 10 (100%) of those receiving SOF, GS-9669,

29 5 (100%) TN patients receiving SOF, LDV, and RBV and 23 of 25 (92%) of those receiving SOF, GS-9669,

30 by 9 (100%) of those receiving SOF, LDV, and RBV and 7 (70%) of those receiving SOF and LDVD without

31 group of TN patients received SOF, LDV, and RBV for 6 weeks (n = 25).

32 patients receiving 6 weeks of SOF, LDV, and RBV, 17 of 25 (68%) achieved SVR12.

33 , regardless of prior response to PegIFN and RBV (simeprevir vs placebo: prior null response, 38%-59%

34 ily) for 12, 24, or 48 weeks plus PegIFN and RBV for 48 weeks (n = 396), or placebo plus PegIFN and R

35 weeks (n = 396), or placebo plus PegIFN and RBV for 48 weeks (n = 66).

36 n of simeprevir or placebo and/or PegIFN and RBV in 8.8% of patients given simeprevir and 4.5% of tho

37 ily) in combination with 48 weeks PegIFN and RBV significantly increased rates of SVR at 24 weeks com

38 or relapsed after treatment with PegIFN and RBV, randomly assigned to receive simeprevir (100 or 150

39 infection previously treated with PegIFN and RBV.

40 red with patients given placebo, PegIFN, and RBV and was generally well tolerated.

41 When utilized with peginterferon and RBV for 12 weeks in treatment-naive patients with genoty

42 fa-2a) as well as the combination of SOF and RBV for the treatment of patients infected with hepatiti

43 SOF and RBV provide high rates of SVR in patients with severe re

44 t of SOF, RBV and peg-IFN-alfa-2a or SOF and RBV.

45 Sofosbuvir and RBV have also been studied without interferon and repres

46 Pase activity, on-treatment anemia, SVR, and RBV levels in hepatitis C virus genotype 1 (HCV-1) patie

47 the host IFN response, has been proposed as RBV's mechanism of action.

48 eron-free hepatitis C treatment regimens, as RBV alone does not inhibit hepatitis C virus (HCV) repli

49 blet of LDV-SOF once-daily plus weight-based RBV (1,000 or 1,200 mg/day) for 12 weeks.

50 CV-SOF (60 + 400 mg daily) with weight-based RBV for 12 or 16 weeks.

51 0 mg GLE + 120 mg PIB with 800 mg once-daily RBV (arm B), or 300 mg GLE + 120 mg PIB without RBV (arm

52 sessed them for the presence of any discrete RBV positional shifts (2 graders) and for traditional me

53 ) DRV 600 mg; all received OBV/PTV/r + DSV + RBV for 12 weeks.

54 the efficacy and safety of OBV/PTV/r + DSV + RBV in coinfected patients on stable, DRV-containing ant

55 During RBV pretreatment, both the frequency of CD56(dim) NK cel

56 fA1) prevented ENT1 degradation and enhanced RBV antiviral activity.

57 In regression models, adjustment for RBV levels attenuated the association between Hb decline

58 However, RBV and IFN alfa were highly synergistic for antiviral e

59 and 3, 12-week administration of SOF+Peg-IFN+RBV provided high SVR rates, irrespective of cirrhosis s

60 lus peginterferon and ribavirin (SOF+Peg-IFN+RBV) administered for 12 weeks to treatment-experienced

61 9%) had previously received SOF plus Peg-IFN-RBV, 20 (39%) had received SOF-RBV, 5 (10%) had received

62 (10%) had received SOF placebo plus Peg-IFN-RBV, and 1 (2%) received GS-0938 monotherapy.

63 g every 8 hours with efavirenz) plus peg-IFN/RBV for 12 weeks and peg-IFN/RBV for 32-56 weeks accordi

64 d response-guided therapy (RGT) with peg-IFN/RBV for 24 or 48 weeks.

65 z) plus peg-IFN/RBV for 12 weeks and peg-IFN/RBV for 32-56 weeks according to virological response at

66 and patients with cirrhosis received peg-IFN/RBV for 48 weeks.

67 who previously failed >/=12 weeks of peg-IFN/RBV for HCV genotype 1 coinfection were enrolled in a si

68 regarding the use of telaprevir plus peg-IFN/RBV in this population.

69 G-IFN)/ribavirin (RBV) for 48 weeks, PEG-IFN/RBV plus boceprevir (BOC) or telaprevir (TEL) for 48 wee

70 uncommonly (6/266 [2.3%]) in MK-5172/peg-IFN/RBV recipients.

71 ts who were null responders to prior peg-IFN/RBV standard therapy and on a raltegravir-based regimen

72 ubsequently broke through during the peg-IFN/RBV tail 16 weeks after completion of MK-5172.

73 vent (AE) rates were consistent with peg-IFN/RBV therapy (fatigue, headache, nausea, neutropenia).

74 lts suggest that a shorter course of peg-IFN/RBV therapy may be sufficient in this population.

75 nts with undetectable HCV RNA during peg-IFN/RBV therapy were enrolled.

76 s' absolute lymphocyte counts during peg-IFN/RBV therapy; peg-IFN dose reductions may be a considerat

77 bining daclatasvir, asunaprevir, and peg-IFN/RBV was associated with a very high cure rate.

78 pegylated interferon alfa/ribavirin (peg-IFN/RBV) during a phase 2 trial.

79 ylated interferon alfa-2a/ribavirin (peg-IFN/RBV) for 12 weeks.

80 with pegylated interferon/ribavirin (peg-IFN/RBV) have shown promising results in HCV-monoinfected pa

81 pegylated interferon plus ribavirin (peg-IFN/RBV) therapy remain unknown.

82 received a 4-week lead-in phase with peg-IFN/RBV, followed by 24 weeks of asunaprevir (100 mg twice d

83 5%) met RGT criteria for 24 weeks of peg-IFN/RBV, of whom 87.0% (47/54) achieved SVR12.

84 daclatasvir (60 mg once daily), and peg-IFN/RBV.

85 h TG4040 followed by TG4040 and PEG-IFNalpha/RBV achieved a cEVR compared with patients who received

86 for 48 weeks (group A, n = 31), PEG-IFNalpha/RBV for 4 weeks followed by PEG-IFNalpha/RBV for 44 week

87 pha/RBV for 4 weeks followed by PEG-IFNalpha/RBV for 44 weeks with 6 injections of TG4040 (group B, n

88 y to 1 of the following groups: PEG-IFNalpha/RBV for 48 weeks (group A, n = 31), PEG-IFNalpha/RBV for

89 eeks (7 injections) followed by PEG-IFNalpha/RBV for 48 weeks with 6 injections of TG4040 (group C, n

90 with patients who received only PEG-IFNalpha/RBV therapy.

91 than 10 IU/mL after 12 weeks of PEG-IFNalpha/RBV treatment.

92 The combination of TG4040 and PEG-IFNalpha/RBV was reasonably well tolerated.

93 erferon alpha-2a and ribavirin (PEG-IFNalpha/RBV) in patients with chronic HCV infection.

94 Furthermore, HCV replication impaired RBV uptake, because of reduced expression of the nucleos

95 s induces an autophagy response that impairs RBV uptake by preventing the expression of equilibrative

96 se could be used as a strategy for improving RBV antiviral activity against HCV infection.

97 ia occurred in 13% of patients, primarily in RBV-based regimens.

98 onse could be used as a strategy to increase RBV antiviral activity against HCV infection.

99 (RBV), n = 53; SOF + pegylated interferon + RBV, n = 25; SOF + RBV, n = 36; and SOF + ledipasvir, n

100 d 82% previously failed pegylated interferon/RBV-based regimens) received treatment and were followed

101 tivity, on-treatment hemoglobin (Hb) levels, RBV levels, and SVR were tested using regression modelin

102 h ALV monotherapy, high body weight, and low RBV levels in patients that received ALV plus RBV.

103 mg ABT-530 with or without once-daily 800 mg RBV for 12 weeks; treatment-experienced patients who wer

104 The antiviral activity of RBV against HCV was progressively impaired in the persis

105 12 weeks of treatment and/or the addition of RBV.

106 To determine whether graders' assessments of RBV positional shifts were false-positives, a control gr

107 imited data are available on the efficacy of RBV-free regimens posttransplant, particularly the use o

108 The impact of RBV-free pan-genotypic regimen with SOF and velpatasvir

109 a potential mechanism for the impairment of RBV antiviral activity in persistently HCV-infected cell

110 were infected with CHIKV in the presence of RBV and/or IFN alfa, and viral production was quantified

111 These studies illustrate the promise of RBV plus IFN alfa as a potential therapeutic strategy fo

112 redicted that a standard clinical regimen of RBV plus IFN alfa would inhibit CHIKV burden by 2.5 log1

113 ociated with clinically relevant regimens of RBV and IFN alfa as combination therapy.

114 Use of RBV did not impact the efficacy of LDV/SOF regimens in t

115 The use of RBV did not increase SVR12 and was associated with anemi

116 The use of RBV may not be necessary to achieve SVR in this patient

117 ents with and 32 patients without 4 weeks of RBV pretreatment, who all received subsequent pegylated

118 F, 138 LDV/SOF + RBV, 28 OPrD, and 73 OPrD + RBV.

119 ting 12 weeks of LDV/SOF +/- RBV or OPrD +/- RBV.

120 taprevir/ritonavir plus dasabuvir (OPrD) +/- RBV in HIV/HCV genotype 1 (GT1)-coinfected patients init

121 Peg-IFN or RBV dose reduction was required in 23% and 43% of patien

122 uired erythropoietin, blood transfusions, or RBV dose reduction for anemia.

123 = 0.35 d(-1) vs. 0.21 d(-1) in patients +/- RBV, respectively; P = 0.0001).

124 FR to <60 mL/min compared to patients on PEG/RBV 1/109 (0.9%) (P < 0.05).

125 ed with peginterferon alfa-2a/ribavirin (PEG/RBV) with or without TVL or BOC.

126 LI4W-W8UTND) received 24 weeks of BOC/PEGIFN/RBV (total: 28 weeks [W28]).

127 NA at week 8 received 44 weeks of BOC/PEGIFN/RBV (total: 48 weeks [W48]).

128 ylated interferon-alpha-2a/ribavirin (PEGIFN/RBV) lead-in, patients with target-not-detectable HCV-RN

129 interferon plus ribavirin treatment (PegIFN/RBV) have not been fully illustrated yet.

130 C infection who had been treated with PegIFN/RBV were enrolled, including 27 (45%) with sustained vir

131 NR in GT-1 CHC patients treated with PegIFN/RBV, while baseline serum level of CCL4 is the only pred

132 f 19 patients treated with SOF/peginterferon/RBV.

133 Plasma RBV levels were measured using high-performance liquid c

134 h another direct-acting antiviral agent plus RBV achieved SVR12-9 of 9 (100%) of those receiving SOF,

135 ent duration and different doses of ALV plus RBV on sustained virologic response (SVR).

136 BV levels in patients that received ALV plus RBV.

137 cacy and safety of ledipasvir (LDV)-SOF plus RBV in patients with genotype 1 hepatitis C virus (HCV)

138 Twelve weeks of LDV-SOF plus RBV was an effective and safe treatment for patients who

139 LDV/SOF plus RBV was associated with a greater incidence of AEs as we

140 ents were to receive 24-48 weeks of SOF plus RBV.

141 ith sofosbuvir-velpatasvir-voxilaprevir plus RBV were fatigue, anemia, gastroenteritis, and nausea.

142 eek, or peg-IFN alfa-2a 180 microg/week plus RBV.

143 osage of Peg-IFN-alpha2a (135 mug/week) plus RBV (10 mg/kg per day) were given for 4 weeks to treatme

144 eived peg-IFN alfa-2a (180 microg/week) plus RBV (1000-1200 mg/day) for 4 weeks, followed by telaprev

145 nter; 55% cohort A and 44% cohort B received RBV.

146 Patients that received RBV had a significantly faster rate of viral decline, wh

147 In the 25 patients who received RBV, 72% developed anemia requiring intervention.

148 Receiving RBV was an independent predictor of PRO impairment in mu

149 those receiving RBV and those not receiving RBV was the same (97%).

150 24 weeks of treatment, in patients receiving RBV or not, and in treatment-naive vs experienced patien

151 Patients receiving RBV with LDV/SOF were more likely to require dose modifi

152 The rate of SVR in those receiving RBV and those not receiving RBV was the same (97%).

153 ciation between Hb decline and SVR reflected RBV levels rather than actual Hb level.

154 Ribavirin (RBV) and interferon have been used successfully for trea

155 Ribavirin (RBV) continues to be an important component of interfero

156 Ribavirin (RBV) is an important component of interferon (IFN)-based

157 Ribavirin (RBV) remains an important component of interferon-free h

158 gylated interferon (Peg-IFN), and ribavirin (RBV) achieved sustained virological response (SVR) rates

159 interferon alpha (IFN-alpha) and ribavirin (RBV) can effectively cure HCV infection in a significant

160 nd 3 contain sofosbuvir (SOF) and ribavirin (RBV) for 12 or 24 weeks.

161 e with peginterferon (PEGINF) and ribavirin (RBV) in patients with chronic genotype 1.

162 egylated interferon (Peg-IFN) and ribavirin (RBV) in patients with genotype 1 hepatitis C virus (HCV)

163 ginterferon-alpha2a (PegIFN), and ribavirin (RBV) in patients with HCV genotype-1 infection previousl

164 5B inhibitor tegobuvir (TGV), and ribavirin (RBV) in treatment-naive patients with chronic hepatitis

165 egylated interferon (PEG-IFN) and ribavirin (RBV) is poor.

166 We provided sofosbuvir (SOF) and ribavirin (RBV) on a compassionate-use basis to patients with sever

167 egylated interferon (peg-IFN) and ribavirin (RBV) results in poor sustained virological response (SVR

168 eatment with interferon (IFN) and ribavirin (RBV) significantly impairs quality of life and other pat

169 ed-interferon alfa (Peg-IFN), and ribavirin (RBV) significantly increases the chances of sustained vi

170 e 1 infection with sofosbuvir and ribavirin (RBV), and explored associations with treatment outcome.

171 treated with interferon (IFN) and ribavirin (RBV), between 2000 and 2008.

172 egylated interferon (Peg-IFN) and ribavirin (RBV), with (n = 3) or without (n = 13) asunaprevir (ASV;

173 197 patients treated with SOF and ribavirin (RBV), with or without peginterferon, including 54% with

174 interferon (IFN)-free or IFN- and ribavirin (RBV)-free treatment regimens with shorter durations and

175 lpha (IFN-alpha), IFN-lambda, and ribavirin (RBV).

176 red to subjects receiving SOF and ribavirin (RBV; FUSION trial, N=201, 34% cirrhosis; VALENCE trial:

177 This shift was blocked by ribavirin (RBV), an antiviral drug that reduces relapse in HCV pati

178 ofosbuvir (SOF) + daclatasvir +/- ribavirin (RBV) was used in 123 patients, SOF + RBV in 30, SOF + si

179 h dasabuvir (OBV/PTV/r + DSV) +/- ribavirin (RBV) is approved for hepatitis C virus (HCV) genotype 1

180 + dasabuvir (OBV/PTV/r + DSV) +/- ribavirin (RBV).

181 ategies: peg-interferon (PEG-IFN)/ribavirin (RBV) for 48 weeks, PEG-IFN/RBV plus boceprevir (BOC) or

182 ors for infections during peg-IFN/ribavirin (RBV) therapy.

183 uated the antiviral activities of ribavirin (RBV) and interferon (IFN) alfa as monotherapy and combin

184 eek treatment and the addition of ribavirin (RBV).

185 ransplantation include the use of ribavirin (RBV).

186 lated interferon (Peg-IFN) and/or ribavirin (RBV), which further compromised work productivity during

187 ir (GLE) + pibrentasvir (PIB) +/- ribavirin (RBV) in HCV genotype 1-infected patients with prior viro

188 ) rates during peginterferon plus ribavirin (RBV) therapy.

189 ived pegylated IFN (PEG-IFN) plus ribavirin (RBV) therapy.

190 n alpha-2a (Peg-IFN-alpha2a) plus ribavirin (RBV) to prevent of HCV recurrence.

191 ) and LDV (90 mg once daily) plus ribavirin (RBV) were given for 12 weeks to treatment-naive (TN) pat

192 atment with sofosbuvir (SOF) plus ribavirin (RBV) with or without pegylated interferon (Peg-IFN) do n

193 reated with sofosbuvir (SOF) plus ribavirin (RBV).

194 ed regimens (SOF + simeprevir +/- ribavirin (RBV), n = 53; SOF + pegylated interferon + RBV, n = 25;

195 8, 12, or 24 weeks of LDV/SOF +/- ribavirin (RBV).

196 combination of sofosbuvir (SOF), ribavirin (RBV) and peg-interferon-alfa-2a (peg-IFN-alfa-2a) as wel

197 logic response (SVR) of LDV/SOF+/-ribavirin (RBV) in routine medical practice.

198 SMV)/SOF, 94% (16/17) for SMV/SOF/ribavirin (RBV), and 52% (16/31) for SOF/RBV.

199 osbuvir (SOF) in combination with ribavirin (RBV) for 12 or 24 weeks is the current standard of care

200 y (N = 50) evaluated DCV-SOF with ribavirin (RBV) in treatment-naive (n = 13) or treatment-experience

201 ir and sofosbuvir with or without ribavirin (RBV) for 12 weeks resulted in high sustained virologic r

202 svir-voxilaprevir with or without ribavirin (RBV) for 12 weeks.

203 -493 plus ABT-530 with or without ribavirin (RBV) in GT1- or GT3-infected patients with compensated c

204 (SVR) of SIM+SOF with and without ribavirin (RBV) in patients with Child-Pugh (CP)-B/C versus CP-A ci

205 sbuvir (LDV/SOF) with and without ribavirin (RBV) resulted in high rates of sustained virological res

206 sofosbuvir (SOF) with or without ribavirin (RBV) results in high sustained virological response (SVR

207 or 12 to 24 weeks with or without ribavirin (RBV).

208 rent doses of ALV with or without ribavirin (RBV).

209 + pegylated interferon + RBV, n = 25; SOF + RBV, n = 36; and SOF + ledipasvir, n = 6) between Januar

210 , and compared between the SOF/VEL and SOF + RBV groups.

211 nitiated therapy: 757 LDV/SOF, 138 LDV/SOF + RBV, 28 OPrD, and 73 OPrD + RBV.

212 avirin (RBV) was used in 123 patients, SOF + RBV in 30, SOF + simeprevir in 11, and SOF + ledipasvir

213 .0% for the use of SOF/VEL (reference: SOF + RBV).

214 In contrast, those in the SOF + RBV group had a modest decline in their PROs starting at

215 epatitis C antibody therapy with LDF/SOF +/- RBV support the prescription labeling suggesting that pa

216 PPI use with LDV/SOF +/- RBV did not affect SVR (89.7% [131/146] with PPI and 91.

217 veterans initiating 12 weeks of LDV/SOF +/- RBV or OPrD +/- RBV.

218 an American race or PPI use with LDV/SOF +/- RBV was not associated with lower SVR rates, but cirrhos

219 buvir with or without ribavirin (LDV/SOF +/- RBV) and ombitasvir/ paritaprevir/ritonavir plus dasabuv

220 SMV/SOF +/- RBV is an effective option with minimal adverse effects

221 N = 654) with LDV/SOF (N = 1,080) or LDV/SOF+RBV (N = 872).

222 for LDV/SOF and 92.0% (527/573) for LDV/SOF+RBV (P = 0.65).

223 he other hand, during treatment with LDV/SOF+RBV, PRO scores declined (up to -5.5% regardless of trea

224 Treatment with SOF+RBV with or without Peg-IFN is tolerated by HCV patients

225 V genotype 1 patients treated with LDV/SOF+/-RBV (ION-1, -2, and -3).

226 real-world cohort, SVR rates with LDV/SOF+/-RBV nearly matched the rates reported in clinical trials

227 HCV-infected veterans treated with LDV/SOF+/-RBV.

228 ALENCE trial: N=333, 21% cirrhosis) and SOF, RBV, and pegylated interferon (Peg-IFN; NEUTRINO trial:

229 eived either a combination treatment of SOF, RBV and peg-IFN-alfa-2a or SOF and RBV.

230 The all-oral regimen of DCV-SOF-RBV was well tolerated and resulted in high and similar

231 plus Peg-IFN-RBV, 20 (39%) had received SOF-RBV, 5 (10%) had received SOF placebo plus Peg-IFN-RBV,

232 he base-case scenario, SOF/SMV dominated SOF/RBV in a modeled 50-year-old cohort of treatment-naive a

233 SOF/ribavirin (RBV), and 52% (16/31) for SOF/RBV.

234 e of SMV/SOF/RBV was higher than that of SOF/RBV (P < .01).

235 ment for genotype 1 CHC than 24 weeks of SOF/RBV among IFN-ineligible/intolerant individuals, support

236 A 24-week course of SOF/RBV costs approximately US$169,000, with sustained virol

237 l response to a 12- to 16-week course of SOF/RBV treatment in these patients was more similar to resp

238 prevention of relapse upon withdrawal of SOF/RBV.

239 otype 1 infection: sofosbuvir/ribavirin (SOF/RBV) for 24 weeks or sofosbuvir/simeprevir (SOF/SMV) for

240 ofosbuvir in combination with ribavirin (SOF/RBV) treatment.

241 The SVR rates of SMV/SOF/RBV and SMV/SOF did not differ significantly in this sma

242 In a per protocol analysis, SMV/SOF/RBV had a higher SVR rate than SOF/RBV: 100% (16/16) vs

243 However the SVR rate of SMV/SOF/RBV was higher than that of SOF/RBV (P < .01).

244 , SMV/SOF/RBV had a higher SVR rate than SOF/RBV: 100% (16/16) vs 57% (16/28) (P < .01).

245 Ys) for the average subject, compared to SOF/RBV ($165,336 and 14.69 QALYs vs. $243,586 and 14.45 QAL

246 mmune activation in those who respond to SOF/RBV therapy and a potential role in predicting treatment

247 ategy saved $91,590 per SVR, compared to SOF/RBV.

248 in those with cirrhosis, treatment with SOF/RBV was suboptimal, highlighting the need for new therap

249 Of 178 patients treated with SOF/RBV, 60% achieved SVR at 12 weeks (SVR12), compared with

250 For patients treated with SOF/RBV, the SVR12 rate was 58% in treatment-naive patients

251 eline viral load, previous treatment status, RBV use, or GT1 subtype did not impact SVR 12.

252 In the HFIM system, RBV plus IFN alfa at clinical exposures resulted in a 2.

253 d membrane expression of ENT1 and terminated RBV uptake.

254 terferon-free regimen containing LDV/VDV/TGV/RBV was well tolerated and led to SVR12 in up to 63% of

255 nd in 100% (27 of 27; 95% CI, 88-100) in the RBV-containing arm.

256 (27 of 28; 95% CI, 82-99) of patients in the RBV-free arm (1 relapse), and in 100% (27 of 27; 95% CI,

257 nearly all adverse events were lower in the RBV-free SOF/VEL group (all P < .03).

258 In this study, we investigated the RBV resistance mechanism using a persistently HCV-infect

259 treatment compared with those receiving the RBV-containing regimen.

260 and prior failure of DAA-containing therapy; RBV coadministration did not improve efficacy.

261 The regimen is well tolerated, though RBV use may require a reduction or interruption to manag

262 In vitro or in vivo exposure of NK cells to RBV improved the pSTAT4 (P < 0.01) but not pSTAT1 respon

263 and SVR is not mechanistic, but is linked to RBV levels.

264 To assess whether RBV has a direct effect on NK cells and/or improves the

265 study provides a potential mechanism for why RBV antiviral activity is impaired in persistently HCV-i

266 The reason why RBV alone does not inhibit HCV replication effectively h

267 s treated with the DAA sofosbuvir along with RBV, IFNL4-DeltaG is associated with slower early viral

268 rogression was statistically associated with RBV shift (odds ratio [OR], 2.2; 95% CI, 1.1-4.5; P = 0.

269 ther variables significantly associated with RBV shift included neuroretinal rim loss (OR, 21.9; 95%

270 l change, were significantly associated with RBV shift.

271 n = 43, respectively) or in combination with RBV (10.6 mg/kg/day) for 12 weeks (arm 3, n = 43).

272 ead investigational DAAs in combination with RBV with or without Peg-IFN.

273 t-term treatment with IFN alfa combined with RBV decreases HIV expression, in part through inhibition

274 Eyes with RBV positional change progressed more rapidly than those

275 d, especially given that viral isolates with RBV resistance have been recently identified.

276 fixed-dose combination of SOF and LDV, with RBV (n = 9) or without RBV (n = 10).

277 dicted 71% and 79% SVR after ALV 400 mg with RBV 400 mg twice-daily for 24 and 36 weeks, respectively

278 patients (of whom 872 received LDV/SOF with RBV and 1,080 received LDV/SOF alone) were analyzed.

279 perienced patients who were not treated with RBV received 16 weeks of therapy.

280 I, 80-100) receiving the same treatment with RBV.

281 and 45% of patients treated with and without RBV, respectively, including fatigue, insomnia, irritabi

282 rability profile of LDV-SOF with and without RBV.

283 ir and sofosbuvir (LDV/SOF) with and without RBV.

284 ty of SOF/LDV fixed-dose combination without RBV in patients with HCV recurrence posttransplant.

285 The combination of SOF/LDV without RBV for 12 or 24 weeks produced 100% SVR 12 in patients

286 SOF/LDV without RBV was used for 12 weeks in patients with early-stage f

287 of sofosbuvir (SOF)/ledipasvir (LDV) without RBV in this patient population.

288 70%) of those receiving SOF and LDVD without RBV.

289 of SOF and LDV, with RBV (n = 9) or without RBV (n = 10).

290 tients, ABT-493 plus ABT-530 with or without RBV achieved SVR12 rates of 96%-100% and was well tolera

291 l protocol utilizing SMV+SOF with or without RBV at three transplant centers were retrospectively rev

292 ng simeprevir and sofosbuvir with or without RBV for 12 weeks was very well tolerated and resulted in

293 The regimen of SMV+SOF with or without RBV for 12 weeks was very well tolerated and resulted in

294 tolerability of SOF and SMV with or without RBV in compensated and decompensated patients with cirrh

295 12, and 24 weeks of LDV/SOF with or without RBV.

296 (arm B), or 300 mg GLE + 120 mg PIB without RBV (arm C).

297 ated for 12 weeks with SOF plus SIM, without RBV.

298 LDV/SOF without RBV is an effective and safe treatment option for patien

299 cirrhosis treated with SIM+SOF with/without RBV for 12 weeks.

300 SIM+SOF with/without RBV has lower efficacy and higher rates of AEs in patien

301 0 patients treated with SIM+SOF with/without RBV, 35% had CP-B/C and 64% had CP-A, with median baseli