ライフサイエンスコーパス: SVR

1 SVR affected overall mortality (HR, 0.27 compared with p

2 SVR appears durable in the majority of patients at 5 yea

3 SVR at 12 weeks (SVR12) was assessed in the modified ful

4 SVR is associated with a reduced risk of liver cirrhosis

5 SVR rates in HCV genotype 1 to 4 are virtually identical

6 SVR rates in HIV/HCV GT1-coinfected patients were high.

7 SVR rates were 91.3% (3,191/3,495) for LDV/SOF and 92.0%

8 SVR was achieved by 60.5% of patients (52.9% with HCV ge

9 SVR was associated with a decreased incidence of hepatoc

10 SVR was associated with a reduced risk of liver mortalit

11 SVR was considered as a time-dependent covariate; its ef

12 SVR was higher and cardiac output and ascites volume wer

13 SVR was similar between African Americans (90.5% [546/60

14 nts with HCV genotype 4 and resulted in 100% SVR for all patients who received all 12 weeks of study

15 without RBV for 12 or 24 weeks produced 100% SVR 12 in patients with HCV recurrence after liver trans

16 was sustained virological response [SVR]12 (SVR of HCV RNA <15 IU/mL 12 weeks after the end of thera

17 regulatory authorities have begun to accept SVR at 12 weeks post-treatment (SVR12) as a valid effica

18 Of the 5 patients who did not achieve SVR, 1 withdrew consent, 2 had confirmed virologic relap

19 riple therapy could be sufficient to achieve SVR in patients with undetectable viremia at week 1, but

20 e use of RBV may not be necessary to achieve SVR in this patient population.

21 comprised patients who had failed to achieve SVR on previous NS5A-based therapy with daclatasvir (DCV

22 0.007) patients were less likely to achieve SVR than white patients, a difference that was not expla

23 <6,000,000 IU/mL were less likely to achieve SVR with 8 weeks compared to 12 weeks of therapy, althou

24 ication of treatment and capacity to achieve SVR.

25 However, a subset of patients who achieve SVR will remain at long-term risk for progression to cir

26 cipants (98% [95% CI, 89% to 100%]) achieved SVR 12 weeks after end of treatment, whereas 1 patient e

27 f 497 patients treated for HCV, 257 achieved SVR and had at least 1 subsequent RNA measurement.

28 f 58.2 months, 668 patients (50.5%) achieved SVR.

29 patients treated with SOF/RBV, 60% achieved SVR at 12 weeks (SVR12), compared with 84% of 19 patient

30 received treatment, of whom 10,817 achieved SVR.

31 patients, and 395 patients (95.9%) achieved SVR at 12 weeks: 96.6%, 94.5%, and 90.9% among LT, KT, a

32 chronic hepatitis C virus who have achieved SVR.

33 e and safe in patients who have not achieved SVR with earlier regimens of one or more DAAs plus Peg-I

34 d compensated cirrhosis who had not achieved SVR with previous treatments and 544 with genotype 3 HCV

35 516 patients achieved SVR, a response rate of 86% (95% CI, 83.0% to 88.7%), wi

36 IU ml-1 after 4 weeks of treatment achieved SVR 12 only in 30% (n = 17/56, p < 0.0001) of cases and

37 t differed between participants who achieved SVR vs those who relapsed was ribavirin concentration at

38 main elevated in GT2/3 patients who achieved SVR, suggesting differential immune activation in those

39 All patients achieving SVR after HCV treatment were followed with HCV RNA measu

40 e significantly lower for patients achieving SVR compared with non-SVR in all 3 populations.

41 rd ratio of mortality for patients achieving SVR vs non-SVR was 0.50 (95% CI, .37-.67) in the general

42 al [CI]) for mortality in patients achieving SVR vs non-SVR, and pooled estimates for the 5-year mort

43 In addition, subjects achieving SVR had increasing expression of the transcription facto

44 py was more impressive among those achieving SVR.

45 fibrosis remains an impediment to achieving SVR with short-duration DAA therapy.

46 PPI use with LDV/SOF +/- RBV did not affect SVR (89.7% [131/146] with PPI and 91.5% [613/670] withou

47 Because HIV coinfection does not affect SVR rates or toxicity with DAA-containing therapy, exclu

48 sent in 13 patients at baseline and 25 after SVR, although only 3 patients had increased pulmonary re

49 es are not reliable in ruling out CSPH after SVR.

50 re associated with persistence of CSPH after SVR.

51 LSMs can rule out the presence of CSPH after SVR.

52 trong risk factors for HCC development after SVR has been achieved.

53 ad the highest annual incidence of HCC after SVR (1.82 vs 0.34/100 person-years in patients without c

54 sk factors and incidence rates for HCC after SVR in HCV patients with pretreatment advanced liver dis

55 rrhosis have a low risk to develop HCC after SVR, and the benefit of HCC surveillance for this group

56 Systemic hemodynamics improved after SVR.

57 kPa before treatment to 18 (14-28) kPa after SVR (P < .05).

58 h a reduction in LSM to below 13.6 kPa after SVR still had CSPH.

59 8) before treatment to 13 (10-16) mmHg after SVR (reduction of 2.1 +/- 3.2 mmHg; P < .01).

60 g 589 person-years of follow-up (PYFU) after SVR, 18 (7%) became HCV RNA positive.

61 IV had smaller transaminase reductions after SVR.

62 assessed risk factors for reinfection after SVR in a representative cohort of Canadian coinfected pa

63 rate (per 1000 PYFU) in the first year after SVR was highest in those who reported high-frequency IDU

64 or HCC decreased significantly 2 years after SVR had been achieved.

65 p HCC diminishes significantly 2 years after SVR.

66 An SVR 12 weeks after treatment completion (SVR12) was achi

67 An SVR was associated with lower risk for HCC (HR, 0.25; 95

68 or treatments were less likely to achieve an SVR.

69 nts with stage 2 disease (18.1%) achieved an SVR (P = .003).

70 6% of patients (95% CI, 91%-99%) achieved an SVR in both treatment groups, which was significantly su

71 ncluded in the CirVir cohort who achieved an SVR.

72 tion of patients with stage 2 disease and an SVR died from causes secondary to HCC (2.0%) compared wi

73 tion of patients with stage 1 disease and an SVR died from HCC (2.9%), compared with those without an

74 Patients with stage 1 disease and an SVR were less likely to develop EVs than stage 1 patient

75 h hepatitis C virus-associated cirrhosis, an SVR to all-oral therapy significantly reduced HVPG, comp

76 We found an SVR to reduce overall mortality and risk of death from l

77 e interval [CI], 93%-97%) of patients had an SVR to 8 weeks of sofosbuvir-velpatasvir-voxilaprevir; t

78 at month 2 with a virological response or an SVR was observed.

79 of sofosbuvir-velpatasvir, which produced an SVR in 98% of patients (95% CI, 96%-99%; difference in t

80 7 locus was significantly associated with an SVR.

81 m HCC (2.9%), compared with those without an SVR (11.9%) (P = .03) or developed liver decompensation

82 ents with stage 2 disease with or without an SVR (12.1% vs 25.4%; P = .15).

83 to HCC (2.0%) compared with those without an SVR (18.4%) (P = .003).

84 develop EVs than stage 1 patients without an SVR (hazard ratio [HR], 0.23; 95% confidence interval [C

85 ratio [HR] compared with patients without an SVR, 0.29; 95% confidence interval [CI], 0.19-0.43; P <

86 iver decompensation (none vs 7.1% without an SVR; P = .009).

87 In an intention-to-treat analysis, SVR rates were 76% (31/41) for simeprevir (SMV)/SOF, 94%

88 t (interferon with or without ribavirin) and SVR (RNA test negative at least 12 weeks after the end o

89 Treatment with PrOD or LDV/SOF and SVR are associated with a significant mortality benefit,

90 ecreases in MIP-1beta early in treatment and SVR.

91 icipants through HCV care and treatment, and SVR rates demonstrate the real-world ability of achievin

92 979860 genes polymorphisms accurately assure SVR in naive CHC G4 patients treated with low cost stand

93 We determined the association between SVR attainment and each outcome event, in terms of the r

94 study was to assess the concordance between SVR at various post-treatment time points in phase III c

95 culated the annual incidence rates of HCC by SVR.

96 In this real-world cohort, SVR rates with LDV/SOF+/-RBV nearly matched the rates re

97 ated with greater odds of SVR12 CONCLUSIONS: SVR rates were acceptable in patients with GT3 HCV witho

98 weeks versus a composite historical control SVR rate.

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

100 high-dose PPI was associated with decreased SVR, although patients taking twice-daily PPI achieved a

101 less, CSPH persists in most patients despite SVR, indicating persistent risk of decompensation.

102 Following SVR, mean change in HbA1c was -0.022 +/- 0.53%; however,

103 e investigated hemodynamic changes following SVR in patients with CSPH and whether liver stiffness me

104 idence of 8.9 per 1000 person-years: 6.9 for SVR and 21.6 for NSVR per 1000 person-years.

105 apy was an independent predictive factor for SVR, and a decreased HEV concentration of 0.5 log copies

106 of 50; 95% confidence interval, 60%-85%) had SVR achieved 12 weeks after the end of treatment.

107 virus-associated cirrhosis and CSPH who had SVR to interferon-free therapy at 6 Liver Units in Spain

108 High SVR rates across multiple HCV genotypes were achieved by

109 High SVR rates of 93% and 100% in GT1a- and GT1b-infected pat

110 mbination DAA therapy, we demonstrate a high SVR rate in response to 12 weeks of LDV/SOF, even for pa

111 mg, was well-tolerated and resulted in high SVR in patients infected with HCV genotypes 1 to 6.

112 e 3D-plus-ribavirin regimen resulted in high SVR rates among patients co-infected with HCV genotype 1

113 and sofosbuvir (LDV/SOF) can result in high SVR rates in patients without cirrhosis.

114 Direct-acting antivirals produce high SVR rates in white, black, Hispanic, and Asian/Pacific I

115 inistration of SOF+Peg-IFN+RBV provided high SVR rates, irrespective of cirrhosis status.

116 The phase 2 COSMOS study reported high SVR rates in treatment-naive and prior null-responder HC

117 ment groups and could not reproduce the high SVR rates observed.

118 protocol analysis, SMV/SOF/RBV had a higher SVR rate than SOF/RBV: 100% (16/16) vs 57% (16/28) (P <

119 hereas Asian race was associated with higher SVR rates compared to white patients.

120 However, SVR did not affect whether patients with stage 2 disease

121 atus, RBV use, or GT1 subtype did not impact SVR 12.

122 Viral load did not impact SVR rates in cohort B.

123 therapy, although the numeric difference in SVR rates was small.

124 all studies assessing all-cause mortality in SVR and non-SVR patients.

125 There is substantial room for improvement in SVRs among persons with cirrhosis and genotype 2 or 3 in

126 modify mean arterial pressure, and increased SVR.

127 n of ribavirin was associated with increased SVR rates for certain DAA regimens and patient groups.

128 Ribavirin did not influence SVR rates and was more often used in those with higher B

129 lant recipients; ribavirin did not influence SVR, and graft rejection was rare.

130 HCV-1 patients with POAE have a lower SVR rate to 48-week therapy if they achieve complete EVR

131 ild-Turcotte-Pugh class C disease, had lower SVR rates (78% to 87%) than other populations.

132 rapy, black patients had significantly lower SVR than white patients when treated for 8 weeks but not

133 e 3 (GT3) HCV remains a challenge with lower SVR rates reported, particularly in patients with cirrho

134 DV/SOF +/- RBV was not associated with lower SVR rates, but cirrhosis was.

135 ) and with baseline HCV RNA<6,000,000 IU/mL, SVR rates were 93.2% (1,020/1,094) for those who complet

136 hird DAA to LDV/SOF may result in a moderate SVR rate, lower than that observed in patients without c

137 assessing all-cause mortality in SVR and non-SVR patients.

138 loss to follow-up was the major cause of non-SVR.

139 mortality for patients achieving SVR vs non-SVR was 0.50 (95% CI, .37-.67) in the general population

140 r mortality in patients achieving SVR vs non-SVR, and pooled estimates for the 5-year mortality in ea

141 for patients achieving SVR compared with non-SVR in all 3 populations.

142 tment) and 1 relapse accounted for the 2 non-SVRs.

143 We found that to predict observed SVR rates it was necessary to assume that ledipasvir, GS

144 A post hoc per protocol analysis of SVR was performed on patients who completed treatment an

145 Primary outcomes were effects of SVR on the hepatic, pulmonary, and systemic hemodynamics

146 nfection, reverses the beneficial effects of SVR.

147 At week 24, the primary endpoint of SVR of 35% or more was achieved by 42 (19%) patients in

148 ta-analysis aimed to determine the impact of SVR on long-term mortality risk compared with nonrespond

149 dipasvir-sofosbuvir provided a high level of SVR in those without cirrhosis.

150 ntly associated with decreased likelihood of SVR; age, sex, body mass index, decompensated liver dise

151 nificantly associated with increased odds of SVR (odds ratio = 1.44; 95% confidence interval [CI] = 1

152 ace was no longer a significant predictor of SVR but FIB-4 >3.25 (odds ratio 0.35, 95% confidence int

153 0.02) was the only independent predictor of SVR in HCV non-genotype 1 patients.

154 were independent pre-treatment predictors of SVR following PEG-IFN-based therapy in HCV genotype 1 pa

155 8B C/C genotype increased the probability of SVR from 80 % to reach 87.8 %, 93 % and 100 %.

156 8B C/C genotype increased the probability of SVR from 82 % to reach 100 % and from 29 % to reach 80 %

157 icacy was owing primarily to a lower rate of SVR (92%) among patients with HCV genotype 1a infection

158 We observed a high rate of SVR 12 with SOF-based treatment regimes, however probabl

159 termine the effect of PPI use on the rate of SVR in a real-world cohort of 1,979 patients with chroni

160 The rate of SVR in those receiving RBV and those not receiving RBV w

161 DHCR7 rs12785878 GT/TT had a higher rate of SVR than those with the GG allele (59.7% vs. 43.4%, P =

162 sofosbuvir was associated with high rates of SVR and infrequent treatment discontinuation.

163 The rates of SVR at 12 weeks after end of treatment (SVR 12) were as

164 d genotype 2 HCV infection had high rates of SVR in all groups.

165 otype 3 who had cirrhosis, compared rates of SVR in both groups with a performance goal of 83%.

166 eks, but the 2 regimens had similar rates of SVR in patients with HCV genotype 3 and cirrhosis.

167 SOF and RBV provide high rates of SVR in patients with severe recurrent HCV, including pat

168 ton pump inhibitor use may increase rates of SVR.

169 ibavirin for 12 weeks produces high rates of SVR.

170 Patients with stage 2 disease, regardless of SVR, were at greater risk than patients with stage 1 dis

171 and/or presence of cirrhosis at the time of SVR are associated with a high enough risk to warrant su

172 clinically relevant threshold (67%; based on SVR reported for pegylated interferon and ribavirin) to

173 on the remaining cysteine residues based on SVR training.

174 on of ribavirin had no detectable effects on SVR.

175 PP, mean arterial pressure, cardiac output, SVR, and ascites volume were also measured after 6 days.

176 Overall SVR rates were 89.8% (95% confidence interval [CI] 89.2-

177 The overall SVR rate was 84% (675 of 802 patients, 95% confidence in

178 ined as confirmed HCV RNA detectability post-SVR.

179 inical) associated with HCC development post-SVR.

180 Diabetes is also a risk factor for post-SVR HCC.

181 tified studies analysing HCV recurrence post-SVR.

182 available to guide clinicians on which post-SVR patients should be monitored vs discharged, how to m

183 present before treatment initiation predict SVR and eventual development of a higher frequency of fu

184 otype 1 subtype, and regimen did not predict SVR.

185 rhosis, and hepatic decompensation predicted SVR at 12 weeks.

186 cell proliferation before therapy predicted SVR and was associated with the magnitude of the HCV-spe

187 Cirrhosis was predictive of reduced SVR (0.51 [95% confidence interval {CI}, .31-.87]; P = .

188 rimary endpoint was spleen volume reduction (SVR) of 35% or more from baseline to week 24 in the inte

189 iac output and systemic vascular resistance (SVR) assessed at 30-minute intervals for 90 minutes.

190 4.8% had a 12-week sustained viral response (SVR) following HCV therapy.

191 Sustained viral response (SVR) is the optimal outcome of hepatitis C virus (HCV) t

192 e the effects of a sustained viral response (SVR) on outcomes of patients with hepatitis C virus (HCV

193 e the effects of a sustained viral response (SVR) on outcomes of patients with hepatitis C virus (HCV

194 essary to increase sustained viral response (SVR) rates.

195 d, 592 (36%) had a sustained viral response (SVR).

196 a 90% rate of sustained virologic response (SVR) 4 weeks after treatment, a second cohort receiving

197 high rates of sustained virologic response (SVR) after 12 weeks of treatment with the nucleotide pol

198 hievement of a sustained virologic response (SVR) after treatment for Hepatitis C infection is associ

199 Rates of sustained virologic response (SVR) at 12 weeks were available on 412 patients, and 395

200 predictors of sustained virologic response (SVR) at 24 weeks following discontinuation of therapy we

201 eillance after sustained virologic response (SVR) has been achieved.

202 treatment with sustained virologic response (SVR) improves survival in liver transplant (LT) recipien

203 the benefit of sustained virologic response (SVR) in patients with HCV and cirrhosis without (stage 1

204 iate models of sustained virologic response (SVR) included age, race, cirrhosis, proton pump inhibito

205 was to assess sustained virologic response (SVR) of LDV/SOF+/-ribavirin (RBV) in routine medical pra

206 ns showed high sustained virologic response (SVR) rates (>95%) in patients with HCV genotype 1 infect

207 sulted in high sustained virologic response (SVR) rates along with minimal adverse events in non-live

208 High sustained virologic response (SVR) rates have been observed after 6 weeks of anti-HCV

209 weeks achieves sustained virologic response (SVR) rates of 95% in some patients.

210 lower rate of sustained virologic response (SVR) than those without POAE (44.1% vs 74.0%; P = .0002)

211 lower rates of sustained virologic response (SVR) to interferon-based treatments for chronic hepatiti

212 attainment of sustained virologic response (SVR) were associated with significantly lower mortality

213 igher rates of sustained virologic response (SVR), and the role of HCV infection diagnostic tests has

214 ry outcome was sustained virologic response (SVR), defined as the level of HCV RNA below quantificati

215 high rates of sustained virologic response (SVR), generally exceeding 90%.

216 not differ by sustained virologic response (SVR), HIV, diabetes, or fibrosis.

217 high rates of sustained virologic response (SVR).

218 high rates of sustained virologic response (SVR).

219 nitiators) had sustained virologic response (SVR).

220 could predict sustained virologic response (SVR).

221 nfection after sustained virologic response (SVR).

222 0%) achieved sustained virological response (SVR) 12.

223 l to achieve sustained virological response (SVR) after treatment with sofosbuvir (SOF) plus ribaviri

224 9%) achieved sustained virological response (SVR) at 12 weeks after the end of treatment, with a high

225 achieving a sustained virological response (SVR) at post-treatment week 12 (SVR12).

226 Sustained virological response (SVR) at week 12 (SVR12) was achieved in 78% (92 of 118)

227 ved rates of sustained virological response (SVR) considerably in recent trials.

228 ase rates of sustained virological response (SVR) for patients taking concomitant PPI and ledipasvir/

229 or achieving sustained virological response (SVR) in hepatitis C virus (HCV)-infected patients.

230 can lead to sustained virological response (SVR) in over 90% of people.

231 igh rates of sustained virological response (SVR) in patients chronically infected with genotype 1 he

232 A sustained virological response (SVR) occurred in 63%.

233 d to achieve sustained virological response (SVR) on a DAA-based regimen were randomized to receive t

234 he impact of sustained virological response (SVR) on cognitive function and mood disorders.

235 ients with a sustained virological response (SVR) or nonsustained virological response (NSVR).

236 ults in high sustained virological response (SVR) rates along with minimal adverse events (AEs) in pa

237 and compares sustained virological response (SVR) rates in the HIV coinfected with those in the HCV m

238 achieve high sustained virological response (SVR) rates on sofosbuvir (SOF)-containing regimens in cl

239 therapy upon sustained virological response (SVR) rates, fibrosis progression, and HCC development am

240 d suboptimal sustained virological response (SVR) rates.

241 atients with sustained virological response (SVR) remains unclear.

242 chieve lower sustained virological response (SVR) than patients without cirrhosis, especially if trea

243 te achieving sustained virological response (SVR) to therapy, remain at risk of liver decompensation.

244 (HCC) after sustained virological response (SVR) with direct-acting antivirals (DAA) is unclear.

245 e to achieve sustained virological response (SVR) with hepatitis C virus (HCV) direct-acting antivira

246 7 (45%) with sustained virological response (SVR), 11 (18%) with relapse after 48 weeks of treatment

247 arance and a sustained virological response (SVR), but a significant proportion of patients do not re

248 e, we report sustained virological response (SVR), safety data, health-related quality-of-life (HRQOL

249 who achieved sustained virological response (SVR).

250 gical response sustain virological response (SVR)12 was 91.8% and 86% of cohorts A and B, respectivel

251 ents (328 with sustained virologic response [SVR]).

252 5 treated with sustained virologic response [SVR], 43 during treatment, and 281 treated without SVR),

253 endpoint was sustained virological response [SVR]12 (SVR of HCV RNA <15 IU/mL 12 weeks after the end

254 of therapy (sustained virological response [SVR]12).

255 oximately 40% sustained virologic responses (SVR).

256 safety and sustained virological responses (SVR) of SIM+SOF with and without ribavirin (RBV) in pati

257 brosis progression measured by FIB-4 scores, SVR rates, and incident HCC (iHCC).

258 erated and induced significant and sustained SVR and symptom reduction, even in patients with severe

259 aluated using the primary endpoint of SVR12 (SVR 12 weeks post-treatment); on-treatment response was

260 The SVR rates of SMV/SOF/RBV and SMV/SOF did not differ sign

261 However the SVR rate of SMV/SOF/RBV was higher than that of SOF/RBV

262 ng 76 patients with genotype 1 infection the SVR 12 rate was 74% (n = 56), among 14 patients with gen

263 ng 14 patients with genotype 2 infection the SVR 12 rate was 79% (n = 11), among 24 patients with gen

264 ong 5 patients with genotype 4 infection the SVR 12 rate was 80% (n = 4).

265 ng 24 patients with genotype 3 infection the SVR 12 rate was 92% (n = 22) and among 5 patients with g

266 in HCV non-genotype 1-infected patients, the SVR rate did not differ between the two groups (63.3% an

267 Thus, SVR in chronic HCV infection is associated with a strong

268 s of SVR at 12 weeks after end of treatment (SVR 12) were as follows: Among 76 patients with genotype

269 After a median 5-year follow-up, SVR was found to be associated with a significant decrea

270 The primary efficacy endpoint was SVR rate 12 weeks after end of treatment (SVR12).

271 The primary outcome was SVR at 12 weeks after the end of treatment.

272 The primary end point was SVR at 24 weeks after treatment (SVR24).

273 Achieving a 12-week SVR was found to be protective for depression.

274 The primary endpoints were SVR at 12 weeks (SVR12) and safety.

275 and 21 completed HCV treatment (n = 16 with SVR and n = 5 without).

276 2,500 patients treated with DAA (19,518 with SVR; 2982 without SVR), the mean (standard deviation) ag

277 657 genes were independently associated with SVR [OR 6.453 & 3.536, p < 0.01 respectively].

278 s and treatment response was even lower with SVR 12 of 25% (n = 5/20, p = 0.0016) in the subgroup of

279 endpoint was the proportion of patients with SVR at 12 weeks after treatment (SVR12).

280 Patients with SVR displayed significant improvement in immediate (p =

281 Patients with SVR may still have a risk of HCC and need to be regularl

282 mononuclear cells (PBMCs) from patients with SVR upregulated TRAIL, as well as IFN-gamma and the chem

283 The associated risk of HCC in patients with SVR was 0.37 (0.22-0.63) for those without cirrhosis and

284 Among patients with SVR, advanced age, male gender, cirrhosis, decreased pla

285 However, in patients with SVR, the absolute risk of HCC remained high in patients

286 ion factor STAT1 in PBMCs from patients with SVR.

287 cases of HCC, including 183 in patients with SVR.

288 ciated with incident HCC among patients with SVR.

289 eated participants without SVR vs those with SVR had a higher risk of liver events (IRR, 6.79 [95% CI

290 mpared with patients without SVR, those with SVR had a significantly reduced risk of HCC (0.90 vs 3.4

291 ted HCV RNA-positive patients and those with SVR.

292 Patients with SVRs also had a lower risk of cardiovascular events (HR,

293 of hepatocellular carcinoma in patients with SVRs, but not in patients with viremia.

294 ated with DAA (19,518 with SVR; 2982 without SVR), the mean (standard deviation) age was 61.6 (6.1) y

295 difference between patients with and without SVR.

296 ve individuals, treated participants without SVR vs those with SVR had a higher risk of liver events

297 Compared with patients without SVR, those with SVR had a significantly reduced risk of

298 ity (HR, 0.27 compared with patients without SVR; 95% CI, 0.18-0.42; P < .001) and death from liver-r

299 isk of HCC in patients with vs those without SVR and to identify factors associated with incident HCC

300 43 during treatment, and 281 treated without SVR), and 2503 HCV-seronegative controls.