ライフサイエンスコーパス: virologic

1 ond-line therapy, NRTIs retained substantial virologic activity without evidence of increased toxicit

2 Virologic analysis revealed the emergence of multiple in

3 ivariate models were constructed to identify virologic and clinical variables predictive of clinical

4 hRSV) and human metapneumovirus (hMPV) share virologic and epidemiologic features and cause clinicall

5 Vigilant virologic and epidemiologic surveillance is needed to mo

6 analysis of high-throughput omics data with virologic and histopathologic data uncovered relationshi

7 Serial measurements of safety parameters, virologic and host immune correlates, and adherence were

8 These vectors exhibit virologic and immunologic characteristics that make them

9 vely characterized the clinical, laboratory, virologic and immunologic features of KICS by evaluating

10 virus (SVV), a homolog of VZV, recapitulates virologic and immunologic hallmarks of VZV infection in

11 lex subunits in HIV-1 infection, we analyzed virologic and integration site targeting properties of a

12 n study design, patient characteristics, and virologic and safety outcomes sequentially and assessed

13 d for further evaluation because of its good virologic and toxicologic profile and its ability to del

14 ween fibrosis progression and epidemiologic, virologic, and disease-associated factors were analyzed

15 Clinical, virologic, and immunologic evaluations were performed at

16 rough systematic imaging and biochemical and virologic approaches, we identified a dynamic associatio

17 ment response (undetectable virus) and 4 had virologic breakthrough between weeks 4 and 12 of therapy

18 ders without cirrhosis and 1 with cirrhosis; virologic breakthrough occurred in 1 null responder with

19 ant unmet needs, including data defining the virologic characteristics and clinical significance of h

20 The clinical and virologic characteristics of Ebola virus disease (EVD) i

21 sitivity (ts) of MP-12 vaccine to understand virologic characteristics.

22 Coincident virologic clearance was confirmed by in situ hybridizati

23 r refractory CMV are suboptimal, in terms of virologic clearance, renal dysfunction, and mortality.

24 ss (ARI), defined by specified symptoms with virologic confirmation.

25 cers may differ depending on immunologic and virologic context during development.

26 vel proviral reservoirs might predict longer virologic control after discontinuation of treatment.

27 Rapid virologic control after initiation of cART also limits t

28 mph nodes and peripheral blood, and improved virologic control and delayed viral rebound following di

29 tion of TLR7 (Toll-like receptor 7) improves virologic control and delays viral rebound following dis

30 cted CD4 T cells in individuals with natural virologic control by sequencing viruses, T cell receptor

31 voir can be sufficiently targeted to improve virologic control following discontinuation of antiretro

32 g on ritonavir-boosted lopinavir (LPV/r) for virologic control in children infected with human immuno

33 ease, suggesting that this natural long term virologic control may be coming at an immunologic and cl

34 e to seasonal influenza vaccination, despite virologic control of HIV.

35 he complexity and multidimensional nature of virologic control of lentivirus infection.

36 f HBV therapeutics to achieve functional and virologic cure in various phases of HBV infection.

37 y because most infected patients can achieve virologic cure.

38 ipants in the HCV-TARGET study with complete virologic data (per-protocol population).

39 reviewed available clinical, laboratory, and virologic data from all patients with laboratory-confirm

40 t epidemiological situation, we analyzed the virologic data of wild poliovirus type 1 (WPV1) strains

41 Clinical and virologic data were collected.

42 We collected demographic, clinical, and virologic data, as well as reports of adverse outcomes,

43 Infants with a CMV diagnosis or virologic detection of CMV prior to day of life 21 were

44 Prospective studies to characterize the virologic determinants of CLAD and define the underlying

45 re well tolerated and associated with a high virologic efficacy in cirrhotic HIV/HCV-coinfected patie

46 Safety and virologic efficacy were evaluated.

47 n can safely omit NRTIs without compromising virologic efficacy.

48 efore, either new ways of using the existing virologic endpoints and laboratory values or entirely ne

49 The virologic factors that limit the transmission of swine i

50 virologic suppression (88%-93%), subsequent virologic failure (0.1%-0.6%/month), and Medicaid-discou

51 ignificantly associated with shorter time to virologic failure (hazard ratio [HR], 2.03; P = .035), a

52 Calendar trends in virologic failure (VF) among human immunodeficiency viru

53 vel (primary) and determination of confirmed virologic failure (VF) from longitudinal samples.

54 avir/ritonavir (LPV/r) monotherapy following virologic failure (VF) on first-line human immunodeficie

55 ary endpoint: stopping randomized treatment, virologic failure (VF), or death by 6 months.

56 fected with hepatitis C virus who experience virologic failure after treatment with direct-acting ant

57 Identification of virologic failure and early management mitigates the gre

58 Associations between selected covariates and virologic failure and resistance were evaluated using ge

59 tical or behavioral interventions to prevent virologic failure and to stimulate complete recovery of

60 ase in CD4 cell count, and a smaller risk of virologic failure at 12 months for atazanavir compared w

61 ess or death, and 0.91 (95% CI, .84-.99) for virologic failure at 12 months.

62 HLA class I alleles subsequently experienced virologic failure compared to those without protective a

63 By TaqMan 2.0, virologic failure defined as HIV-1 RNA >/= 50 copies/mL

64 Virologic failure during treatment and relapse after tre

65 No patients had virologic failure during treatment, and no patients had

66 (baseline) drug resistance and subtype with virologic failure in a multinational, randomized clinica

67 on with nevirapine was a strong predictor of virologic failure in our cohort, which was not explained

68 (1%) and was only associated with increased virologic failure in patients treated for short duration

69 Virologic failure in subtype C is characterized by high

70 and V321A in 5% (17 of 353) of patients with virologic failure in the SOF studies.

71 high rates of sustained virologic response, virologic failure may still occur, potentially leading t

72 Virologic failure occurred in 13 (33%) of 39 and relapse

73 Virologic failure occurred in 13 patients (4%), includin

74 On-treatment virologic failure occurred in 3 patients with HCV genoty

75 Virologic failure occurred in 34 patients (8%) overall.

76 Virologic failure occurred in no patients in arm A and i

77 .83]) and no difference in the likelihood of virologic failure or CD4 cell gain.

78 cy virus (HIV)-infected women are at risk of virologic failure postpartum.

79 countries (LMICs) experience higher rates of virologic failure than adults.

80 HCV genotype 1-infected patients with prior virologic failure to HCV DAA-containing therapy.

81 Virologic failure was defined as 2 consecutive human imm

82 Fifty-four children (49%) experienced virologic failure, and 2 (2%) died.

83 Of 44 ART-experienced children, 57% had virologic failure, most never virologically suppressed.

84 pregnancy, elimination of food restrictions, virologic failure, or drug toxicities.

85 in a subset of patients treated with SOF at virologic failure.

86 reappeared at relapse in all 3 patients with virologic failure.

87 0.98; 95% CI, .97-.99) decreased the risk of virologic failure.

88 ce of L159F or V321A to 2% (1 of 50 each) at virologic failure.

89 1 subtype were independently associated with virologic failure.

90 Relapse accounted for all cases of virologic failure.

91 ion of antiretroviral therapy and to prevent virologic failure.

92 l, Mozambique, were previously evaluated for virologic failure.

93 No patient had virologic failure.

94 pleted treatment in either study experienced virologic failure.

95 .15; 95% CI, 1.03-1.28) were associated with virologic failure.

96 Thirteen of these 23 (56.5%) virologic failures resuppressed after a median of 8.0 mo

97 as performed at baseline and periodically in virologic failures throughout the 24-week posttherapy fo

98 ith the detection of R155K/D168A in NS3 from virologic failures treated with simeprevir but not grazo

99 The clinical, serologic, and virologic features were compared between the 2 groups.

100 of HCV from infected cancer patients confers virologic, hepatic, and oncologic advantages.

101 We demonstrated that virologic markers of HBV disease activity (hepatitis B e

102 iding robust adherence support, and ensuring virologic monitoring for children receiving ART are esse

103 e after initiation of ART heralded a lack of virologic or clinical response, and hence their monitori

104 Virologic or complete cure additionally includes loss of

105 s with respect to clinical, immunologic, and virologic outcomes using data from prospective studies o

106 ns may overestimate successful retention and virologic outcomes.

107 ased intensive farming practices rather than virologic properties.

108 No patient had confirmed HIV-1 virologic rebound.

109 SVR12 after 8 weeks of treatment experienced virologic relapse after stopping therapy.

110 lure during treatment, and no patients had a virologic relapse after the end of treatment.

111 retreatment, it is important to distinguish virologic relapse from reinfection when patients in whom

112 nalysis of multiple HCV genes to distinguish virologic relapse from reinfection.

113 Distinguishing reinfection from virologic relapse has implications for determining true

114 g 5 patients with late recurrent viremia had virologic relapse in which the HCV present at baseline p

115 Virologic relapse occurred in 3 null responders without

116 eve SVR, 1 withdrew consent, 2 had confirmed virologic relapse or breakthrough, and 2 patients had cl

117 g regimen had a significantly higher rate of virologic relapse than patients given simeprevir and sof

118 Overall, 11 patients (22%) experienced virologic relapse, and 1 (2%) was lost to follow-up at 4

119 velpatasvir, both with HCV genotype 1, had a virologic relapse.

120 Neither virologic relapses nor serious adverse events were noted

121 ly restriction of HIV-1 reservoirs to enable virologic remission and cure.

122 a formidable obstacle to achieving sustained virologic remission in HIV-infected individuals after an

123 achieving reservoir reduction and sustained virologic remission.

124 nd ribavirin, 101 patients (48%) had a rapid virologic response (defined as undetectable levels of he

125 CV genotype 1 (HCV-1) who had complete early virologic response (EVR) and received 48 weeks of therap

126 as the proportion of patients with sustained virologic response (HCV RNA <25 IU/mL) at posttreatment

127 The primary efficacy endpoint was sustained virologic response (HCV RNA below the limit of quantitat

128 of 12 weeks of therapy; all had a sustained virologic response (no detectable serum HCV RNA 12 weeks

129 The primary end point was sustained virologic response (serum HCV RNA <25 IU/mL) 12 weeks af

130 If this cohort had a 90% rate of sustained virologic response (SVR) 4 weeks after treatment, a seco

131 (HCV) infection have high rates of sustained virologic response (SVR) after 12 weeks of treatment wit

132 Achievement of a sustained virologic response (SVR) after treatment for Hepatitis C

133 Rates of sustained virologic response (SVR) at 12 weeks were available on 4

134 Pre-treatment predictors of sustained virologic response (SVR) at 24 weeks following discontin

135 d continued HCC surveillance after sustained virologic response (SVR) has been achieved.

136 Antiviral treatment with sustained virologic response (SVR) improves survival in liver tran

137 notype 2 or 3 infection produces a sustained virologic response (SVR) in 70%-80% of patients.

138 We evaluated the benefit of sustained virologic response (SVR) in patients with HCV and cirrho

139 Multivariate models of sustained virologic response (SVR) included age, race, cirrhosis,

140 he aim of this study was to assess sustained virologic response (SVR) of LDV/SOF+/-ribavirin (RBV) in

141 Six DAA regimens showed high sustained virologic response (SVR) rates (>95%) in patients with H

142 RBV) for 12 weeks resulted in high sustained virologic response (SVR) rates along with minimal advers

143 High sustained virologic response (SVR) rates have been observed after

144 virals (DAAs) for 6 weeks achieves sustained virologic response (SVR) rates of 95% in some patients.

145 ents with POAE had a lower rate of sustained virologic response (SVR) than those without POAE (44.1%

146 ere associated with lower rates of sustained virologic response (SVR) to interferon-based treatments

147 l [CI], .33-.57) and attainment of sustained virologic response (SVR) were associated with significan

148 tment duration and higher rates of sustained virologic response (SVR), and the role of HCV infection

149 The primary outcome was sustained virologic response (SVR), defined as the level of HCV RN

150 are associated with high rates of sustained virologic response (SVR), generally exceeding 90%.

151 were minimal and did not differ by sustained virologic response (SVR), HIV, diabetes, or fibrosis.

152 s is associated with high rates of sustained virologic response (SVR).

153 t, and 119 (91% of initiators) had sustained virologic response (SVR).

154 ed therapies lead to high rates of sustained virologic response (SVR).

155 of the host response could predict sustained virologic response (SVR).

156 greater risk of reinfection after sustained virologic response (SVR).

157 vels at end of treatment (EOT) for sustained virologic response (SVR12) during interferon-sparing dir

158 therapy on completion, adherence, sustained virologic response (SVR12), and safety of ledipasvir/sof

159 not impact completion, adherence, sustained virologic response (SVR12), or safety.

160 -up or thereafter was assumed as a sustained virologic response (SVR12).

161 red in the W28 arm, resulting in a sustained virologic response (SVR12TND) rate of 100% (12/12).

162 Primary endpoint was sustained virologic response 12 weeks after end of treatment (12 w

163 1-infected patients, high rates of sustained virologic response 12 weeks after planned end of treatme

164 The primary efficacy endpoint was sustained virologic response 12 weeks after the end of treatment (

165 The primary endpoint was sustained virologic response 12 weeks after the end of treatment (

166 e recurrent viremia (patients with sustained virologic response 12 weeks after the end of treatment b

167 Eight of 9 (89%) achieved sustained virologic response 12 weeks after the end of treatment.

168 The primary end point was a sustained virologic response 12 weeks after the end of treatment.

169 s had detectable HCV RNA following sustained virologic response 12 weeks after the end of treatment.

170 whether patients who maintained a sustained virologic response 12 weeks after therapy (SVR12) with d

171 The primary endpoint was sustained virologic response 12 weeks after treatment (SVR12).

172 The primary end point was sustained virologic response 12 weeks after treatment (SVR12).

173 ssess completion of treatments and sustained virologic response 12 weeks after treatment (SVR12).

174 the percentage of patients with a sustained virologic response 12 weeks after treatment (SVR12).

175 class B/C, n = 175), 90% achieved sustained virologic response 12 weeks after treatment (SVR12).

176 avirin, demonstrated high rates of sustained virologic response 12 weeks after treatment ended (SVR12

177 Sustained virologic response 12 weeks after treatment was achieved

178 The primary end point was sustained virologic response 12 weeks after treatment.

179 Sustained virologic response 12 weeks post-treatment (SVR12) was 9

180 L 12 weeks after stopping therapy (sustained virologic response [SVR12]).

181 e comprised 903 patients (328 with sustained virologic response [SVR]).

182 HCV RNA positive, 345 treated with sustained virologic response [SVR], 43 during treatment, and 281 t

183 iver biopsies from 8 patients (n=7 sustained virologic response [SVR]; n=1 relapse) and unpaired EOT

184 vir for HCV infection, the rate of sustained virologic response across all genotypes was 97.0% after

185 Rates of sustained virologic response across all genotypes were 97.0% (95%

186 ronic HCV infection who achieved a sustained virologic response after 12 weeks of treatment with sofo

187 ks in patients who did not achieve sustained virologic response after prior treatment with direct-act

188 HCV-RNA in the explant achieved a sustained virologic response after receiving their liver transplan

189 virus (HCV) and who do not have a sustained virologic response after treatment with regimens contain

190 or 12 weeks provided high rates of sustained virologic response among both previously treated and unt

191 or 12 weeks provided high rates of sustained virologic response among patients across HCV genotypes i

192 The rate of sustained virologic response among patients receiving sofosbuvir-v

193 ignificant differences in rates of sustained virologic response among the three study groups.

194 storation of T-cell immunity correlated with virologic response and protection from virus-related mor

195 Primary endpoints included sustained virologic response as defined as negative viral load at

196 r plus ribavirin, concordance of a sustained virologic response at 12 and 24 weeks supports the use o

197 A/PR Therapy) demonstrated a 96.2% sustained virologic response at 12 weeks (SVR12) rate using the NS

198 Sustained virologic response at 12 weeks (SVR12).

199 L 12 weeks after stopping therapy (sustained virologic response at 12 weeks [SVR12]).

200 n therapy and 100% have achieved a sustained virologic response at 12 weeks after completion of ledip

201 e proportion of patients achieving sustained virologic response at 12 weeks after the cessation of tr

202 The primary endpoint was sustained virologic response at 12 weeks after the end of therapy

203 Overall, 322 patients (96%) had a sustained virologic response at 12 weeks after the end of therapy

204 end point for the two trials was a sustained virologic response at 12 weeks after the end of therapy.

205 The primary end point was a sustained virologic response at 12 weeks after the end of therapy.

206 The primary end point was sustained virologic response at 12 weeks after the end of therapy.

207 The primary end point was sustained virologic response at 12 weeks after the end of treatmen

208 The primary endpoint was sustained virologic response at 12 weeks after the end of treatmen

209 The primary efficacy end point was sustained virologic response at 12 weeks after therapy (SVR12).

210 rements: The primary end point was sustained virologic response at 12 weeks after therapy ended (SVR1

211 The primary end point was sustained virologic response at 12 weeks after therapy ended (SVR1

212 the percentage of patients with a sustained virologic response at 12 weeks posttreatment.

213 Per protocol rates of sustained virologic response at 12 weeks were 98.1% (622/634) in t

214 The 2 patients who did not achieve sustained virologic response at 12 weeks were lost to follow-up ei

215 atients, 30 (70%) had a post-transplantation virologic response at 12 weeks, 10 (23%) had recurrent i

216 terval, 82%-97%) patients achieved sustained virologic response at 12 weeks, including 36 of 37 (97%;

217 rval 93%-100%) of patients reached sustained virologic response at 12 weeks.

218 navir) plus ribavirin, the rate of sustained virologic response at 24 weeks after treatment was 88% a

219 inhibitor) has shown high rates of sustained virologic response at post-treatment week 12 (SVR12) in

220 The primary efficacy measure was sustained virologic response at posttreatment week 12 (SVR12) in p

221 Sustained virologic response at posttreatment week 12 (SVR12).

222 as the percentage of patients with sustained virologic response at posttreatment week 12 (SVR12).

223 By intent-to-treat analysis, sustained virologic response at posttreatment week 12 was achieved

224 The primary end point was a sustained virologic response at week 12 after the end of therapy a

225 dred percent of patients exhibited sustained virologic response at week 12 after the end of treatment

226 Proportion of patients with sustained virologic response at week 12 after treatment (SVR12).

227 With multivariate analysis, virologic response at week 4 of treatment was an indepen

228 t durations and increased rates of sustained virologic response compared with existing therapies but

229 regimens have shown high rates of sustained virologic response in both clinical trials and real-worl

230 -acting agents to achieve complete sustained virologic response in humans.

231 patasvir resulted in high rates of sustained virologic response in patients chronically infected with

232 or 12 weeks provided high rates of sustained virologic response in patients coinfected with HIV-1 and

233 iral therapy, with higher rates of sustained virologic response in patients with genotype 2 (hazard r

234 24 weeks resulted in high rates of sustained virologic response in patients with HCV infection and de

235 2 weeks resulted in a high rate of sustained virologic response in patients with stage 4 or 5 chronic

236 s with HCV genotype 2, the rate of sustained virologic response in the sofosbuvir-velpatasvir group w

237 s with HCV genotype 3, the rate of sustained virologic response in the sofosbuvir-velpatasvir group w

238 The overall sustained virologic response rate 12 weeks after the end of treatm

239 The sustained virologic response rate was 98% (102 of 104 patients; 95

240 sk of advanced fibrosis and lowest sustained virologic response rate.

241 have revolutionized therapy, with sustained virologic response rates (undetectable viral load 12 wee

242 In 413 HIV/HCV-coinfected patients with a virologic response sustained for 12 weeks after treatmen

243 r-velpatasvir resulted in rates of sustained virologic response that were superior to those with stan

244 started treatment, and 9 achieved sustained virologic response thus far.

245 In POLARIS-1, the rate of sustained virologic response was 96% with sofosbuvir-velpatasvir-v

246 Sustained virologic response was documented for 10 of 17 patients

247 Extended rapid virologic response was highly predictive of SVR12.

248 Among patients with genotype 1, a sustained virologic response was reported in 96.4% (95% confidence

249 Overall rates of sustained virologic response were 83% (95% confidence interval [CI

250 Rates of sustained virologic response were similar regardless of previous t

251 week total therapy, 87% achieved a sustained virologic response with undetectable HCV RNA by the High

252 Ten patients (66%) exhibited a rapid virologic response within 4 weeks (HCV GT1a, n = 4; HCV

253 The other 5 patients exhibited a virologic response within 8 (HCV GT 1b, n = 4) or 12 wee

254 the 13 patients who did not have a sustained virologic response, 10 had a relapse after the end of tr

255 risk for disease progression after sustained virologic response, the optimal approach to current DAA

256 on have demonstrated high rates of sustained virologic response, virologic failure may still occur, p

257 ring treatment and after achieving sustained virologic response.

258 esistance polymorphisms achieved a sustained virologic response.

259 RNA by Abbott RealTime achieved a sustained virologic response.

260 svir who did not meet the criteria for early virologic response.

261 following enrollment and achieving sustained virologic response.

262 nts; three of these patients had a sustained virologic response.

263 6 patients receiving placebo had a sustained virologic response.

264 nd ribavirin, 49% had a post-transplantation virologic response.

265 treatment initiation date and duration, and virologic response.

266 All patients achieved sustained virologic response.

267 atients treated, 30 (97%) achieved sustained virologic response.

268 rget-not-detectable HCV-RNA at week 8 (rapid virologic response; LI4W-W8UTND) received 24 weeks of BO

269 ribavirin yields approximately 40% sustained virologic responses (SVR).

270 onal study to determine real-world sustained virologic responses 12 weeks after treatment (SVR12) wit

271 Immunologic and virologic responses to antiretroviral therapy were unaff

272 clonal B cells of MC patients with sustained virologic responses to direct-acting antivirals (DAAs),

273 Data were collected on virologic responses, mortality, and nephrotoxicity.

274 s in several measures of exposure to ART and virologic status, including declines in HIV drug resista

275 ian hospitals were evaluated clinically, and virologic studies were completed for 42 of the patients.

276 ly in sensitivity analyses, included 48-week virologic suppression (88%-93%), subsequent virologic fa

277 this is an immediate or long-term effect of virologic suppression (VS) in perinatal infection is unk

278 global treatment target aims to achieve 73% virologic suppression among HIV-infected persons worldwi

279 tting, as it improves retention in care with virologic suppression among patients with early clinical

280 t Pace of detection, linkage, retention, and virologic suppression and (2) NHAS investments in expand

281 e show that HIV/CMV co-infected persons with virologic suppression and recovered CD4(+) T cells compa

282 h node tissue specimens from 8 subjects with virologic suppression during long-term ART at 2 time poi

283 infection "functional cure" whereby durable virologic suppression is sustained after discontinuation

284 eferred strategy only when DTG + 3TC 48-week virologic suppression rate exceeded 90%.

285 Despite lower exposure, virologic suppression was maintained and no perinatal tr

286 elow the prespecified threshold of >80%, and virologic suppression was maintained.

287 L) relative to antiretroviral therapy (ART), virologic suppression, and CD4 count is important.

288 ART initiation, time from ART initiation to virologic suppression, detectable CMV DNA pre-ART, and a

289 Should DTG + 3TC demonstrate high rates of virologic suppression, this regimen will be cost-effecti

290 inflammation than optimal adherence, despite virologic suppression.

291 infected partner, permitting time to achieve virologic suppression.

292 HIV-infected patients, including those with virologic suppression.

293 exhibit residual inflammation regardless of virologic suppression.

294 tently low CRP level, despite achievement of virologic suppression.

295 collected beyond the first year of sustained virologic suppression.

296 n care but is declining with improvements in virologic suppression.

297 ns in efavirenz mid-dosing concentrations or virologic suppression.

298 ng and ART initiation improves retention and virologic suppression.

299 Several pathways may lead to 73% overall virologic suppression; these were examined in sensitivit

300 rategies targeting swine workers, as well as virologic surveillance in areas with large concentration