ライフサイエンスコーパス: virological

1 Virological analyses and gross pathology, histopathology

2 Detailed histopathological and virological analyses revealed that IRF-1 preferentially

3 Based on extensive virological analyses, we determined that Ifi27l2a protec

4 g a combination of evolutionary, genetic and virological analyses.

5 Therefore, virological analysis of RSV isolates in conjunction with

6 Based on extensive virological analysis, we demonstrate greater levels of a

7 ng, and Participants: For this retrospective virological analysis, we recruited 25 HIV+ MSM with AGWs

8 Using virological and behavioral data collected 12 months afte

9 of nerve fibers relative to biopsies during virological and clinical quiescence.

10 associated with the subsequent occurrence of virological and clinical relapses in CHB patients who di

11 nterquartile range [IQR], 10.6-25.3) months, virological and clinical relapses occurred in 94 and 49

12 Virological and clinical relapses were defined as viral

13 We assessed virological and gene-expression changes using quantitati

14 Virological and histological analyses revealed greater i

15 d gene deletion of Ifitm3 Based on extensive virological and immunological analyses, we determined th

16 CN54) (NYVAC-Gag-Pol-Nef), and defined their virological and immunological characteristics in culture

17 ssion of virus replication affected the main virological and immunological features of this nonpathog

18 to individual-level viral load data to test virological and immunological hypotheses explaining inte

19 ffer valuable resources for further in-depth virological and immunological study.

20 We analyzed the virological and lymphoproliferative disease response (LD

21 ica without real-time VL monitoring had good virological and resistance outcomes over 4 years, regard

22 antly increases the speed and sensitivity of virological and serological assays.

23 We aimed to evaluate virological and social outcomes of HIV-infected adolesce

24 (HRs) for potential predictors (demographic, virological, and clinical) associated with HCC developme

25 o disease progression and assesses clinical, virological, and serological parameters of chikungunya d

26 One patient in the 12-week group experienced virological breakthrough and one discontinued prematurel

27 tment-experienced patients, respectively; no virological breakthrough was observed, and >/=99% of pat

28 ment in non-cirrhotic CHB patients without a virological breakthrough.

29 virological relapse, and one (2%) of 44 had virological breakthrough; no virological failures were r

30 There were 4 relapses (2 per group) and no virological breakthroughs.

31 tridium difficile (97/1048 (9.3%) tested) or virological causes (9/172 (5.7%) tested).

32 Baseline sociodemographic, clinical, and virological characteristics did not differ between group

33 vestigated in detail the epidemiological and virological characteristics of asymptomatic and mild ill

34 We compared the epidemiologic, clinical, and virological characteristics of US-born African Americans

35 with respect to clinical, immunological and virological characteristics.

36 RT had failed (assessed by WHO criteria with virological confirmation) were randomly assigned to a bo

37 educe the extent of reservoirs and allow for virological control after ART discontinuation.

38 l replication ex vivo In some cases, loss of virological control was associated with reduction in the

39 ic kidney disease resulted in a high rate of virological cure compared with placebo.

40 t baseline is associated with lower rates of virological cure in certain groups of patients, such as

41 Although most treated patients achieve virological cure, HCV resistance to DAAs has an importan

42 significantly increased the likelihood of a virological cure.

43 Demographic, clinical, and virological data from 4140 antiretroviral-naive human im

44 These data demonstrate the virological effect of potent MAbs and support future cli

45 vantage over protease inhibitor plus NRTI in virological efficacy or safety.

46 An in-depth understanding of the basic virological elements that can affect the epidemiology of

47 provides a means for monitoring intrahepatic virological events in chronic HBV infection.

48 However, the cellular and virological events that occur in the female reproductive

49 These observations provide direct virological evidence for nonsterilizing immunity in indi

50 Here, we assayed virological factors and AKT expression in liver tissues

51 llow-up (October, 2014), 96 participants had virological failure (46 in the raltegravir group and 50

52 ate hazard ratios (HR) for time-to-secondary virological failure (detectable viral load after initial

53 arunavir/ritonavir patients remained free of virological failure (estimated difference 6.3%; 95% CI,

54 on to assess factors associated with primary virological failure (failure to suppress HIV-1 within 9

55 mia was associated with increased hazards of virological failure (hazard ratio [HR] 2.6, 95% CI 2.5-2

56 DAA-resistant HCV is generally dominant at virological failure (most often relapse).

57 Outcomes were WHO-defined virological failure (one or more viral load measurement

58 e patients (1%) experienced protocol-defined virological failure (two in the 8-week group; one in the

59 The primary endpoint was time to confirmed virological failure (two measurements of HIV-1 RNA viral

60 We evaluated risk factors for virological failure (VF) in a logistic regression model

61 prospectively investigated risk factors for virological failure (VF) of bPI-based ART in the combine

62 ity have been identified in individuals with virological failure (VF) while receiving a boosted PI (P

63 Primary outcome was confirmed virological failure (viral load >400 copies per mL) by w

64 h threshold 500, the 24 month risk ratios of virological failure (viral load more than 200 copies per

65 difficult and the incidence of triple-class virological failure after initiation of antiretroviral t

66 Virological failure among patients treated for 12 weeks

67 Higher risk of virological failure among PWUD with TDR may be explained

68 tion of baseline virological resistance with virological failure and emergent resistance on study.

69 ccurred frequently and increased the risk of virological failure and switch to second-line ART.

70 e use of lamivudine was associated with more virological failure at week 48 compared to emtricitabine

71 d, highlighting the importance of confirming virological failure before switching to second-line ther

72 d by comparing the cumulative probability of virological failure by 48 weeks.

73 erapy group achieved the primary endpoint of virological failure by week 48 compared with 23 (18%) pa

74 oth 8 and 24 weeks had 5 times the hazard of virological failure compared to more adherent participan

75 ee NtRTIs (NtRTI-group) in participants with virological failure composed of a first-line regimen of

76 Virological failure during follow-up occurred in 14 380

77 drug resistance may not be a risk factor for virological failure during treatment with a non-NNRTI-co

78 ce were transmitted are at increased risk of virological failure during treatment with a non-NNRTI-co

79 ons are associated with an increased risk of virological failure during treatment with NNRTI-containi

80 ho discontinued early for reasons other than virological failure had HCV RNA less than 25 IU/mL at th

81 valuated whether subtype influenced rates of virological failure in a cohort of 8746 patients from th

82 Incidence of virological failure in Latin America and the Caribbean w

83 We aimed to examine factors associated with virological failure in patients in a standardised nation

84 Our findings suggest an increased risk of virological failure in patients with HIV-1C, especially

85 Poor adherence was a major determinant of virological failure in people on second-line ART.

86 stimates of CD4 less than 100 cells per muL, virological failure incidence, and loss to follow-up wer

87 Risk of virological failure increased further with higher ranges

88 The gold standard for detecting virological failure is plasma human immunodeficiency vir

89 usted difference 4.1%, 95% CI 1.6-6.7), with virological failure noted in ten and six patients, respe

90 ified in sub-Saharan Africa in patients with virological failure of first-line combination antiretrov

91 ne analogue mutations (TAM) in patients with virological failure of first-line tenofovir-containing A

92 Virological failure of the WHO-recommended first-line NN

93 antiretrovirals, and 169 (15%) had previous virological failure on a non-darunavir regimen.

94 e screening), and patients with a history of virological failure on non-darunavir regimens were allow

95 on, and a composite endpoint of the first of virological failure or major regimen modification.

96 ase inhibitors had earlier time-to-secondary virological failure than did those with HIV-1B given sim

97 Participants with TDR had higher risk of virological failure than those without TDR (log-rank P =

98 By 48 weeks, the cumulative probability of virological failure was 10.3% (95% CI 6.5-14.0) in the r

99 rly measure HIV RNA, cumulative incidence of virological failure was 7.8% (95% CI 7.2-8.5) 1 year aft

100 o acid positions in subjects who experienced virological failure were also noted and further evaluate

101 No participant had virological failure with resistance in the integrase inh

102 Of 6450 patients with confirmed virological failure, 58.0% (95% CI 56.5-59.6) switched b

103 DS-defining illness or death, risk ratios of virological failure, and mean differences in CD4 cell co

104 outcomes were time from ART initiation until virological failure, major regimen modification, and a c

105 up and six (5%) in the pravastatin group had virological failure, with no significant difference betw

106 ing might be necessary to reduce the risk of virological failure.

107 inued treatment because of adverse events or virological failure.

108 nd explore which factors are associated with virological failure.

109 re associated with increased risk of primary virological failure.

110 per muL on ART but lost to follow-up or with virological failure.

111 riple-therapy arm developed protocol-defined virological failure.

112 There were no seroconversions on PrEP and 7 virological failures on early ART among women remaining

113 (2%) of 44 had virological breakthrough; no virological failures were recorded in the ribavirin-cont

114 ration snapshot algorithm), protocol-defined virological failures, and safety events through 96 weeks

115 n of 15 viral breakthroughs considered to be virological failures.

116 terized longitudinally the immunological and virological features that may explain divergence in dise

117 We describe the clinical, biological, and virological follow-up of a case of Ebola virus disease.

118 Virological, histopathological, and immunohistochemical

119 Virological investigations included RT-PCR for Zika viru

120 ide a unique opportunity to do such in-depth virological investigations.

121 ts with preexisting rt204 LAM-R mutations or virological load refractory to LAM undergoing liver tran

122 technique from >500 patients were tested for virological markers used to diagnose and monitor HCV inf

123 However, more frequent virological monitoring might be necessary to reduce the

124 expect our findings will be generalisable to virological monitoring of patients with HIV receiving AR

125 in sub-Saharan Africa with limited access to virological monitoring.

126 sociated with non-adherence to ART, and with virological non-suppression (prevalence ratios [PR] adju

127 -adherence at the time of the questionnaire; virological non-suppression (viral load >50 copies per m

128 on-adherence to ART and 219 (9%) of 2405 had virological non-suppression in cross-sectional analysis.

129 antiretroviral therapy (ART) non-adherence, virological non-suppression, and virological rebound, in

130 d viral load at baseline (P<0.05), (ii) poor virological outcome at day 49 after anti-CMV therapy, (i

131 lar inflammation and is associated with late virological outcome in these patients.

132 was no clinical benefit when a difference in virological outcome was identified.

133 ween January 2006 and May 2013 that reported virological outcomes among human immunodeficiency virus

134 idence for the effect of cross-resistance on virological outcomes is limited.

135 , and assessed its impacts on first-line ART virological outcomes.

136 The serum level of HBsAg was associated with virological (P < 0.001) and clinical (P = 0.01) relapses

137 rological response, clinical parameters, and virological parameters among children with laboratory-co

138 n addition, considering various clinical and virological parameters, IFNalpha therapy was independent

139 sk to develop HHV8-related disease underwent virological posttransplant monitoring by quantitative re

140 tient did not achieve SVR12 because of a non-virological reason, and seven patients without cirrhosis

141 d from the primary efficacy analysis for non-virological reasons (death, lost-to-follow-up [n=2], non

142 come was the proportion of participants with virological rebound (confirmed viral load >/=50 copies p

143 139 (8%) of 1740 individuals had subsequent virological rebound (rate=3.6/100 person-years).

144 o (cross-sectional analysis); and subsequent virological rebound (viral load >200 copies per mL) in t

145 ession within 48 weeks or the probability of virological rebound after successful virological suppres

146 regimen was non-inferior to the control for virological rebound cumulative through week 48 (19 [2.5%

147 -adherence, virological non-suppression, and virological rebound, in HIV-positive people on ART in th

148 All 3 patients who did not achieve SVR12 had virological relapse within 4 weeks of the end of treatme

149 two (5%) of 42 treatment-naive patients had virological relapse, and one (2%) of 44 had virological

150 ing therapy, 13 of 15 patients experienced a virological relapse.

151 patients subsequently developed clinical and virological relapses.

152 s including patients who discontinued NAs in virological remission (VR) and were followed for >/=12 m

153 health-related quality-of-life (HRQOL), and virological resistance analyses in patients in C-SURFER

154 We report the relation of baseline virological resistance with virological failure and emer

155 There was no evidence of virological resistance.

156 atients in each group achieved an ultrarapid virological response (18 [69%]).

157 (25%), and 19 of these 24 achieved sustained virological response (79%).

158 the proportion of patients with a sustained virological response (HCV RNA <15 IU/mL) 12 weeks after

159 the proportion of patients with a sustained virological response (HCV RNA <25 IU/mL) at post-treatme

160 l studies have shown high rates of sustained virological response (hepatitis C virus [HCV] RNA <15 IU

161 d virological response (SVR) or nonsustained virological response (NSVR).

162 in each group (1:1:1) achieved an ultrarapid virological response (plasma HCV RNA <500 IU/mL by day 2

163 Forty-five patients (57.0 %) showed a rapid virological response (RVR).

164 All 46 patients (100%) achieved sustained virological response (SVR) 12.

165 Patients who fail to achieve sustained virological response (SVR) after treatment with sofosbuv

166 virus (HCV) has improved rates of sustained virological response (SVR) considerably in recent trials

167 cently suggested decrease rates of sustained virological response (SVR) for patients taking concomita

168 therapy is essential for achieving sustained virological response (SVR) in hepatitis C virus (HCV)-in

169 epatitis C virus (HCV) can lead to sustained virological response (SVR) in over 90% of people.

170 in (RBV) resulted in high rates of sustained virological response (SVR) in patients chronically infec

171 n who previously failed to achieve sustained virological response (SVR) on a DAA-based regimen were r

172 aim was to evaluate the impact of sustained virological response (SVR) on cognitive function and moo

173 cinoma (HCC) among patients with a sustained virological response (SVR) or nonsustained virological r

174 ut ribavirin (RBV) results in high sustained virological response (SVR) rates along with minimal adve

175 eficiency virus (HIV) achieve high sustained virological response (SVR) rates on sofosbuvir (SOF)-con

176 ose with cirrhosis, had suboptimal sustained virological response (SVR) rates.

177 arcinoma (HCC) among patients with sustained virological response (SVR) remains unclear.

178 ns, but consistently achieve lower sustained virological response (SVR) than patients without cirrhos

179 mHg or greater), despite achieving sustained virological response (SVR) to therapy, remain at risk of

180 hepatocellular cancer (HCC) after sustained virological response (SVR) with direct-acting antivirals

181 Failure to achieve sustained virological response (SVR) with hepatitis C virus (HCV)

182 enrolled, including 27 (45%) with sustained virological response (SVR), 11 (18%) with relapse after

183 re crucial for HCV clearance and a sustained virological response (SVR), but a significant proportion

184 Here, we report sustained virological response (SVR), safety data, health-related

185 higher in individuals who achieved sustained virological response (SVR).

186 Sustained virological response sustain virological response (SVR)12 was 91.8% and 86% of cohort

187 h was observed, and >/=99% of patients had a virological response (VR) at the end of treatment.

188 Statin use was associated with improved virological response (VR) rates to antiviral therapy and

189 le HCV RNA 12 weeks posttreatment (sustained virological response 12 weeks after completion of study

190 oportion of participants achieving sustained virological response 12 weeks after the end of all study

191 After 24 weeks' treatment, sustained virological response 12 weeks after the end of treatment

192 as the proportion of patients with sustained virological response 12 weeks after the end of treatment

193 he study regimen well and achieved sustained virological response 12 weeks after treatment (SVR12).

194 proportion of patients achieving a sustained virological response 12 weeks after treatment (SVR12).

195 VR12, three relapsed, two achieved sustained virological response 4 weeks after the end of treatment

196 The primary efficacy endpoint was sustained virological response [SVR]12 (SVR of HCV RNA <15 IU/mL 1

197 weeks after completion of therapy (sustained virological response [SVR]12).

198 ns with consistently high rates of sustained virological response across hepatitis C genotypes.

199 All patients with sustained virological response also experienced a sustained clinic

200 alysis of the relationship between sustained virological response and liver fibrosis progression amon

201 the proportion of patients with a sustained virological response at 12 weeks (SVR12) after treatment

202 oportion of participants achieving sustained virological response at 12 weeks (SVR12; HCV RNA less th

203 The primary outcome was sustained virological response at 12 weeks after treatment complet

204 and end-of-treatment response and sustained virological response at 12 weeks after treatment end (SV

205 revir plus pibrentasvir achieved a sustained virological response at 12 weeks.

206 The primary efficacy endpoint was sustained virological response at post-treatment week 12 (HCV RNA

207 The primary endpoint was sustained virological response at post-treatment week 12 (SVR12).

208 The primary efficacy endpoint was sustained virological response at posttreatment week 12 (SVR12).

209 Sustained virological response at week 12 (SVR12) was achieved by

210 A sustained virological response at week 12 after finishing DAAs was

211 erence was observed in the rate of sustained virological response between the HCV group and both the

212 3.47; P = 0.021); and absence of a sustained virological response during follow-up (HR, 3.02; 95% CI,

213 LT was highly effective, achieving sustained virological response in all patients who completed 12 we

214 as well tolerated and effective at achieving virological response in patients with HCV genotype 1 inf

215 rentasvir, has shown high rates of sustained virological response in phase 2 and 3 studies.

216 eated patients within 4 weeks, and sustained virological response in three patients for 76 weeks.

217 ome of these extrahepatic effects; sustained virological response is associated with resolution of co

218 In genotype 1 patients the analysis of early virological response may predict treatment response in S

219 without cirrhosis who achieved an ultrarapid virological response on triple direct-acting antiviral r

220 n trough level on day 7 or at month 2 with a virological response or an SVR was observed.

221 Sustained virological response rate at 12 weeks (SVR12) was 83% ov

222 gravir once daily had a significantly higher virological response rate than did those taking ritonavi

223 Overall, the sustained virological response rate was 97% (95% confidence interv

224 With current treatment and sustained virological response rates (status quo), chronic prevale

225 acceptable safety profile and high sustained virological response rates 12 weeks after the end of tre

226 Sustained virological response rates were sourced from ASTRAL-4, S

227 ity of patients post-LT, treatment sustained virological response rates, LT costs, and baseline Model

228 Patients with an ultrarapid virological response received 3 weeks of therapy.

229 Sustained virological response sustain virological response (SVR)1

230 pact of these DRMs on ARV susceptibility and virological response to first- and later-line treatment

231 All patients who achieved an ultrarapid virological response were included in the safety analysi

232 All patients with an ultrarapid virological response who were given 3 weeks of triple th

233 1) use of a "validated" surrogate (sustained virological response) for a primary endpoint, (2) shorte

234 ents in fibrosis stages F0-F3 post-sustained virological response, and in the transition probabilitie

235 recipients, without achieving HEV sustained virological response, and may induce a biopsy-proven reg

236 antivirals (DAAs; 8-12 weeks, 95% sustained virological response, pound3300/week).

237 The aim of this study was to report on the virological response, safety, and tolerability of SOF an

238 ents (99%, 95% CI 98-100) achieved sustained virological response, with one (1%) relapse at post-trea

239 mplications were less likely after sustained virological response.

240 MC is a negative prognostic factor of virological response.

241 atitis C has led to an increase in sustained virological response.

242 ence is markedly decreased after a sustained virological response.

243 g 12 weeks of follow-up achieved a sustained virological response.

244 o clear the virus, and establish a sustained virological response.

245 l ongoing) but without achieving a sustained virological response.

246 We assessed the safety and sustained virological responses (SVR) of SIM+SOF with and without

247 /=1 to </=2 log-reduction in 2 weeks; n = 2) virological responses were observed in 15 (83%) brincido

248 fovir episodes compared to only 2 (9%) major virological responses with cidofovir (P < .0001).

249 Health-state transition probabilities, virological responses, and utility values were obtained

250 xicity and good clinical, immunological, and virological responses.

251 Mutagenesis and virological studies demonstrate that RSV F residue 201 i

252 ted using electron microscopic, genetic, and virological studies, which identified a parvovirus with

253 Through week 48, virological success (HIV-1 RNA <50 copies per mL) was ma

254 e or E/C/F/tenofovir disoproxil fumarate had virological success.

255 aged 6-11 years, weighed 25 kg or more, had virological suppression (<50 copies of HIV-1 RNA per mL)

256 viral therapy (ART), and 90% of those having virological suppression (90-90-90).

257 All participants maintained virological suppression (HIV-1 RNA <50 copies per mL) at

258 Summary estimates of virological suppression after 6, 12, 24, 36, 48, and 60

259 at high levels of adherence to treatment and virological suppression are sustained.

260 have emphasized the importance of long-term virological suppression as a key measure of program perf

261 Early antiretroviral therapy (ART) and virological suppression can affect evolving antibody res

262 ranges, most patients will likely experience virological suppression during receipt of currently avai

263 citabine, and tenofovir alafenamide achieved virological suppression in 92% of previously untreated a

264 y and could have a substantial effect on HIV virological suppression in children and adolescents, a g

265 inferior to boosted lopinavir plus NRTIs for virological suppression in resource-limited settings.

266 T (HR 5.2, 4.4-6.1; p<0.0001]) compared with virological suppression of less than 50 copies per mL.

267 Summary estimates of virological suppression remained >80% for up to 60 month

268 ne with tenofovir alafenamide, high rates of virological suppression were maintained.

269 INTERPRETATION: At 48 weeks, virological suppression with the bictegravir regimen was

270 tabine in cART did not influence the time to virological suppression within 48 weeks or the probabili

271 failure (detectable viral load after initial virological suppression).

272 95% CI 67.5-73.0) of HIV-infected people had virological suppression, close to the UNAIDS target of 7

273 Among women with virological suppression, sCD163 remained associated with

274 kg (IQR 27.5-33.0), and all participants had virological suppression.

275 lity of virological rebound after successful virological suppression.

276 f individuals achieve the desired outcome of virological suppression.

277 d directly observed therapy had no effect on virological suppression.

278 tart treatment, and 90% achieve and maintain virological suppression.

279 of antiretroviral therapy and high rates of virological suppression.

280 of this approach enhanced the findings from virological surveillance and epidemiological studies bet

281 To facilitate virological surveillance and epidemiological studies, we

282 (i) the national surveillance database, (ii) virological surveillance records from all provinces, and

283 icient way of HIV-1 spread and occurs at the virological synapse (VS).

284 res seen by electron microscopy in the HIV-1 virological synapse.

285 lease of infectious virus particles into the virological synapse.

286 Virological synapses (VS) are adhesive structures that f

287 nfected to uninfected CD4(+) T cells through virological synapses (VS) has been found to require grea

288 cell spread at intercellular contacts called virological synapses (VS), where the virus preferentiall

289 t cell-cell transmission that takes place at virological synapses (VS).

290 trovirus-induced immune cell contacts called virological synapses (VS).

291 large number of particles transferred across virological synapses has also been implicated in reduced

292 A hallmark of virological synapses is that viruses can be transmitted

293 directional assembly of viral components at virological synapses, thereby facilitating cell-to-cell

294 h trimerized Env during its biosynthesis, at virological synapses, with innate immune effectors (such

295 e lymph node to spread the infection through virological synapses.

296 ls directly contact uninfected cells to form virological synapses.

297 viral structures created by transfer across virological synapses.

298 influenza infection dynamics model fitted to virological, systemic and respiratory symptoms to invest

299 The DBS sample matrix facilitates virological testing in remote areas.

300 een June 2015 and May 2016, biomolecular and virological tests were performed on 845 clinical samples