ライフサイエンスコーパス: virological

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

2 nding this high mortality, detailed clinical virological analyses were performed in specimens from 18

3 A postmortem, virological analysis of multiple organs, such as the kid

4 Here we report a detailed virological analysis of nine cases of COVID-19 that prov

5 Therefore, virological analysis of RSV isolates in conjunction with

6 Virological analysis revealed that mice lacking IFN-alph

7 By these means, together with virological and biochemical methods, we identify the vir

8 l events and their correlation with baseline virological and biochemical parameters as well as interf

9 Virological and biochemical parameters, interferon and n

10 rivir should be tested without delay on both virological and clinical endpoints in patients with or a

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

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

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

14 Virological and clinical relapses were defined as viral

15 We assessed virological and gene-expression changes using quantitati

16 Virological and histological analyses revealed greater i

17 The sequential pathology, virological and immune cell kinetics (CD4(+), CD8(+) T-l

18 n vitro, were associated with more sustained virological and immunological benefits of continued DTG

19 We provide detailed clinical, virological and immunological data of a B-cell depleted

20 (LoC) to investigate possible mechanisms and virological and immunological events related to the sudd

21 Here, we describe the virological and immunological factors that play a role i

22 ological status of COVID-19 and consider the virological and immunological lessons, animal models, an

23 and showed a distinctive trend of increasing virological and immunological response rates through 96

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

25 Using virological and immunological techniques, we examined th

26 Here we compared virological and innate immunological aspects of two ZIKV

27 e the impact of clinical interventions using virological and phylogenetic analysis.

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

29 Our objective was to identify virological and serological predictors of anal high-grad

30 Through multiple years of virological and serological surveillance in a single ord

31 Relying on routine virological and serological testing may not identify exp

32 andomized study comparing the immunological, virological, and clinical responses to cART based on 2 n

33 als with ATIs also intend to determine host, virological, and immunological markers that are predicti

34 A comprehensive clinical, virological, and immunological study was performed.

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

36 Biochemical and virological assays were performed to analyze the effects

37 scopy, transmission electron microscopy, and virological assays.

38 Concentrations of HBV serological/virological biomarkers (HBV DNA, HBsAg, HBcrAg, and HBV

39 The concentrations of HBV serological/virological biomarkers (HBV DNA, HBsAg, HBcrAg, HBV RNA)

40 favourable outcomes, with increasing risk of virological breakthrough as MPR fell.

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

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

43 , should be evaluated in other studies using virological case confirmation.

44 etween baseline clinical, immunological, and virological characteristics and the HIV reservoir size m

45 We compared all virological characteristics between the local and import

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

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

48 Here, we report the epidemiological and virological characteristics of the COVID-19 outbreak.

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

50 Our findings highlight virological characteristics-both genetic and functional-

51 with respect to clinical, immunological and virological characteristics.

52 liver damage, and coagulopathy as defined by virological, clinical, and pathological criteria.

53 unt an immune response to SARS-CoV-2 without virological confirmation of infection, raising the possi

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

55 asma samples from ECs who spontaneously lost virological control (transient controllers [TCs]), at 2

56 IV-positive organ transplantation is loss of virological control because of donor-derived HIV superin

57 rol group of ECs who persistently maintained virological control during the same follow-up period (pe

58 However, 25% lose virological control over time.

59 HIV-infected subjects under virological control still exhibit a persistent proinflam

60 proteomic profile that preceded this loss of virological control to identify potential biomarkers.

61 ture associated with the spontaneous loss of virological control was characterized by higher levels o

62 ts of whom 29 were coinfected with HIV under virological control.

63 IV-1 infected child with long-term sustained virological control.

64 this population at risk of poor post-partum virological control.

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

66 We analyzed epidemiological and virological data at molecular level to comprehend the cu

67 We show that virological data from sequential infection experiments c

68 Clinical and virological data from these patients were collected.

69 We analyzed epidemiological and virological data to comprehend the current epidemiologic

70 standing of the clinical, immunological, and virological determinants of reservoir size is critical t

71 of previously hypothesised environmental and virological drivers of influenza epidemics.

72 hate exhibits a long half-life and prolonged virological effects.

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

74 Although the virological, epidemiological, clinical, and management o

75 addition to the bioinformatics analysis, the virological evaluation of the results can be important i

76 cell counts to identify potential immune and virological factors that were responsible for initial vi

77 unpredictable but depends on ecological and virological factors.

78 tment containing an NNRTI and two NRTIs, had virological failure (confirmed HIV-1 RNA >=400 copies pe

79 ed evolution of PI resistance mutations from virological failure (confirmed VL >1000 copies/mL) until

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

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

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

83 VS (<400 copies/mL), confirmed virological failure (VF) (2 consecutive viral loads >100

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

85 g 537 DAA-treated patients who experienced a virological failure (VF) in France between 2015 and 2018

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

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

88 xed virions at the earliest recorded time of virological failure (VF).

89 252 (32%) of 786 patients had virological failure (viral load >=1000 copies per mL).

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

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

92 f-care regimen for at least 6 months without virological failure and be aged 18 years or older.

93 004-2017, from 9 South African cohorts, with virological failure and complete baseline data.

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

95 5%) of 400 participants in the OLA group had virological failure at month 12 of ART (95% CI 6.0-11.7)

96 6f infection and cirrhosis had on-treatment virological failure at treatment week 12, and one patien

97 proportion of patients with protocol-defined virological failure at week 96 was low in all treatment

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

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

100 Virological failure during follow-up occurred in 14 380

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

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

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

104 Our finding that OLA testing for PDR reduced virological failure in only those with specific PDR muta

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

106 Risk of virological failure increased further with higher ranges

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

108 Switching therapy for virological failure is relatively rare at this time, and

109 IV-2 integrase (231INS)-in 6 patients at the virological failure of a raltegravir-based regimen.

110 ravir, elvitegravir, and raltegravir) at the virological failure of an INSTI-based regimen.

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

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

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

114 inical management of patients with confirmed virological failure on a dolutegravir-based regimen can

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

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

117 and that the value of PDR testing to reduce virological failure should be assessed for antiretrovira

118 ment - these patients were classified as non-virological failure since viral clearance could not be d

119 Province were more likely to experience non-virological failure than patients in Kigali, likely due

120 s suggests that PDR poses less of a risk for virological failure than that predicted by past prevalen

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

122 nts given efavirenz were less likely to have virological failure than were those receiving nevirapine

123 Among participants with PDR, virological failure was lower in the OLA-guided therapy

124 tion between preexisting LA-DRVs and risk of virological failure whereas 14/25 (56.0%) did not.

125 In case of confirmed virological failure, a switch to second-line ART is indi

126 %) achieved SVR12, 304 (34%) experienced non-virological failure, and 50 (6%) experienced virological

127 IV-1, was associated with a low frequency of virological failure, and had a favourable safety profile

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

129 2 months after ART initiation, which defined virological failure, assessed in all participants who re

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

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

132 (92%) achieved SVR12 and 50 (8%) experienced virological failure.

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

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

135 unfavourable therapeutic outcomes, including virological failure.

136 A above the median split was associated with virological failure.

137 virological failure, and 50 (6%) experienced virological failure.

138 There were 3 protocol-defined virological failures (2 DTG, no acquired resistance; 1 E

139 and two (<1%, every 4 weeks group) confirmed virological failures (two sequential measures >=200 copi

140 We observed 121 virological failures during 18'447 person-years of follo

141 There were 5 virological failures in the DTG-I arm and 5 (1 while on

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

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

144 (SVR) with glecaprevir/pibrentasvir, with no virological failures.

145 lity of life despite impressive clinical and virological improvements in HIV care.

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

147 humanized mice controlled HBV infection and virological markers declined 4-5 log or below detection

148 ub-Saharan Africa combined with weak routine virological monitoring has driven increasing HIV drug re

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

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

151 patient-years of data that were linked with virological (n = 5910 swabs) data.

152 of data, which were linked with hospital and virological (n=5,910 swabs) data.

153 No difference in clinical, virological or pathological parameters were observed in

154 Virological outcome was assessed using Cox regression in

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

156 We compared virological outcomes by pre-ART CD4 count, where univers

157 possession ration (MPR) and its relation to virological outcomes in a large multi-centre hospital ou

158 evirapine or efavirenz have suggested poorer virological outcomes in the presence of pretreatment dru

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

160 with CD4 counts >=500 cells/uL had very good virological outcomes, being better than those with CD4 c

161 cDNA, to characterise this dissociation, and virological outcomes.

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

163 DNA), to characterize this dissociation, and virological outcomes.

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

165 the CLIV Score based on clinical and immune-virological parameters is potentially useful to stratify

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

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

168 as potential biomarker for the prediction of virological progression and as therapeutic target in ECs

169 on for HIV-1/O variants, suggesting specific virological properties and physiopathology that now need

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

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

172 while only age and race were associated with virological rebound in 2012-2017.

173 homelessness were associated with increased virological rebound in earlier time periods, while only

174 c form responsible for viral persistence and virological relapse after treatment withdrawal.

175 patients subsequently developed clinical and virological relapses.

176 egative at baseline and failure to remain in virological remission were associated with an increased

177 is largely dependent upon the maintenance of virological remission, since viral load is found to be t

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

179 (25%), and 19 of these 24 achieved sustained virological response (79%).

180 n treatment, which can result in a sustained virological response (effective cure).

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

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

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

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

185 as the proportion of patients with sustained-virological response (SVR) at 12 and/or 24 weeks post-tr

186 The primary outcome was sustained virological response (SVR) at 12 weeks after completion

187 with hepatitis C virus (HCV) with sustained virological response (SVR) develop hepatic complications

188 Some HCV-infected patients with sustained virological response (SVR) develops hepatic complication

189 ticenter study aimed to assess the sustained virological response (SVR) in a large cohort of solid or

190 Sustained virological response (SVR) is a non-validated surrogate

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

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

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

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

195 HCV-infected patients who achieve sustained virological response (SVR) with direct-acting antiviral

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

197 notype 5 or 6 infection achieved a sustained virological response (SVR) with glecaprevir/pibrentasvir

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

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

200 ting antiviral (DAA) treatment and sustained virological response (SVR).

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

202 primary outcome was achievement of sustained virological response 12 weeks after completion of glecap

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

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

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

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

207 proportion of participants with a sustained virological response 12 weeks after therapy (SVR12).

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

209 The primary endpoint was sustained virological response 12 weeks after treatment (SVR12).

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

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

212 Sustained virological response after 12 weeks of follow-up was ach

213 e becoming increasingly related to sustained virological response after hepatitis C, suppressed hepat

214 Sustained virological response among primary care participants (98

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

216 Sustained virological response at 12 weeks post-treatment (SVR12)

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

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

219 after the end of treatment (for a sustained virological response at Week 12; SVR12).

220 Sustained virological response for 12 weeks for Dactavira or Dacta

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

222 Conclusion: The lower rates of sustained virological response in patients infected with subtype 4

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

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

225 he per-protocol population, 67/67 (100%) had virological response in the dolutegravir monotherapy gro

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

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

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

229 d velpatasvir has resulted in high sustained virological response rates in patients chronically infec

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

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

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

233 Sustained virological response sustain virological response (SVR)1

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

235 e models to estimate the effect of sustained virological response to hepatitis C virus treatment on t

236 on (which was treated, achieving a sustained virological response when she was 18 years old), and sec

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

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

239 th LD and HCC were age, absence of sustained virological response, and severity of cirrhosis, but not

240 The primary efficacy endpoint was sustained virological response, defined as HCV RNA less than 15 IU

241 observe a temporally correlated clinical and virological response, leading to clinical resolution and

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

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

244 ence is markedly decreased after a sustained virological response.

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

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

247 mplications were less likely after sustained virological response.

248 All patients achieved sustained virological response.

249 evaluate the impact of HEV RNA mutations on virological response.

250 /=1 to </=2 log-reduction in 2 weeks; n = 2) virological responses were observed in 15 (83%) brincido

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

252 sments included pharmacokinetic analyses and virological responses.

253 our estimates for epidemiological processes, virological sample positivity, vaccine uptake and effica

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

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

256 In the randomised cohort, rates of virological suppression (HIV-1 RNA <40 copies per mL) in

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

258 rence and human immunodeficiency virus (HIV) virological suppression (VS) among clinically well peopl

259 We assessed the impact of PDR on virological suppression (VS; <50 copies/mL) in individua

260 ether these properties would allow sustained virological suppression after simplification of cART to

261 However, natural virological suppression and absence of immune dysfunctio

262 To improve virological suppression and address the emerging threat

263 There is a paucity of data on virological suppression and clinical management of patie

264 The secondary endpoints included virological suppression at 48 weeks according to the US

265 We aimed to investigate virological suppression before giving birth with doluteg

266 In this study, 90% virological suppression below the threshold of 1,000 cop

267 inexpensive point mutation assay can improve virological suppression by identifying PDR to guide drug

268 gramme on HIV/AIDS (UNAIDS) to have achieved virological suppression in 90% of all persons receiving

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

270 rvice delivery can substantially improve HIV virological suppression in adolescents with HIV and shou

271 o characterise safety, pharmacokinetics, and virological suppression in adults who are HIV positive.

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

273 (DTG) monotherapy could be used to maintain virological suppression in people living with human immu

274 ug antiretroviral regimen for maintenance of virological suppression in people with HIV-1.

275 Monitoring of virological suppression is recommended at 6 months of tr

276 n of dolutegravir plus rilpivirine sustained virological suppression of HIV-1, was associated with a

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

278 port a large-scale multicenter assessment of virological suppression over time and management of vire

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

280 Among women with virological suppression, sCD163 remained associated with

281 Virological suppression, switch to second-line ART, deat

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

283 of antiretroviral therapy and high rates of virological suppression.

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

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

286 To facilitate virological surveillance and epidemiological studies, we

287 Dendritic cells (DCs) form a virological synapse (VS) with CD4(+) T cells, enabling t

288 tact, virions pass to target cells through a virological synapse or cellular conduits or are transfer

289 lease of infectious virus particles into the virological synapse.

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

291 Virological synapses (VS) are adhesive structures that f

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

293 mune system and delivering it to T cells via virological synapses (VS).

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

295 viral structures created by transfer across virological synapses.

296 atories' ability to perform high-sensitivity virological testing for SARS-CoV-2.

297 r care from acute respiratory infection, and virological testing of acute respiratory infections at t

298 uenza infections were identified through the virological testing of samples taken from patients diagn

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

300 tively between 2011 and 2017, using accurate virological tools.