ライフサイエンスコーパス: HCV RNA

1 HCV RNA levels were significantly higher with CAP/CTM th

2 HCV RNA present in the patient liver specimen was undete

3 HCV RNA results were provided in a mean of 2 days.

4 HCV RNA testing was performed in 90 % (9/10) of HCV AB-p

5 HCV RNA was detected DBS from the vast majority of patie

6 HCV RNA was detected in 23% (325/1386).

7 HCV RNA was detected in 45 (30% [95% CI 23-38]) of 150 p

8 HCV RNA was measured using a reverse-transcription polym

9 HCV RNA was readily detected in all control mice challen

10 HCV-RNA is commonly detectable in rectal and nasal fluid

11 nstrated that 97% had post-treatment Week 12 HCV RNA >10 000 IU/mL, above reported sensitivity limits

12 ological response at post-treatment week 12 (HCV RNA <15 IU/mL).

13 t a computational model of the hAgo2:miR-122:HCV RNA complex at the 5' terminus of the viral genome a

14 ive Canadian Co-infection Cohort (n = 1423), HCV RNA-positive participants in whom IFN-lambda genotyp

15 IA and HCV-WES was determined by testing 205 HCV RNA-negative/anti-HCV-positive samples, of which 149

16 chronically infected with HCV genotypes 1-6 (HCV RNA >/=10 000 IU/mL) with or without compensated cir

17 795 HCV RNA + patients without HCC from University of Michig

18 At week 8 HCV RNA was undetectable in 15/28 patients.

19 f lipid rafts, from autophagosomes abolished HCV RNA replication.

20 therapy using highly sensitive and accurate HCV RNA assays.

21 All patients achieved HCV RNA below lower limit of quantification (<12 IU/mL)

22 Following RG-101 administration, HCV RNA declined in all patients (mean decline at week 2

23 HCV antibodies were measured from all HCV RNA-positive samples.

24 Of all HCV RNA+, 49% reported current injection drug use (82 of

25 omes to these core clusters without altering HCV RNA colocalization with NS5A.

26 were significantly higher among men with an HCV RNA load of >/=2 x 10(6) IU/mL, compared with findin

27 fficacy was measured by SVR12, defined as an HCV-RNA level less than 25 IU/mL.

28 ty were screened for anti-HCV antibodies and HCV RNA, and viremic women were tested for quantitative

29 HCV antibody and HCV RNA prevalence were 58.8% (95% confidence interval [

30 proteins colocalize with apolipoproteins and HCV RNA in Sec31-coated COPII vesicles.

31 % sensitivity compared to serum anti-HCV and HCV RNA reverse-transcription polymerase chain reaction

32 atients for anti-HCV antibody (anti-HCV) and HCV RNA.

33 n reads, which included the expected HIV and HCV RNA sequences.

34 umulative HCV treatment uptake, outcome, and HCV RNA prevalence were evaluated, with follow-up throug

35 umulative HCV treatment uptake, outcome, and HCV RNA prevalence were evaluated, with follow-up throug

36 dependently analyzed HCV drug resistance and HCV RNA measurement results that were submitted to the U

37 d received shorter courses of treatment, and HCV RNA was undetectable in serum for shorter periods be

38 Tests included hepatitis C antibody, HCV RNA, HCV genotype (nucleic acid tests [NAT]), liver

39 with a sustained viral response, defined as HCV RNA concentration less than 15 IU/mL at 12 weeks aft

40 s sustained virological response, defined as HCV RNA less than 15 IU/mL at 12 weeks after completion

41 end of all study therapy (SVR12), defined as HCV RNA less than the lower limit of quantification (eit

42 tection of other bloodborne viruses, such as HCV RNA and SEN virus D.

43 athway includes HCV antibody (Ab), automatic HCV RNA for Ab-positive patients, coinfection and liver

44 different widely used commercially available HCV RNA test.

45 Baseline HCV RNA < 400,000 IU/ml (OR = 1.96; 95% CI, 1.13-3.39; P

46 is, HCV treatment history, GT , and baseline HCV RNA did not affect SVR12.

47 of the end of treatment; all 3 had baseline HCV RNA >/=800,000 IU/mL, a non-CC IL-28B genotype, and

48 rrhotic patients, respectively, had baseline HCV RNA levels below 4M and 6M IU/mL with ART.

49 fections, including those with high baseline HCV RNA loads.

50 The median baseline HCV RNA load was 6.17 log10 IU/mL (interquartile range 4

51 Median baseline HCV RNA was 2 280 000 IU/mL (interquartile range, 272 00

52 SVR12 was related to baseline HCV RNA (</=6 log10 IU/mL, P = 0.018) and early on-treat

53 naive, non-cirrhotic patients with baseline HCV RNA levels <6 million IU/mL (6.8 log10 IU/mL).

54 t-naive, noncirrhotic patients with baseline HCV RNA levels of <4 or <6 million (M) IU/mL based on po

55 (defined by FIB-4 </=3.25) and with baseline HCV RNA<6,000,000 IU/mL, SVR rates were 93.2% (1,020/1,0

56 6-70 kPa; cirrhosis, n = 9); median baseline HCV-RNA level was 1.38 x 10(6) IU/mL.

57 f follow-up (PYFU) after SVR, 18 (7%) became HCV RNA positive.

58 a multifunctional protein implicated in both HCV RNA replication and virus particle assembly.

59 serve as a promising target to inhibit both HCV RNA replication and virus assembly, representing a n

60 oylation likely allows NS2 to fine tune both HCV RNA replication and infectious-particle assembly.IMP

61 ity of patients with active replication, but HCV RNA levels were substantially lower than in serum sp

62 steps: anti-HCV test to screen, followed by HCV RNA reverse-transcription polymerase chain reaction

63 entify perinatally-exposed infants tested by HCV-RNA RT-PCR at age 2-6 months.

64 We estimated the association between chronic HCV (RNA+) and time to MI adjusting for demographic char

65 We estimated the association between chronic HCV (RNA+) and time to MI while adjusting for demographi

66 donor hearts without detectable circulating HCV RNA were followed using a reactive approach and star

67 Among patients with HCV coinfection, HCV RNA replication status at retransplantation was the

68 ere anti-HCV positive underwent confirmatory HCV RNA testing, and those with detectable HCV RNA were

69 Recurrence was defined as confirmed HCV RNA detectability post-SVR.

70 icons with 13 potently and durably decreased HCV RNA levels for gt1a, gt2a, and gt3a.

71 To thoroughly delineate HCV RNA populations, we developed conditions that fully

72 Treatment algorithm 2 (a detectable HCV RNA result followed by 2 sequential HCV RNA test res

73 lts) and treatment algorithm 5 (a detectable HCV RNA result followed by 2 sequential HCV RNA test res

74 2 minutes and 80% (261/325) had a detectable HCV RNA result in <=40 minutes.

75 surface antigen measurements and detectable HCV RNA, or a positive HCV antibody test result if HCV R

76 surface antigen measurements and detectable HCV RNA, or a positive HCV antibody test result if HCV R

77 ks after the end of treatment but detectable HCV RNA at follow-up week 24) and used refined phylogene

78 SOF, only 12 of 3004 patients had detectable HCV RNA following sustained virologic response 12 weeks

79 Patients with undetectable versus detectable HCV RNA had a survival probability of 80% versus 39% at

80 Among people with detectable HCV RNA (n = 325), median time to HCV RNA detection was

81 y HCV RNA testing, and those with detectable HCV RNA were genotyped.

82 urvival in recipients of HCV-viremic donors (HCV-RNA positive as measured by nucleic acid testing [NA

83 Using the composite case definitions, early HCV-RNA screening demonstrated sensitivity of 100% (87.5

84 If the proportion of eligible (HCV RNA positive) patients using DAAs stays at 65% per y

85 CV RNA-negative); or HCV treatment failures (HCV RNA-positive).

86 tima HCV provides a suitable alternative for HCV RNA testing on serum and DBS samples.

87 tivity of the Xpert HCV Viral Load assay for HCV RNA detection in plasma collected by venepuncture wa

88 tivity of the Xpert HCV Viral Load assay for HCV RNA detection in samples collected by finger-stick w

89 gest that NS2 palmitoylation is critical for HCV RNA replication by promoting NS2-NS3 autoprocessing.

90 mal Pro(314)-Trp(316) turn, is essential for HCV RNA replication, and its disruption alters the subce

91 h HCV genotype 1 infection were included for HCV RNA analysis with 2 widely used assays, Cobas AmpliP

92 me RNA testing of a high-risk population for HCV RNA might identify more infected persons than routin

93 r mRNAs, the entire eIF3 is not required for HCV RNA translation, favoring viral expression under con

94 The assay is specific for HCV RNA and is free of interference from non-HCV pathoge

95 ificity of the Xpert HCV Viral Load test for HCV RNA detection by venepuncture and finger-stick colle

96 tive for hepatitis C were further tested for HCV RNA genotyping.

97 ite constant negative results from tests for HCV RNA in serum.

98 opulation-based and systematic screening for HCV-RNA among MSM from the SHCS.

99 ewly identified or never treated for HCV had HCV RNA testing, of which 31 (51%) resulted positive (3.

100 Sixty-three percent had HCV RNA levels below the lower limit of quantification a

101 lved HCV; chronic, untreated HCV; cured HCV (HCV RNA-negative); or HCV treatment failures (HCV RNA-po

102 Patients with low and high HCV RNA levels were at higher risk of ESRD than those wh

103 The primary efficacy endpoint was SVR12 (ie, HCV RNA <15 IU/mL at 12 weeks post-treatment), assessed

104 were tested for presence of HCV RNA and, if HCV RNA positive, patients underwent treatment discussio

105 A, or a positive HCV antibody test result if HCV RNA measurements were not available.

106 A, or a positive HCV antibody test result if HCV RNA measurements were not available.

107 reduced NS2-NS3 autoprocessing and impaired HCV RNA replication.

108 promise in closing gaps, including improving HCV RNA testing, communicating diagnoses, and assessing

109 tent of which correlated with the decline in HCV RNA, suggesting HCV compartmentalization within the

110 we found a sharp and significant decrease in HCV RNA in the tumor compared with surrounding nontumoro

111 osis, or after 4 weeks if no 2-log10 drop in HCV RNA level occurs, promises rapid HCV elimination.

112 that two major functions of NS2 involved in HCV RNA replication and virus assembly, i.e., NS2-NS3 au

113 primarily binding to the poly U/UC motifs in HCV RNA.

114 g of NS2-NS3 precursor, an essential step in HCV RNA replication.

115 Reactivation was defined as an increase in HCV-RNA >/=1 log10 IU/mL over baseline and hepatitis fla

116 cellular HCV replication models that include HCV RNA secretion and/or virus assembly and release.

117 ected CTLs were polyfunctional and inhibited HCV RNA replication through antigen-specific cytotoxicit

118 Interestingly, HCV RNA was detected in most liver explants (67%).

119 nd that in spite of decreasing intracellular HCV RNA and extracellular virus concentration, low level

120 .018) and early on-treatment viral kinetics (HCV RNA below the level of quantitation at week 1, P = 0

121 All pretreatment labs (HCV RNA, genotype, and noninvasive fibrosis assessments)

122 CV RNA test result >=12 weeks after the last HCV RNA result; sensitivity for all 4 algorithms was 79%

123 extracellular virus concentration, low level HCV RNA secretion may continue as long as intracellular

124 ce interval {CI}, 1.88-2.73], P < .001), log HCV RNA (HR, 1.19 [95% CI, 1.02-1.38], P = .02), tobacco

125 00 HCV and cobas 4800 HCV were linear at low HCV RNA concentrations (<0.3 log10 IU/ml difference betw

126 The low HCV RNA prevalence and HCV incidence rates confirm that

127 Moreover, lower HCV RNA prevalence was associated with female gender, em

128 s (HCV) infection is determined by measuring HCV RNA at specific time points throughout therapy using

129 ction was 29 weeks (range 13, 52) and median HCV RNA was 6.2 log(10) IU/mL (range 0.9, 7.7).

130 At baseline, median HCV RNA was 5.4 log10 IU/mL (interquartile range 4.4-6.8

131 rified from HCV replicon cells could mediate HCV RNA replication in a lipid raft-dependent manner, as

132 V antibody-positive persons and 0.25 million HCV RNA-positive persons not part of the 2013-2016 NHANE

133 tivity, hepatocellular carcinoma, or missing HCV RNA or FIB-4 scores.

134 at least 18 years, with more than 1000 IU/mL HCV RNA, and a laboratory result at screening indicating

135 Modern HCV-RNA RT-PCR assays have excellent sensitivity for dia

136 We hypothesized that modern HCV-RNA RT-PCR platforms would adequately detect infecte

137 A negative HCV RNA result at 12 weeks of follow-up or thereafter wa

138 2'930/3'538 (83%) MSM with a prior negative HCV-RNA and identified 13 (0.4%) with a new HCV infectio

139 Among 742 infants with negative HCV-RNA results, 226 received follow-up anti-HCV testing

140 significantly reduced HCV infection but not HCV RNA replication.

141 duals were seen by an HCV specialist (57% of HCV RNA+), 72 started treatment (43%), and 69 (41%) comp

142 mplying that only the presence or absence of HCV RNA or changes in the HCV RNA level should be taken

143 valuable for surveillance in the absence of HCV RNA testing.

144 R system for rapid quantitative detection of HCV RNA in human EDTA-plasma and serum, and the performa

145 For the first 3 d after electroporation of HCV RNA, intracellular virus predominates over secreted

146 It is unclear which forms of HCV RNA are associated with ISG induction and IFN resist

147 ts without cirrhosis and a baseline level of HCV RNA <6 million IU/mL.

148 ogic response (SVR), defined as the level of HCV RNA below quantification at least 64 days after the

149 therapy was defined as undetectable level of HCV RNA by polymerase chain reaction assay (<50 IU/mL) 1

150 D and suggests that elevated serum levels of HCV RNA (>167,000 IU/mL) and HCV genotype 1 are strong p

151 Levels of HCV RNA in explants were significantly higher in patient

152 easured HCV binding, intracellular levels of HCV RNA, and expression of target genes.

153 Measurements of HCV RNA were performed using the Roche COBAS TaqMan HCV

154 in the presence of the 3' poly U/UC motif of HCV RNA.

155 In these two settings, the percentage of HCV RNA-positive patients identified as a result of refl

156 CV RNA (metagenomics), (ii) preenrichment of HCV RNA by probe capture, and (iii) HCV preamplification

157 The presence of HCV RNA and age of >=65 years were significantly associa

158 ositive patients were tested for presence of HCV RNA and, if HCV RNA positive, patients underwent tre

159 We evaluated the quantification of HCV RNA in serum and plasma by the Cepheid Xpert HCV Vir

160 t is the in vivo dose dependent reduction of HCV RNA observed in HCV infected (GT1a and GT3a) human h

161 stained virological response [SVR]12 (SVR of HCV RNA <15 IU/mL 12 weeks after the end of therapy).

162 negative HCV antibody result at the time of HCV RNA positivity.

163 We demonstrated that the transport of HCV RNA on the polysomes is Stau1-dependent, being mainl

164 ers and primary care settings, where omitted HCV RNA analyses had absolute reductions of 76.4 and 20.

165 e of anti-HCV-positive patients with omitted HCV RNA determination remarkably decreased in most setti

166 ate the assembly of miR-122/Ago complexes on HCV RNA, preferentially directing miR-122/Ago2 to S1 whi

167 n time to HCV RNA detection was dependent on HCV RNA level.

168 l P-body protein DCP1a that has no effect on HCV RNA production or infectivity of progeny virus.

169 own of E-cadherin, however, had no effect on HCV RNA replication or internal ribosomal entry site (IR

170 incorrect treatment duration based solely on HCV RNA test method used.

171 eron alpha (IFNalpha), but have no effect on HCV-RNA replication.

172 Using only HCV RNA cutoff of 6 million IU/mL, 29.55% of subjects wo

173 d by first positive anti-HCV antibody and/or HCV RNA within 6 months of enrollment and either acute c

174 ed by the presence of anti-HCV antibodies or HCV RNA.

175 Of 695 anti-HCV-positive patients, HCV RNA was tested in 520 (74.8%; 48.9% to 92.9% by prac

176 nces of two recently developed real-time PCR HCV RNA assays, cobas HCV for use on the cobas 6800/8800

177 k did not seem to be dependent of persistent HCV RNA.

178 notype 4 for at least 6 months with a plasma HCV RNA concentration of more than 1000 IU/mL at screeni

179 h HCV genotype 1 or 4 infection and a plasma HCV RNA concentration of more than 1000 IU/mL at screeni

180 the presence of detectable levels of plasma HCV RNA at the end of treatment even in patients that ul

181 d an ultrarapid virological response (plasma HCV RNA <500 IU/mL by day 2, measured by COBAS TaqMan HC

182 l [CI], 7.4%-42.9%), correlating with plasma HCV RNA (Spearman rank correlation r = 0.9); at biopsy 2

183 c infection with HCV genotype 5, with plasma HCV RNA of at least 10,000 IU/mL.

184 h a positive HCV antibody who had a positive HCV RNA was 0.5 (95% confidence interval, 0.42-0.55); th

185 Reinfection was defined as new positive HCV RNA within 6 months of enrollment and evidence of pr

186 ical Case Registry in patients with positive HCV RNA between October 1999 and August 2009 and follow-

187 virus assembly sites, which in turn promote HCV RNA replication and infectious-particle assembly, re

188 d region (UTR) and this interaction promotes HCV RNA accumulation, although the precise role of miR-1

189 l and nasal swabs were collected to quantify HCV-RNA levels within rectal and nasal fluids.

190 V VL FS) is a point-of-care test quantifying HCV RNA in <1 hour, enabling same-visit diagnosis and tr

191 nt-naive persons with available quantitative HCV RNA testing results.

192 d viremic women were tested for quantitative HCV RNA at 3, 6, 9, and 12 months postpartum.

193 Algorithms using serial quantitative HCV RNA results can serve as proxy measures for evaluati

194 ted retrospectively with the Abbott RealTime HCV RNA test (ART).

195 e, and 100% of Ab-positive patients received HCV RNA testing.

196 tment with simeprevir or daclatasvir reduced HCV RNA levels initially, but the levels later rebounded

197 ls with DAA and anti-miR-122 sharply reduced HCV RNA amounts.

198 CTLs expressing the NS5-specific TCR reduced HCV RNA replication by a noncytotoxic mechanism, the NS3

199 vigation, and anti-HCV screening with reflex HCV RNA testing.

200 engaged from care were more likely to remain HCV RNA positive.

201 engaged from care were more likely to remain HCV RNA positive.

202 only one of four 3/11-treated mice remained HCV-RNA negative throughout the observation period, wher

203 on: 1) infected children had positive repeat HCV-RNA testing or positive anti-HCV at age >=24 months;

204 ytes and cells with autonomously replicating HCV RNA, we found that levels of IRF5 mRNA and protein e

205 .016), but most patients (85%) with residual HCV-RNA in the explant achieved a sustained virologic re

206 y endpoint was sustained virologic response (HCV RNA below the limit of quantitation [<15 IU/mL]) 12

207 ients with a sustained virological response (HCV RNA <15 IU/mL) 12 weeks after the last dose of study

208 ients with a sustained virological response (HCV RNA <25 IU/mL) at post-treatment week 12 (SVR12) in

209 uggested that HCV-infected cells can secrete HCV RNA carrying exosomes that can infect cells in a rec

210 h HCV, suggests that initially most secreted HCV RNA derives from intracellular cytosolic plus-strand

211 c plus-strand RNA, but subsequently secreted HCV RNA derives equally from the cytoplasm and the repli

212 able HCV RNA result followed by 2 sequential HCV RNA test results >6 weeks apart) had the highest sen

213 able HCV RNA result followed by 2 sequential HCV RNA test results) and treatment algorithm 5 (a detec

214 eveloped multiple algorithms that use serial HCV RNA test results as proxy measures for initiation of

215 ined virologic response (no detectable serum HCV RNA 12 weeks after the end of antiviral therapy).

216 had chronic HCV genotype 1 infection (serum HCV RNA >/=2000 IU/mL), and stage 3-4 liver fibrosis.

217 oint was sustained virologic response (serum HCV RNA <25 IU/mL) 12 weeks after treatment ended (SVR12

218 owest limit of detection equivalent to serum HCV RNA levels of 150-250 IU/mL; using nondenaturation o

219 of the HCV-Ags EIA were equivalent to serum HCV RNA levels of approximate 150-250 IU/mL.

220 eron-free regimen and had undetectable serum HCV RNA at the time of liver transplantation.

221 Using ROC-curve analysis, serum HCV-RNA cut-offs for ruling in-/out any HCV+SS were esta

222 Using ROC-curve analysis, serum HCV-RNA cutoffs for ruling in/out any HCV+SS were establ

223 nd HIV-negative HCV patients with high serum HCV-RNA, independently of the suspected route of HCV tra

224 utes, especially in patients with high serum HCV-RNA.

225 utes, especially in patients with high serum HCV-RNA.

226 s with HCV+SS had significantly higher serum HCV-RNA levels than patients with HCV-negative SS (6.28

227 s with HCV+SS had significantly higher serum HCV-RNA levels than patients with HCV-negative SS (6.28

228 for 8-week regimens on the basis of a single HCV RNA determination may not be reliable because viral

229 U were more active than 22-3G in stabilizing HCV RNA and promoting its replication, whereas 21-3U was

230 miR-122 stabilizes the positive-strand HCV RNA genome and promotes its synthesis by binding two

231 V-positive participants underwent successful HCV RNA testing, of whom 230 (81%) were viraemic.

232 Mov10 overexpression suppresses HCV RNA in both infectious virus and subgenomic replicon

233 ned virological response at 12 weeks (SVR12; HCV RNA less than the lower limit of quantitation at 12

234 2015 and May 2016, we performed a systematic HCV RNA-based screening among HIV-infected MSM participa

235 A systematic HCV RNA-based screening among HIV-infected MSM revealed

236 d with the Xpert HCV VL FS test, rather than HCV RNA quantification, although the current platform do

237 nated on an iodixanol gradient revealed that HCV RNA is enriched in the highly buoyant COPII vesicle

238 lpha reduced Ser-235 phosphorylation and the HCV RNA levels in the infected cells.

239 ence or absence of HCV RNA or changes in the HCV RNA level should be taken into consideration for the

240 y of new virions, likely via transfer of the HCV RNA genome to viral particle assembly sites.

241 y of new virions, likely via transfer of the HCV RNA genome to viral particle assembly sites.

242 mprised 52% (standard deviation, 28%) of the HCV RNA in the livers of patients with chronic infection

243 HCV antibody test result at the time of the HCV RNA positivity.

244 This study evaluated time to HCV RNA detection using the Xpert HCV VL FS assay.

245 detectable HCV RNA (n = 325), median time to HCV RNA detection was 32 minutes and 80% (261/325) had a

246 Median time to HCV RNA detection was dependent on HCV RNA level.

247 Pre-treatment HCV RNA above the median split was associated with virol

248 At the end of treatment, HCV RNA was nonquantifiable in 89% (n = 17).

249 Sixty-two HCV RNA-positive patients (24% human immunodeficiency vi

250 obust in sensing and quantifying unamplified HCV RNA in clinical samples.

251 d, 770 perinatally-exposed infants underwent HCV-RNA testing at age 2-6 months.

252 rithm definitions and having an undetectable HCV RNA test result >=12 weeks after the last HCV RNA re

253 with HBV or HCV coinfection but undetectable HCV RNA.

254 er (47 versus 51 years) and had undetectable HCV RNA at LT (19% versus 9%) more frequently than non-H

255 l 12 weeks of treatment and had undetectable HCV RNA at their final treatment visit.

256 Three patients had undetectable HCV RNA levels 76 weeks after a single dose of RG-101.

257 ntly change in patients who had undetectable HCV RNA levels by week 8 post-RG-101 injection.

258 d sustained virologic response (undetectable HCV RNA 12 weeks after completing treatment with glecapr

259 Among people with undetectable HCV RNA (n = 1061), median time to result was 57 minutes

260 n of patients in the ITG with unquantifiable HCV RNA 12 weeks posttreatment (sustained virological re

261 NGS methods using (i) unselected HCV RNA (metagenomics), (ii) preenrichment of HCV RNA by

262 th spontaneous HCV clearance, 1294 untreated HCV RNA positive, 345 treated with sustained virologic r

263 ant differences were found between untreated HCV RNA-positive patients and those with SVR.

264 classified into strata based on time-updated HCV RNA measurements and HCV treatment, as either HCV an

265 eated a rationale for utilizing HCV-viremic (HCV-RNA-positive) donors, including into HCV-negative re

266 Hepatitis C virus (HCV) RNA and genotypes were determined in anti-HCV-posit

267 alyzes replication of the hepatitis C virus (HCV) RNA genome and therefore is central for its life cy

268 assessed the presence of hepatitis C virus (HCV) RNA in liver explants from 39 patients awaiting liv

269 and reliable detection of Hepatitis C Virus (HCV) RNA is a cornerstone in the management and control

270 e analyzed post-treatment hepatitis C virus (HCV) RNA levels from 330 subjects who experienced virolo

271 Hepatitis C virus (HCV) RNA quantitation is the primary method by which act

272 We performed hepatitis C virus (HCV) RNA screening among all men who have sex with men (

273 Point-of-care hepatitis C virus (HCV) RNA testing offers an advantage over antibody testi

274 ned virological response (hepatitis C virus [HCV] RNA <15 IU/mL) at post-treatment week 12 (SVR12) in

275 r sensitivity for very low viral load (VLVL; HCV RNA <=3000 IU/mL).

276 RNA positive/anti-HCV negative, and 15 were HCV RNA and anti-HCV negative, the specificity and sensi

277 were HCV RNA and anti-HCV positive, 15 were HCV RNA positive/anti-HCV negative, and 15 were HCV RNA

278 well-characterized samples, of which 40 were HCV RNA and anti-HCV positive, 15 were HCV RNA positive/

279 Of those, 44.4 % (4/9) were HCV RNA-positive, and all 4 (100 %) were linked to careg

280 hundred thirteen of 120 (94%) patients were HCV RNA undetectable at end of treatment, and SVR12 was

281 ximately 2.4 (2.0-2.8) million persons, were HCV RNA-positive (indicating current infection).

282 r time points, including 3 patients who were HCV RNA-negative 76 weeks postdosing.

283 nts who received organs from donors who were HCV-RNA negative (DNAT(-) ).

284 o received an allograft from donors who were HCV-RNA positive (DNAT(+) ) were compared to outcomes fo

285 ould be achieved by monitoring the time when HCV RNA is first detected with the Xpert HCV VL FS test,

286 in increased fluidity of the membrane where HCV RNA replication occurs.

287 This study aimed to determine whether HCV RNA level and genotype affect the risk of developing

288 infected with HCV genotypes 1, 2, or 3, with HCV RNA of at least 10 000 IU/mL, without evidence of ci

289 nosis (2.56; 1.74-3.76) were associated with HCV RNA positivity.

290 FH) cells were significantly associated with HCV RNA reduction, expansion of memory B and plasmablast

291 subgroups; those without cirrhosis but with HCV RNA<6,000,000 IU/mL were less likely to achieve SVR

292 tt ARCHITECT, HCVcAg correlated closely with HCV RNA levels greater than 3000 IU/mL.

293 at this fraction is directly correlated with HCV RNA replication efficiency.

294 high specificity, and good correlation with HCV RNA levels greater than 3000 IU/mL and have the pote

295 g SVR after HCV treatment were followed with HCV RNA measurements every 6 months in a prospective coh

296 tes with HCV antibodies and 2.1 million with HCV RNA and an estimated 0.38 million HCV antibody-posit

297 endpoint was the percentage of patients with HCV RNA <15 IU/mL 12 weeks after stopping therapy (SVR12

298 cohorts was the percentage of patients with HCV RNA <15 IU/mL 12 weeks after therapy (SVR12).

299 re transplantation compared to patients with HCV RNA-negative explants (P = .014 and P = .013, respec

300 Patients with HCV RNA-positive explants had received shorter courses o