ライフサイエンスコーパス: HCV RNA

1 HCV RNA concentration and population sequencing to detec

2 HCV RNA levels were correlated in semen and blood (r(2)

3 HCV RNA levels were determined by real-time polymerase c

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

5 HCV RNA polymerase is a key target for the development o

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

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

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

9 HCV RNA was detected in semen during both acute and chro

10 HCV RNA was detected in semen specimens from 29 of 66 me

11 HCV RNA was measured using a reverse-transcription polym

12 HCV RNA was readily detected in all control mice challen

13 HCV RNA was undetectable at week 4 in 77.2% of patients

14 eptor 7 and retinoic acid-inducible gene 1), HCV RNA induced consistent and broad transcription of mu

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

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

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

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 int was the proportion of patients achieving HCV RNA less than 25 IU/mL 12 weeks after end of treatme

23 int was the proportion of patients achieving HCV RNA less than 25 IU/mL at 12 weeks after end of trea

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

25 only independent predictive factor affecting HCV RNA negativity 6 months after liver transplantation

26 tracellular virus assembly without affecting HCV RNA replication.

27 line characteristics, including gender, age, HCV-RNA levels, and interleukin-28B genotype, did not im

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

29 Those with positive results of an HCV RNA test following viral suppression were investigat

30 point was a sustained virologic response (an HCV RNA level of <25 IU per milliliter) 12 weeks after t

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

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

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

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

35 % sensitivity compared to serum anti-HCV and HCV RNA reverse-transcription polymerase chain reaction

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

37 der with chronic HCV genoype 1 infection and HCV RNA at least 10 000 IU/mL in peripheral blood withou

38 er with chronic HCV genotype 1 infection and HCV RNA concentrations of 10 000 IU/mL or higher in peri

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

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

41 d only in PWID infected with genotype 3a and HCV-RNA negative PWID, but not in PWID infected with gen

42 und that Huh7-Lunet cells supported HAV- and HCV-RNA replication with similar efficiency and limited

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

44 Patients in Arm 2 with vRVR, defined as HCV RNA below the lower limit of quantification (LLOQ) f

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

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

47 tained virological response (SVR)-defined as HCV RNA levels below a designated threshold of quantific

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

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

50 different widely used commercially available HCV RNA test.

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

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

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

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

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

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

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

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

59 (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

60 6-70 kPa; cirrhosis, n = 9); median baseline HCV-RNA level was 1.38 x 10(6) IU/mL.

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

62 Depleting AGO2 or PCBP2, which binds HCV RNA in competition with miR-122 and promotes transla

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

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

65 and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-1

66 eplication-competent, genome-length chimeric HCV RNAs encoding GBV-B structural proteins in place of

67 Subjects who cleared HCV RNA (n = 36) showed a significant decrease in anti-H

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

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

70 ized HCV, independent of cell-cell contacts; HCV RNA was translated but not replicated.

71 l role of the NS4A TM domain in coordinating HCV RNA replication and virus particle assembly.

72 onstrated that MCPIP1 could directly degrade HCV RNA.

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

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

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

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

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

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

79 gher (96%) compared to those with detectable HCV RNA (83%).

80 re examined in 483 HCC cases with detectable HCV RNA and 516 controls.

81 lead-in, patients with target-not-detectable HCV-RNA at week 8 (rapid virologic response; LI4W-W8UTND

82 Patients with target-detectable HCV-RNA at week 8 received 44 weeks of BOC/PEGIFN/RBV (t

83 HCV RNA assays and the impacts of different HCV RNA cutoffs on treatment outcome were evaluated.

84 a-driven structural models for three diverse HCV RNA genomes.

85 We show that miR-122 enhances HCV RNA levels by altering the fraction of HCV genomes a

86 We evaluated HCV RNA sequences in serum and liver tissue to distingui

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 red semen and blood samples were assayed for HCV RNA levels.

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 b) followed by a nucleic acid test (NAT) for HCV RNA when the antibody test is positive, are compared

93 NS5A is required for HCV RNA replication and is involved in viral particle fo

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

95 Among 287 patients tested for HCV RNA (91% of all anti-HCV-positive cases), 175 (61%)

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

97 from rhesus macaques are also permissive for HCV-RNA replication and particle production, which is en

98 without GS-9669 or GS-9451, 100% (59/59) had HCV RNA <LLOQ by the Roche assay and 1 relapsed (PPV, 98

99 By the Abbott assay, 90% (53/59) had HCV RNA <LLOQ, of whom 1 patient relapsed (PPV, 98%).

100 r reasons other than virological failure had HCV RNA less than 25 IU/mL at their last study visit.

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

102 ts treated with sofosbuvir and ribavirin had HCV RNA <LLOQ at EOT by the Roche and Abbott assays, but

103 population consisted of 43 patients who had HCV-RNA level less than 25 IU/mL at the time of transpla

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

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

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

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

108 igible for shorter, 24-week total therapy if HCV RNA is undetectable at both weeks 4 and 12.

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

110 In this study, the concordance in HCV RNA assessments between the Roche High Pure System/C

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

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

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

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

115 However, the reason for inefficient HCV RNA replication efficiency in mouse liver cells rema

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

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

118 wn of autophagy genes enhances intracellular HCV RNA and accumulates infectious virus particles in ce

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

120 HCV) across England using routine laboratory HCV RNA testing data.

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

122 00 HCV and cobas 4800 HCV were linear at low HCV RNA concentrations (<0.3 log10 IU/ml difference betw

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

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

125 th acute HCV and HIV coinfection, the median HCV RNA level in blood specimens from those with seminal

126 The median HCV RNA level in blood was 4.0 log IU/mL higher than tha

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

128 Changes in IP-10 levels mirror HCV RNA, suggesting that IP-10 is an indicator of innate

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

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

131 termination of RNA polymerase II, modulates HCV RNA abundance in the cytoplasm, but is counteracted

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

133 significantly reduced HCV infection but not HCV RNA replication.

134 Our studies also demonstrate that NS5B HCV RNA polymerase was able to accommodate 2',4'-diF-rU

135 We evaluated the predictive ability of HCV RNA levels at end of treatment (EOT) for sustained v

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

137 nts who tested positive for trace amounts of HCV RNA more than 6 months after completing pegylated IF

138 We previously reported that trace amounts of HCV RNA, below the sensitivity of the standard clinical

139 se results demonstrate that trace amounts of HCV RNA, which appear sporadically in successfully treat

140 n situ hybridization (ISH) system capable of HCV RNA and ISG mRNA detection in human liver biopsies a

141 minant 5' exoribonuclease mediating decay of HCV RNA and that miR-122 provides protection against it.

142 erent HCV strains and mediating the decay of HCV RNA.

143 Here we study the details of HCV RNA replication by determining crystal structures of

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

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

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

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

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

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

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

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

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

153 (PPV) and negative predictive value (NPV) of HCV RNA less than the lower limit of quantification (<LL

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

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

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

157 ot alter translation or replication rates of HCV RNA, but affected viral RNA stability.

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

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

160 in synthesis and preferential translation of HCV RNA.

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

162 Notably, the level of HCV-RNA after 4 weeks of treatment was a significant pre

163 nt of peginterferon + ribavirin dependent on HCV RNA level at week 12; (2) Harvoni treatment, 12 week

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

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

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

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

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

169 response to HCV treatment, HCV RNA level, or HCV RNA decline at week 4.

170 In 64 patients, HCV-RNA levels were less than 25 IU/mL by week 4 of trea

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

172 Peak HCV RNA level was lower during reinfection than primary

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

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

175 ction, compensated liver disease, and plasma HCV RNA higher than 10 000 IU/mL who were null or partia

176 ted >/=6 months before screening) and plasma HCV RNA levels higher than 10,000 IU/mL.

177 HIV infection raises plasma HCV RNA levels and diminishes the response to exogenous

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

179 tients with sustained viral response (plasma HCV RNA level <12 IU/mL) 12 weeks after end of treatment

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

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

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

183 ividuals, of whom 6,383 (47%) had a positive HCV-RNA test.

184 Quantifiable HCV RNA (range, 15-57 IU/mL) was measured 2 weeks posttr

185 ining treatments, low levels of quantifiable HCV RNA at EOT do not preclude treatment success.

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

187 Pure System/Cobas TaqMan and Abbott RealTime HCV RNA assays and the impacts of different HCV RNA cuto

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

189 A fourth chimpanzee received HCV RNA-negative plasma and PBMCs from healthy blood don

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

191 nhanced JAK1 and IRF9 expression and reduced HCV RNA replication.

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

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

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

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

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

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

198 patients with sustained virologic response (HCV RNA <25 IU/mL) at posttreatment week 12 (SVR12).

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

200 endpoint was sustained virological response (HCV RNA <15 IU/mL) 12 weeks after the end of therapy (SV

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

202 dpoint was a sustained virological response (HCV RNA <25 IU/mL) 12 weeks after the end of treatment (

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

204 stration of miR-122, Xrn2 depletion restored HCV RNA abundance, arguing that Xrn2 depletion eliminate

205 care (CoC) from HCV antibody (Ab) screening, HCV-RNA confirmation, engagement and retention in medica

206 Seminal HCV RNA was detected in >/=1 sample for 26 of 35 men (74

207 Elevated seminal HCV RNA levels could contribute to sexual transmission o

208 iated with an increased frequency of seminal HCV RNA detection.

209 l in blood specimens from those with seminal HCV RNA was higher than that in blood specimens from tho

210 n blood specimens from those without seminal HCV RNA (P = .001).

211 atment completion (SVR12), assessed by serum HCV RNA concentrations lower than 43 IU/mL (the lower li

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

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

214 irin allowed for rapid negativation of serum HCV RNA and was well tolerated despite advanced liver an

215 ction, reaching steady-state levels of serum HCV RNA by day 21.

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

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

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

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

220 erformed after 46 days of undetectable serum HCV RNA.

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

222 L3 was associated with increased spontaneous HCV RNA clearance, with an adjusted odds ratio (95% CI)

223 oma (HCC) among subjects in whom spontaneous HCV RNA clearance did not occur.

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

225 ad negative results of at least 1 subsequent HCV RNA test.

226 onsistent with this, 41H potently suppressed HCV RNA in the 20-day RNA reduction assay.

227 The primary efficacy end point was SVR12 (HCV RNA level below the lower limit of quantification at

228 The primary study outcome was SVR12 (HCV-RNA <25 IU/mL at posttreatment week 12) in patients

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

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

231 dge, for the first time, we demonstrate that HCV-RNA sensing by human trophoblast cells elicits a str

232 We found that HCV-RNA sensing by human trophoblast cells induces robus

233 Furthermore, we observed that HCV-RNA transfection induces a proapoptotic response wit

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

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

236 in recognizes 5' triphosphate (5'ppp) of the HCV RNA and a pathogen-associated molecular pattern (PAM

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

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

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

240 for PI(4,5)P2 binding and replication of the HCV-RNA genome.

241 ter transplantation among patients with this HCV-RNA level at their last measurement before transplan

242 l count, previous response to HCV treatment, HCV RNA level, or HCV RNA decline at week 4.

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

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

245 with HBV or HCV coinfection but undetectable HCV RNA.

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

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

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

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

250 CV treatment, and 18 (0.4%) had undetectable HCV RNA.

251 e number of consecutive days of undetectable HCV RNA before transplantation.

252 Using undetectable HCV RNA as the cutoff, the more sensitive Abbott RealTim

253 Using undetectable HCV RNA at week 4, 34% of the patients would be eligible

254 wever, 92% of the patients with undetectable HCV RNA by Abbott RealTime achieved a sustained virologi

255 stained virologic response with undetectable HCV RNA by the High Pure System or <12 IU/ml by Abbott R

256 total of 1113 CHC patients with undetectable HCV RNA during peg-IFN/RBV therapy were enrolled.

257 The fifth patient had undetectable HCV-RNA levels at the end of triple therapy but subseque

258 the proportion of patients with undetectable HCV-RNA levels 12 weeks after therapy completion (SVR12)

259 Half of the patients achieved undetected HCV RNA at treatment week 4, and their SVR12 rate was si

260 ate-treatment group achieving unquantifiable HCV RNA 12 weeks after treatment (SVR12); adverse events

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

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

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

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

265 In the base-case scenario, total viraemic (HCV RNA-positive) cases of HCV in England will decrease

266 Patients with detectable hepatitis C virus (HCV) RNA at the time of liver transplantation universall

267 tion-competent subgenomic hepatitis C virus (HCV) RNA can be transferred to permissive Huh7 cells, le

268 who achieved undetectable hepatitis C virus (HCV) RNA during pegylated interferon plus ribavirin (peg

269 d to characterize seminal hepatitis C virus (HCV) RNA dynamics in human immunodeficiency virus (HIV)-

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

271 ' noncoding region of the hepatitis C virus (HCV) RNA genome, protecting the viral RNA from degradati

272 oRNA, miR-122, stabilizes hepatitis C virus (HCV) RNA genomes by recruiting host argonaute 2 (AGO2) t

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

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

275 Hepatitis C virus (HCV) RNA loads serve as predictors of treatment response

276 different factors in the hepatitis C virus (HCV) RNA replication complex are not well understood.

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

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

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 ecimens from patients with late relapse were HCV RNA positive at SVR, with sequences nearly identical

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

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

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

285 program involving dynamic associations with HCV RNA and proteins, IKK-alpha, SG, and LD surfaces for

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

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

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

289 has translated into clinical efficacy, with HCV RNA declining by ~3-4 log10 in infected patients aft

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

291 Notably, 6 patients with HCV RNA >/=LLOQ at EOT (range, 14-64 IU/mL) achieved SVR

292 nd point was the percentage of patients with HCV RNA </=15 IU/mL 12 weeks after stopping therapy (sus

293 nd point was the percentage of patients with HCV RNA <15 IU/mL 12 weeks after stopping therapy (susta

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

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

296 measured by the proportion of patients with HCV RNA concentrations less than the lower limit of quan

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

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

299 Patients with HCV-RNA levels >/= 12 IU ml-1 after 4 weeks of treatment

300 nd point was the proportion of patients with HCV-RNA levels less than 25 IU/mL at 12 weeks after tran