ライフサイエンスコーパス: HCV

1 HCV CVLs vary geographically and merit further study as

2 HCV reinfection was observed in 3 participants.

3 HCV treatment outcomes in PWID and patients on OST are s

4 HCV treatment with paritaprevir-ritonavir-ombitasvir plu

5 HCV+ recipients were less likely to receive ATG than HCV

6 HCV-specific CD8(+) T cells cross-reacted with allogenei

7 HCV-specific cytokines were also improved post DAA.

8 1035 HCV-infected patients were included, 667 (64%) coinfecte

9 ion in 29 HCV-infected LTx-recipients and 17 HCV-infected patients during DAA-treatment.

10 ribavirin) that enrolled chronic genotype 1a HCV-infected persons coinfected with suppressed HIV: 5 o

11 with STAT-1 and STAT-4 phosphorylation in 29 HCV-infected LTx-recipients and 17 HCV-infected patients

12 is deaths were related to HBV [39% and 29%], HCV [29% and 26%], ALD [16% and 25%], and NAFLD [8% and

13 safety and efficacy of transplantation of 30 HCV-viremic kidneys into HCV-negative recipients, follow

14 d for ALD (APC = -0.44% [-0.78% to -0.40%]), HCV (APC = -0.50% [-0.81% to -0.18%]), and HBV (APC = -1

15 es in India in 2016-2017, a total of N = 498 HCV and N = 755 HIV strains were classified from N = 975

16 Between 2010-2018, there were a total of 585 HCV initiations among 1130 eligible participants.

17 is reduced by 55-85% (USD 6,730 to 17,720), HCV treatment would be cost-saving within a 5 to 20-year

18 ce among HIV-positive GBM up to 2025 using a HCV transmission model parameterized with Australian dat

19 rolled human infection studies to accelerate HCV vaccine development.

20 e agonist treatment (OAT) programs addresses HCV treatment barriers, but few evidence-based models ex

21 sub-nationally, we calculated age-adjusted, HCV-associated death rates and compared death rate ratio

22 onocytes were decreased in coinfection after HCV treatment.

23 Among HCV patients, receiving a re-LT in the post-DAA era was

24 The recent discovery of an HCV-like rodent hepacivirus (RHV) enabled the developmen

25 s index <21 kg/m (aHR, 1.61; P = 0.006), and HCV (aHR, 1.83; P < 0.001) were associated with graft lo

26 re were no increases for HBV (P = 0.224) and HCV (P = 0.054).

27 rowth biology, hepatocellular carcinoma, and HCV pathogenesis.

28 .5% of HCC and 47.2% of cirrhosis cases, and HCV in 6.4% and 3.7% respectively.

29 patients independently of liver fibrosis and HCV cure.

30 Global and HCV-specific CD4 + CXCR5 + T(FH), CD4 + CXCR5-T and CD19

31 ence-free survival rates compared to HBV and HCV-HCC cases.

32 Subset analyses examined HIV and HCV disease severity markers separately and jointly.

33 We also tracked HIV and HCV infections, overdose deaths, and jail population siz

34 T, respectively, compared to 42% for HIV and HCV LBT.

35 ase notification was 95% and 93% for HIV and HCV RT, respectively, compared to 42% for HIV and HCV LB

36 ionnaires were completed, along with HIV and HCV testing.

37 ment for substance use disorder, and HIV and HCV treatment, as well as diversion program cost.

38 9, national utilization rates for HCV-NV and HCV-V hearts were the same as HCV- hearts (27.6% for HCV

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

40 Anti-HCV therapy comprised pegylated interferon and ribavirin

41 five participants who were reactive for anti-HCV had the HCV genotype 1a and 3a.

42 lacked these criteria and had negative anti-HCV at age >=18 months.

43 ferase > 10 x upper limit of normal) or anti-HCV antibody seroconversion within 18 months.

44 infection was defined by first positive anti-HCV antibody and/or HCV RNA within 6 months of enrollmen

45 tive repeat HCV-RNA testing or positive anti-HCV at age >=24 months; 2) uninfected children lacked th

46 Three children had low-positive anti-HCV results at age 18-24 months that were negative upon

47 Among those anti-HCV positive, viraemic prevalence declined 83% during th

48 , antibodies against hepatitis C virus (anti-HCV).

49 serum HCV-RNA cutoffs for ruling in/out any HCV+SS were established at 6.02 log IU/mL and 4.02 log I

50 In comparison, daclatasvir, an approved HCV drug, suppressed more than 3 log of viraemia but is

51 for HCV-NV and HCV-V hearts were the same as HCV- hearts (27.6% for HCV-NV, 30.9 for HCV-V, and 31.7%

52 We examined the mean age at HCV-associated death, and rates and proportions by sex,

53 ined stable or decreased following DAA-based HCV treatment.

54 ld serve to increase the uptake of DAA-based HCV treatment.

55 with substantial increases in risk behavior, HCV incidence would drop to 0.6 per 100 person-years (76

56 fusion of HCV with hepatic cells by binding HCV envelope protein 1 to prevent fusion.

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

58 mmunodeficiency virus (HIV) and hepatitis C (HCV) coinfected patients with advanced liver disease.

59 ks between DO and autoimmunity, Hepatitis C (HCV) infection, and cancer, but the mechanism of how DO

60 fibrosis stage restrictions on hepatitis C (HCV) treatment initiation rates among people living with

61 The overall engaged-in-care HCV CVL was 4 351 079 copies/mL (standard deviation = 7

62 ol and Prevention, we used acute and chronic HCV infections among persons aged <=40 years as a proxy

63 gher in HCV-infected hepatocytes and chronic HCV-infected liver biopsy specimens.

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

65 (ERCHIVES) database for persons with chronic HCV infection (n = 242 680), we identified those treated

66 e in children 3 to <6 years old with chronic HCV infection.

67 er cells increasingly shaped the circulating HCV-specific CD4+ T cell repertoire, suggesting antigen-

68 We describe a program that colocates HCV management within a syringe service program in New Y

69 Considerable HCV diversity was identified, with different strains pre

70 In contrast, HCV+ recipients who received ATG were at lower risk of a

71 By 2018, cumulative HCV treatment uptake in those ever eligible for treatmen

72 Annual and cumulative HCV treatment uptake, outcome, and HCV RNA prevalence we

73 t implications for HCC surveillance in cured HCV patients.

74 The efficacy of current HCV therapies has created this important opportunity to

75 CRISPR-Cas9-based Mov10 depletion decreases HCV replication and infection levels.

76 sensitivity was low did not have detectable HCV viral load/core antigen.

77 re be used as a preclinical model to develop HCV vaccines.

78 t levels for broad neutralization of diverse HCV isolates.

79 To document HCV-associated deaths sub-nationally, we calculated age-

80 nt cell-mediated cytotoxicity (ADCC), during HCV infection is poorly defined, while no study has expl

81 addition to behavioral interventions, early HCV treatment and retreatment should be implemented for

82 Eighteen HCV seroconversions were reported for an incidence of 19

83 Findings further support expanding HCV treatment to all, irrespective of injection drug use

84 Mental health treatment may facilitate HCV cure.

85 s effect was not observed with the bona fide HCV IRES.

86 ants, 0.5% were positive for HIV and 48% for HCV; 96% received test results in the RT arm and 42% in

87 arts were the same as HCV- hearts (27.6% for HCV-NV, 30.9 for HCV-V, and 31.7% for HCV-, P = .277); (

88 6% for HCV-NV, 30.9 for HCV-V, and 31.7% for HCV-, P = .277); (2) utilization rates of HCV-NV hearts

89 e as HCV- hearts (27.6% for HCV-NV, 30.9 for HCV-V, and 31.7% for HCV-, P = .277); (2) utilization ra

90 application of an RHV outbred rat model for HCV vaccine development.

91 (1) in 2019, national utilization rates for HCV-NV and HCV-V hearts were the same as HCV- hearts (27

92 the minimum treatment duration required for HCV infection.

93 , we establish the mechanism responsible for HCV's effect on intracellular desmosterol, whereby the H

94 s with moderate certainty that screening for HCV infection in adults aged 18 to 79 years has substant

95 The USPSTF recommends screening for HCV infection in adults aged 18 to 79 years.

96 ed for HIV and 65 188 (7.7%) were tested for HCV infections.

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

98 newer, direct-acting antiviral therapies for HCV, our objective was to determine whether chronic infl

99 the development of an effective vaccine for HCV in humans.

100 ssed the efficacy of salvage SOF/VEL/VOX for HCV infection in NS5A-inhibitor experienced participants

101 had ever injected drugs, and 13% (n = 4) had HCV reinfection.

102 The majority had HCV genotype 1 (83%, n = 25), followed by genotype 4 (10

103 ts capacity to predict mortality risk in HIV-HCV-coinfected patients has never been investigated.

104 a risk factor for all-cause mortality in HIV-HCV-coinfected patients independently of liver fibrosis

105 ruses present in residual plasma from an HIV/HCV prevalence study conducted amongst PWID across five

106 20) but there was no association between HIV/HCV coinfection and prevalent PH.

107 During HIV/HCV coinfection, plasma immune activation marker heterog

108 veterans referred for echocardiography, HIV/HCV coinfection was not associated with a clinically sig

109 MD) and biomarkers of bone remodeling in HIV/HCV coinfected patients.

110 ng sofosbuvir-based DAA therapy to treat HIV/HCV-coinfected participants pre- or post-liver transplan

111 nd March 2017, 402 participants who were HIV/HCV antibody positive were enrolled (95% male [80% gay a

112 We determine whether HIV/HCV coinfection is associated with higher pulmonary arte

113 regression analyses to determine whether HIV/HCV mono- or co-infection were associated with PASP and

114 Individuals with HIV/HCV coinfection displayed a higher PASP than uninfected

115 ors of clinical outcomes in persons with HIV/HCV coinfection.

116 without increasing hepatic complications in HCV+ KT recipients.

117 oluble CD163 and neopterin were decreased in HCV mono- and coinfected persons.

118 pective cohorts to assess sex disparities in HCV incidence among PWID exposed to OAT.

119 developing hepatocellular carcinoma (HCC) in HCV-infected patients who achieve sustained virological

120 emonstrated that ATM expression is higher in HCV-infected hepatocytes and chronic HCV-infected liver

121 ive post-DAA era effect was observed only in HCV patients with first graft loss due to disease recurr

122 7; P = .005, and HR: 0.65; P = .004) only in HCV patients.

123 tment scale-up, with a dramatic reduction in HCV infection burden and low reinfection rate among peop

124 The impact of time in HCV treatment and follow-up on longitudinally measured l

125 oinfection and MX1, LGALS3BP, and TNFAIP6 in HCV monoinfection.

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

127 antithymocyte globulin (ATG) might increase HCV-related complications.

128 a rapid rise in hepatitis C virus-infected (HCV+) heart transplantation.

129 ansplantation of 30 HCV-viremic kidneys into HCV-negative recipients, followed by early initiation of

130 rus (HCV)-viremic heart transplantation into HCV-negative recipients with HCV treatment are good.

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

132 sion, we developed a series of intracellular HCV replication models that include HCV RNA secretion an

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

134 s/mL (standard deviation = 7 149 888); local HCV CVLs varied by subgroup and geography.

135 We observed a low HCV prevalence in this large sample of MSM despite a hig

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

137 The main HCV genotypes 1 to 6 are detected with an accuracy of +/

138 At liver biopsy 1, mean %HCV-infected cells = 25.2% (95% confidence interval [CI]

139 opsy 2 (Day 7 in 4 of 5 participants), mean %HCV-infected cells = 1.0% (95% CI, 0.2%-1.7%) (P < .05 f

140 We aimed to (1) deliver and measure HCV treatment effectiveness, and (2) determine the popul

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

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

143 ar patient group, dramatic reductions in new HCV infections can be achieved.

144 infected (HCV-) to those of HCV+ nonviremic (HCV-NV) and viremic (HCV-V) hearts nationally and by UNO

145 here was marked variability in allocation of HCV+ hearts at the OPO level even within the same UNOS r

146 arker for single-particle cryoEM analysis of HCV E2.

147 NV hearts were low in regions 3 and 4 and of HCV-V hearts in regions 3, 4, and 8 even in the contempo

148 expression of miR-181c promoted apoptosis of HCV-infected hepatocytes and can be inhibited by overexp

149 g of HCV that shares many characteristics of HCV infection, we report the development and application

150 both the straight and bent CDRH3 classes of HCV bNAb can be elicited in a single individual, reveali

151 Using the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES) database for persons wi

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

153 ve was to evaluate the cost-effectiveness of HCV treatment in patients of different age groups and to

154 onsiderable evidence of the effectiveness of HCV treatment in people who inject drugs (PWID), and rec

155 We evaluated the cost-effectiveness of HCV treatment models for OAT patients using data from a

156 Direct evidence on the effects of HCV screening on clinical outcomes remains unavailable,

157 Eradication of HCV is a national goal.

158 is known about the effects of eradication of HCV on bone mineral density (BMD) and biomarkers of bone

159 Single-cell longitudinal estimates of HCV clearance from liver have never been reported previo

160 pidemic among PWUD will require expansion of HCV treatment coverage.

161 e show that fluoxazolevir inhibits fusion of HCV with hepatic cells by binding HCV envelope protein 1

162 tively escape the immune response, a goal of HCV vaccine design is to induce neutralizing antibodies

163 Using rodent hepacivirus (RHV), a homolog of HCV that shares many characteristics of HCV infection, w

164 n is characterized by a severe impairment of HCV-specific CD4+ T cell help that is driven by chronic

165 ncidences of NADM or CVD were independent of HCV group, whereas those cured had substantially lower i

166 responses following LT and the influence of HCV eradication.

167 d has direct relevance to the interaction of HCV with cell-surface receptors and neutralising antibod

168 de direct evidence that the profound loss of HCV-specific CD4+ T cell help that results in chronic in

169 -term outcomes using an established model of HCV disease progression and treatment (hepatitis C cost-

170 zed controlled trial that assessed models of HCV care for 150 PWID on OAT.

171 lly and merit further study as predictors of HCV incidence.

172 cation and infectious particle production of HCV as well as dengue virus and Zika virus revealing a c

173 or HCV-, P = .277); (2) utilization rates of HCV-NV hearts were low in regions 3 and 4 and of HCV-V h

174 otential negative consequences of receipt of HCV-viremic hearts.

175 a propensity-matched cohort of recipients of HCV-viremic (RNA positive) versus HCV-naive kidneys.

176 es (hearts transplanted/donors recovered) of HCV-uninfected (HCV-) to those of HCV+ nonviremic (HCV-N

177 87, 667, 101 and 248 nucleotide sequences of HCV NS3 genotypes 1a, 1b, 2b, and 3a, respectively, and

178 major glycoprotein E2 from three strains of HCV.

179 overed) of HCV-uninfected (HCV-) to those of HCV+ nonviremic (HCV-NV) and viremic (HCV-V) hearts nati

180 eflecting either the need for a threshold of HCV for sexual transmission and/or variability in sexual

181 ere are multiple barriers to broad uptake of HCV treatment.

182 In carefully selected patients, the use of HCV-viremic grafts in the DAA era appears to be efficaci

183 Due to the high variability of HCV and its ability to actively escape the immune respon

184 ffect of treatment and behavioral changes on HCV incidence among HIV-positive GBM up to 2025 using a

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

186 Here, we investigate the effect of Mov10 on HCV infection and determine the virus life cycle steps a

187 ermine the population impact of treatment on HCV prevalence and incidence longitudinally.

188 Compared to accepting only HCV-negative hearts, accepting any heart gained 0.14 lif

189 o patients of the same age group with ALD or HCV.

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

191 ed the percentage of PWIDs tested for HIV or HCV within 1 year of an index encounter, and we used mul

192 Only HIV-negative or HCV-negative participants not on medication assisted tre

193 and correctly removes 96.2% of all pairwise HCV sample comparisons, outperforming all previous metho

194 d-containing CDRH3 is specific to particular HCV-infected individuals, we solved a crystal structure

195 Among 8352 patients, HCV prevalence was 48.7%.

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

197 ere used to identify correlates of prevalent HCV, and Bayesian phylogenetic analysis was used to exam

198 be implemented for this subgroup to prevent HCV transmission.

199 to bolster the efficacy of OAT in preventing HCV transmission.

200 an avenue for the development of preventive HCV vaccine candidates that induce bNAbs at higher yield

201 Unexpectedly, endogenous Mov10 promotes HCV replication, as CRISPR-Cas9-based Mov10 depletion de

202 critical for the efficacy of a prophylactic HCV vaccine.

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

204 capture microdissection was used to quantify HCV.

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

206 effective among people with acute and recent HCV infection, supporting further evaluation of shortene

207 Interviews and assessments of recurrent HCV viremia occurred at 6-month intervals for up to 24 m

208 Here, we investigated whether reduced HCV replication after pregnancy is associated with recov

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

210 80%) MSM and identified 177 with replicating HCV infections (4.8%); 150 (85%) of which started DAA tr

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

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

213 LD, underlining the importance of successful HCV treatment for reducing ESLD.

214 ened for hepatitis C virus (HCV), 180 tested HCV antibody positive (34%), and 108 were HCV-ribonuclei

215 ipients were less likely to receive ATG than HCV- recipients (living donor, adjusted odds ratio [aOR]

216 We extrapolate that HCV eradication could occur in these participants by 63

217 Coss et al. showed that HCV-specific CD4+ T cells temporarily recovered in some

218 The HCV genome is a single plus strand of RNA.

219 Interventions are needed to address the HCV-opioid syndemic in this region.

220 We analyzed the HCV reinfection incidence rates of participants in the G

221 ogram, 176/190 MSM (93%) were cured, and the HCV incidence rate declined from 0.53 per 100 patient-ye

222 By elucidating the HCV interactome, we identified the 17-beta-hydroxysteroi

223 pants who were reactive for anti-HCV had the HCV genotype 1a and 3a.

224 iduals, we solved a crystal structure of the HCV E2 ectodomain in complex with AR3X, a bNAb with an u

225 t treatment need suggest that control of the HCV epidemic among PWUD will require expansion of HCV tr

226 ram to discover solubilizing prodrugs of the HCV NS5A inhibitor pibrentasvir (PIB) identified phospho

227 ct on intracellular desmosterol, whereby the HCV NS3-4A protease controls activity of 24-dehydrochole

228 These HCV-specific CD4+ T cells had an effector-memory phenoty

229 vement in polyclonal immune serum binding to HCV pseudoparticles and neutralization of isolates assoc

230 in any patient were deemed likely related to HCV infection or treatment with glecaprevir and pibrenta

231 D81 cholesterol sensing, how this relates to HCV entry, and CD81's function as a molecular scaffold;

232 ion of cell cycle progression in relation to HCV infection.

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

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

235 ndependently associated with shorter time to HCV seroconversion.

236 g current guideline recommendations to treat HCV in these patient populations.

237 inority of those trained have begun treating HCV independently.

238 In clinical trials, HCV salvage treatment with Sofosbuvir/Velpatasvir/Voxila

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

240 planted/donors recovered) of HCV-uninfected (HCV-) to those of HCV+ nonviremic (HCV-NV) and viremic (

241 Universal HCV rescreening among pregnant women was cost-effective

242 Persons with chronic, untreated HCV infections (aIRR 1.47, 95% CI 1.02-2.13) or treatmen

243 ipients of HCV-viremic (RNA positive) versus HCV-naive kidneys.

244 ose of HCV+ nonviremic (HCV-NV) and viremic (HCV-V) hearts nationally and by UNOS region.

245 Hepatitis C virus (HCV) and alcohol use are patient risk factors for accele

246 currence in patients with hepatitis C virus (HCV) and hepatocellular carcinoma (HCC) listed for liver

247 Here, we show that hepatitis C virus (HCV) co-opts the host protein CypA to aid evasion of ant

248 unodeficiency virus (HIV)/hepatitis C virus (HCV) coinfection increases cognitive impairment.

249 alth Organization's (WHO) hepatitis C virus (HCV) elimination target of an 80% reduction in incidence

250 eficiency virus (HIV) and hepatitis C virus (HCV) infection among persons who inject drugs (PWID).

251 s set a goal to eliminate hepatitis C virus (HCV) infection as public health threat by 2030.

252 NK) cell responses during hepatitis C virus (HCV) infection can be restored after viral eradication w

253 global epidemic of acute hepatitis C virus (HCV) infection has been noted in men who have sex with m

254 se as a result of chronic hepatitis C virus (HCV) infection is a global problem.

255 BACKGROUNDChronic hepatitis C virus (HCV) infection is characterized by a severe impairment o

256 Chronic hepatitis C virus (HCV) infection is characterized by activation of natural

257 Hepatitis C virus (HCV) infection is common among people living with human

258 Chronic hepatitis C virus (HCV) infection is one of the major causal factors for he

259 Hepatitis C virus (HCV) infection promotes hepatocyte growth and progress t

260 s of age who have chronic hepatitis C virus (HCV) infection, there are currently no approved treatmen

261 is a hallmark of chronic hepatitis C virus (HCV) infection.

262 viral treatment (DAA) for hepatitis C virus (HCV) infection.

263 Hepatitis C virus (HCV) is a blood borne pathogen mostly transmitted via pe

264 The E2 glycoprotein of hepatitis C virus (HCV) is the major target of broadly neutralizing antibod

265 nsformed the landscape of hepatitis C virus (HCV) management.

266 covery of a pan-genotypic hepatitis C virus (HCV) NS3/4A protease inhibitor based on a P1-P3 macrocyc

267 Clearance of hepatitis C virus (HCV) results in rapid changes in metabolic parameters ea

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

269 es Task Force (USPSTF) of hepatitis C virus (HCV) screening found interferon-based antiviral therapy

270 nderpin hugely successful hepatitis C virus (HCV) therapy.

271 rently, the only approved hepatitis C virus (HCV) treatment for children aged <12 years is pegylated

272 Some people living with hepatitis C virus (HCV) with sustained virological response (SVR) develop h

273 viduals were screened for hepatitis C virus (HCV), 180 tested HCV antibody positive (34%), and 108 we

274 ng mechanistic aspects of hepatitis C virus (HCV)-host interactions, one could discover common strate

275 cognizing motifs found in hepatitis C virus (HCV)-like IRESs, suggesting mechanistic similarities.

276 Outcomes following hepatitis C virus (HCV)-viremic heart transplantation into HCV-negative rec

277 s, hepatitis B virus, and hepatitis C virus (HCV).

278 est Nile virus (WNV), and hepatitis C virus (HCV).

279 ed HCV antibody positive (34%), and 108 were HCV-ribonucleic acid (RNA) positive (20%).

280 tners was 17 (IQR: 6, 50) and 246 (19%) were HCV antibody positive.

281 Predictors of HCC emergence were: HCV genotype 3 [sHR=7.9 (2.5-24.9); p<0.001], MELD score

282 Here, we asked whether HCV-elimination by sofosbuvir-based direct-acting antivi

283 We investigated the mechanisms through which HCV infection modulates donor-specific T cell responses

284 or other countries aiming to achieve the WHO HCV elimination targets.

285 Factors associated with HCV acquisition among females exposed to OAT included no

286 level indicators potentially associated with HCV infection rates were identified.

287 uld be decreased and cognition improved with HCV sustained viral response (SVR) in coinfection.

288 Individuals with HCV+SS had significantly higher serum HCV-RNA levels tha

289 Individuals with HCV/HIV co-infection were prospectively enrolled from pr

290 ent in 59 patients chronically infected with HCV, 39 with advanced liver fibrosis, and 20 with mild-m

291 h alcohol use, older age, and infection with HCV genotype 3.

292 in mice by using a tumor from a patient with HCV-associated HCC and evaluating this model's therapeut

293 We considered 509 consecutive patients with HCV cirrhosis (defined histologically or when liver stif

294 We analyzed data from 1021 patients with HCV infection (506 with genotype 1; 16 with genotype 2;

295 gher serum HCV-RNA levels than patients with HCV-negative SS (6.28 [IQR, 0.85] log IU/mL vs 4.08 [2.4

296 D) with or without ribavirin in persons with HCV-1/HIV coinfection suppressed with antiretroviral the

297 plantation into HCV-negative recipients with HCV treatment are good.

298 Xpert HCV Viral Load Fingerstick assay (Xpert HCV VL FS) is a

299 pert HCV Viral Load Fingerstick assay (Xpert HCV VL FS) is a point-of-care test quantifying HCV RNA i

300 ed time to HCV RNA detection using the Xpert HCV VL FS assay.

301 eaths with a concomitant increase in younger HCV viremic donors after brain death being identified.