ライフサイエンスコーパス: HCV

1 HCV subverts the antiviral actions of these miRNAs by da

2 HCV-infected patients receiving cancer treatment at our

3 cted with the Japanese fulminant hepatitis 1 HCV strain as well as in biopsies of chronic HCV patient

4 However, only NS5A from genotype 2 HCV, and not that from genotype 1, targets NAP1L1 for pr

5 Our findings suggest that non-genotype 3 HCV infection may be protective against HS.

6 r plus ribavirin in patients with genotype 3 HCV infection.

7 44.5 person-years of observation [PYO]), 371 HCV incident infections resulted in an overall incidence

8 iral) and without HCC (n = 309: 39% HBV, 39% HCV, 22% non-viral).

9 This lack of 21-3U HCV host factor activity correlated with reduced recruit

10 In the Middle East, genotype 4 HCV infection is the most common genotype.

11 uvir for patients with acute genotype 1 or 4 HCV infection and HIV-1 coinfection is similar to histor

12 411 patients with HCC (n = 102: 32% HBV, 54% HCV, 14% non-viral) and without HCC (n = 309: 39% HBV, 3

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

14 nt also provides important information about HCV-induced carcinogenesis and the effects of DAAs.

15 therapy using highly sensitive and accurate HCV RNA assays.

16 ns without interferon for treatment of acute HCV in HIV-1 infected individuals (SWIFT-C) is an open-l

17 ir plus ribavirin for the treatment of acute HCV infection in participants with chronic human immunod

18 lizing monoclonal antibodies (bNAbs) against HCV is a major goal of vaccine development.

19 ssion on HCV-infected hepatoma cells against HCV-specific CD8 T cells.

20 tency of the humoral immune response against HCV.

21 ominantly among IgM(+) memory B cells of all HCV-infected patients analyzed.

22 Among HCV patients, individuals who received the minimally eff

23 analysis supported close relationships among HCV sequences from the four male subjects and subsequent

24 promotes HCV infection by functioning as an HCV attachment factor.

25 )-specific CD8 T cells have been shown in an HCV replicon system but not in an authentic infectious H

26 ndoglin expression on the cell surface of an HCV core-expressing hepatocellular carcinoma (HepG2) cel

27 rary to expectations, HIV/HCV-coinfected and HCV-monoinfected adults had significantly less liver fat

28 inoma (HCC) in patients with chronic HBV and HCV infection.

29 population at low risk of diabetes, HBV and HCV infections were associated with diabetes prevalence

30 s a crucial priority for halting the HIV and HCV epidemics.

31 cross-sectional relationship between LLD and HCV or TBV, and 46 studies fulfilled the inclusion crite

32 IGHV4-59, which are closely linked to MC and HCV-associated lymphomas, was specifically seen among Ig

33 their expression in cell culture models and HCV-infected human livers.

34 no apparent resistance to pibrentasvir, and HCV with RAS at amino acid 93 had a low level of resista

35 on, and (3) who lacked prior documented anti-HCV testing.

36 Of 2514 women, 97 (3.9%) had anti-HCV antibodies, 54 (2.1%) were viremic and of those, 52

37 tes have been observed after 6 weeks of anti-HCV treatment using sofosbuvir, ledipasvir and a non-nuc

38 All patients received anti-HCV treatment before or after inclusion (with interferon

39 t inhibiting glutamine metabolism attenuates HCV infection and the oxidative stress associated with H

40 %, 3%, 6%, 12%, or 24%) and varying baseline HCV prevalence in people who inject drugs (30%, 60%, 75%

41 results provide detailed insights into basic HCV T cell immunology and have clinical relevance for re

42 r, male, died from anoxia, more likely to be HCV and antibody reacting to hepatitis B core antigen+,

43 PS-containing liposomes blocked HCV cell attachment and subsequent HCV infection.

44 rectal HCV viral load (VL) with paired blood HCV VL.

45 isms for hepatic stellate-cell activation by HCV-infected hepatocytes are underexplored.

46 Infection of B cells by HCV inhibited the recall reaction to antigen stimulation

47 lly in individuals with chronic hepatitis C (HCV); however, the impact of nonheavy use is not clear.

48 o experiments demonstrated that only certain HCV-NS5B prodrugs elicit bradycardia when combined with

49 response to PEG-IFN-based therapy in chronic HCV genotype 1 infection.

50 n of endoglin/ID1 mRNA expression in chronic HCV patient liver biopsy samples.

51 In the setting of chronic HCV alone, statin initiators had reduced risks of aminot

52 population of Tfr cells in livers of chronic HCV patients that is absent in liver tissues from nonvir

53 HCV strain as well as in biopsies of chronic HCV patients.

54 Regardless of HIV and/or chronic HCV status, statin initiators had a lower risk of ALI an

55 Thirty-two chronic HCV patients infected with HCV genotypes 1, 3, and 4 rec

56 omised women (aged 18-65 years) with chronic HCV genotype 1, 3, or 4 infection diagnosed at least 24

57 biopsy samples from 69 patients with chronic HCV infection and 19 uninfected individuals (controls) a

58 blood samples from 42 patients with chronic HCV infection who achieved a sustained virologic respons

59 ir in renal transplant patients with chronic HCV infection.

60 iral load reduction in patients with chronic HCV infection.

61 This comprehensive HCV-miRNA interaction map provides fundamental insights

62 Consistently, HCV infection increases glutamine use and dependence.

63 been paramount to the VA's success in curing HCV infection.

64 Indeed, curing HCV infection with an oral medication is now reality.

65 on treatment increased rather than decreased HCV dsRNA.

66 ion profiles of 12 human NAbs across diverse HCV strains, assigning the NAbs to two functionally dist

67 in the pathogenesis of liver disease during HCV infection.

68 ferentiation and M2 MPhi polarization during HCV infection.

69 orne pathogens, the natural history of early HCV infection, and the scientific rationale for PEP.

70 ticenter, retrospective cohort study of 2 ED HCV screening programs.

71 viduals who received the minimally effective HCV treatment for dual, triple, or all-oral therapy had

72 promising treatment regimen for eradicating HCV in this patient population.

73 We examined HCV entry in HepG2/microRNA (miR) 122/CD81 cells, which

74 rget cells presenting endogenously expressed HCV proteins.

75 Twenty (13 males and 7 females) HCV genotype 1b-positive subjects, undergoing chemothera

76 ts in glycemia were not identified following HCV clearance irrespective of HIV, diabetes, or fibrosis

77 Financing for HCV treatment and infrastructure resources coupled with

78 dical comorbidities) and tested negative for HCV were less frequently transplanted compared with the

79 -aged women and children who were tested for HCV infection.

80 Of 497 patients treated for HCV, 257 achieved SVR and had at least 1 subsequent RNA

81 inant protein-based prophylactic vaccine for HCV with potential for universal protection.

82 cubated with conditioned medium derived from HCV-exposed human macrophages.

83 ells rapidly revert after disengagement from HCV, whereas virus-specific exhaustion imparts a durable

84 at miR-19a carried through the exosomes from HCV-infected hepatocytes activates HSC by modulating the

85 stigation suggested that CCL5, secreted from HCV-exposed macrophages, activates inflammasome and fibr

86 onal genomics strategies to elucidate global HCV-miRNA interactions.

87 Seventy-two percent of the patients had HCV genotype 1a infection.

88 All patients had HCV infection and biopsy-proven cirrhosis, were Child-Pu

89 recipients with negative pretransplant HBc, HCV, EBV, or CMV serology.

90 V) reactivation (HBV-R) in patients with HBV-HCV co-infection.

91 decompensation, mortality, and HCC in HBV-, HCV-, and alcohol-related cirrhosis.

92 27-0.94) when reinfected with a heterologous HCV genotype.

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

94 The prevalence of HIV, HCV, and HBV among homeless veterans nationally is curre

95 and population prevalence estimates of HIV, HCV, and HBV among homeless veterans nationally.

96 ational testing rates and prevalence of HIV, HCV, and HBV among homeless veterans.

97 characteristics, and the prevalence of HIV, HCV, and HBV among PWID.

98 y profile and SVR12 rates of 96.7% among HIV/HCV co-infected patients participating in an Italian com

99 Among HIV/HCV-coinfected patients, statin initiators had lower ris

100 llowed by the HCV-monoinfected (19%) and HIV/HCV-coinfected (11%) (P = 0.003 across groups).

101 Contrary to expectations, HIV/HCV-coinfected and HCV-monoinfected adults had significa

102 fairs Clinical Case Registry to identify HIV/HCV GT1-coinfected veterans initiating 12 weeks of LDV/S

103 FNy, IL-15) were found to be elevated in HIV/HCV coinfection when compared to both monoinfections.

104 ivirals (DAAs) in predominantly minority HIV/HCV coinfected populations.

105 y of study sites to India, lack of prior HIV/HCV diagnosis confirmation with clinic records, and lack

106 ted populations, including patients with HIV/HCV coinfection, decompensated cirrhosis, liver and kidn

107 fected cells and liver biopsies to study how HCV modulates the glutaminolysis pathway, which is known

108 rease monitoring in high-risk IDU and MSM if HCV elimination targets are to be realized.

109 r liver fibrosis in HCV infection.IMPORTANCE HCV-associated liver fibrosis is a critical step for end

110 strated the importance of apolipoproteins in HCV secretion and infectivity, leading to the notion tha

111 ed epigenetic and transcriptional changes in HCV-infected livers in comparison with control, uninfect

112 These early changes in HCV-specific CD8(+) T cell transcription preceded the ov

113 sed to compare the risk of developing CKD in HCV patients compared with non-HCV patients and treated

114 les for TLR7/8 in induction of fibrocytes in HCV infection.

115 the activation of HSC for liver fibrosis in HCV infection.IMPORTANCE HCV-associated liver fibrosis i

116 score is a better predictor of HD and HCC in HCV-positive persons.

117 upling of the canonical Akt/FoxO1 pathway in HCV protein-expressing hepatocytes.

118 esistance-associated substitutions (RASs) in HCV genes (nonstructural protein [NS]3, NS5A, NS5B) targ

119 + pibrentasvir (PIB) +/- ribavirin (RBV) in HCV genotype 1-infected patients with prior virologic fa

120 ne the importance of individual receptors in HCV cell-free and cell-to-cell transmission.

121 human immunodeficiency virus (HIV)-infected HCV-seropositive and incidence density-matched HCV-seron

122 on system but not in an authentic infectious HCV cell culture (HCVcc) system.

123 ) variants were able to specifically inhibit HCV by interacting with infectious particles.

124 indicated that IRF5 re-expression inhibited HCV protein translation and RNA replication.

125 Among 1391 initially HCV-negative participants followed prospectively (1644.5

126 ction map provides fundamental insights into HCV-mediated pathogenesis and unveils molecular pathways

127 y performs well compared to a market-leading HCV viral load test and should be considered for instanc

128 B7.2 (CD86) as a co-receptor of lymphotropic HCV.

129 ope and 5'-UTR sequences of the lymphotropic HCV strain were responsible for the lymphotropism.

130 eradication rates are pushing 100% for many HCV-infected populations, including patients with HIV/HC

131 nce comparable to that of currently marketed HCV assays when tested across multiple European sites.

132 V-seropositive and incidence density-matched HCV-seronegative participants of the Swiss HIV Cohort St

133 We then measured HCV binding, intracellular levels of HCV RNA, and expres

134 We measured HCV replication, entry, spread, production, and release

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

136 f peripheral blood B cells of 30 MC-negative HCV-infected patients and 15 healthy controls revealed t

137 epitope I, and their serum could neutralize HCV.

138 NNDSS HCV case reports and Quest laboratory data regarding uni

139 loping CKD in HCV patients compared with non-HCV patients and treated patients compared with untreate

140 k of ESRD than those who were nonchronically HCV-infected (HR, 2.11, 95% CI 1.16-3.86, and HR, 3.06,

141 % CI 1.83-7.07) compared with nonchronically HCV-infected subjects.

142 injection, suggesting that NK cells, but not HCV adaptive immunity, may contribute to HCV viral contr

143 significantly reduced HCV infection but not HCV RNA replication.

144 .IMPORTANCE Due to the protective ability of HCV-specific T cells and the hepatotoxic potential that

145 IFN treatment increased the total amount of HCV dsRNA through a process that required de novo viral

146 e understanding of the functional aspects of HCV-specific T cells.

147 ates the exact site where the association of HCV virions with host lipoproteins occurs.

148 e development has been confounded because of HCV's high degree of antigenic variability and the prefe

149 predictors for viral decline in a cohort of HCV-infected postpartum women.

150 al agents (DAA) provide an effective cure of HCV infection without risk of allograft rejection.

151 for further understanding the life cycle of HCV and its interaction with the host cells.

152 me, as the redox probe in the development of HCV core antigen electrochemical immunosensor.

153 nd 1965, (2) who lacked a prior diagnosis of HCV infection, and (3) who lacked prior documented anti-

154 producing enhanced cytolytic elimination of HCV-infected Huh7.5A2 cells.

155 TNF has been reported to increase entry of HCV pseudoparticles into hepatoma cells and inhibit sign

156 Our data suggest that eradication of HCV in coinfected patients is associated not only with a

157 Short exposure of HCV-infected cells to daclatasvir reduced viral assembly

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

159 itical for assessing the potential impact of HCV treatment.

160 re, TLR7 or TLR8 stimulation, independent of HCV, caused monocyte differentiation and M2 MPhi polariz

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

162 through this network with varying levels of HCV treatment coverage (0%, 3%, 6%, 12%, or 24%) and var

163 These findings argue for the prescription of HCV therapy in coinfected patients regardless of fibrosi

164 rted for improving the resistance profile of HCV NS3/4A protease inhibitors.

165 m the societal perspective across a range of HCV(+) liver availability rates.

166 vulnerability resulting from the reliance of HCV on multiple cell surface receptors, suggesting that

167 ells, which support entry and replication of HCV, were transfected these cells with small interfering

168 ontroversial without considering the role of HCV viral load and genotype.

169 d the full genome of both a novel subtype of HCV genotype 6, and a co-infecting human pegivirus.

170 We simulated transmission of HCV and HIV through this network with varying levels of

171 eks is highly effective for the treatment of HCV genotype 2.

172 nalysis to assess diagnosis and treatment of HCV infection in a primary care patient panel with and w

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

174 ked protective effect of PD-L1 expression on HCV-infected hepatoma cells against HCV-specific CD8 T c

175 l effects was blunted by PD-L1 expression on HCV-infected Huh7.5A2 cells, resulting in the improved v

176 In conclusion, patients with HBV or HCV infection, with or without HCC, have distinctly diff

177 nstrable proclivity to transmit HIV, HBV, or HCV needs to be reexamined.

178 occludin (OCLN), explain, at least in part, HCV's limited ability to enter mouse hepatocytes.

179 t prompted primary care providers to perform HCV screening for patients seen in primary care clinic (

180 ve vaccine is highly desirable in preventing HCV (re)infection.

181 and another inhibitory SMAD (SMAD7) promote HCV infection in human hepatoma cells and hepatocytes.

182 ese findings demonstrate that TIM-1 promotes HCV infection by serving as an attachment receptor for b

183 that TIM-1, but not TIM-3 or TIM-4, promotes HCV infection by functioning as an HCV attachment factor

184 red to quantification by the Abbott RealTime HCV assay.

185 milarly misquantified by the Abbott RealTime HCV assay.

186 ompensated cirrhosis patients should receive HCV treatment while awaiting LT is between 23 and 27, de

187 -R is a safety concern in patients receiving HCV DAAs.

188 29 patients with HBV-R receiving HCV DAAs.

189 We compared the rectal HCV viral load (VL) with paired blood HCV VL.

190 wn of TIM-1 expression significantly reduced HCV infection but not HCV RNA replication.

191 eatment-as-prevention strategies on reducing HCV prevalence over 10 years and 20 years versus no trea

192 rmed using 245 clinical samples representing HCV GT 1 to GT 4.

193 road neutralizing activity against all seven HCV genotypes.

194 subjects, patients had significantly smaller HCVs (standardized mean difference = -0.32 [95% confiden

195 However, some HCV-like IRES elements possess an additional sub-domain,

196 g of structural proteins with non-structural HCV proteins, including core, E2, NS4B, and NS5A.

197 s blocked HCV cell attachment and subsequent HCV infection.

198 Successful HCV treatment was associated with a lower incidence of l

199 Recently, we demonstrated that HCV infection leads to monocyte differentiation into pol

200 Our results demonstrated that HCV-exo internalized to HSC and increased the expression

201 and infectivity, leading to the notion that HCV coopts the secretion of very-low-density lipoprotein

202 Our findings suggest that HCV infection should not contraindicate cancer therapy a

203 and HIV-monoinfected (28%), followed by the HCV-monoinfected (19%) and HIV/HCV-coinfected (11%) (P =

204 We evaluate the HCV Continuum of Care for patients identified with HCV i

205 We find the HCV-infected liver to have a pattern of acquisition of D

206 13%, 45.57%, and 40.50% respectively, in the HCV group, and the corresponding rates in the healthy co

207 This work provides a unique insight into the HCV LVP assembly process within infected cells and offer

208 ble patients who completed each stage of the HCV Continuum of Care.

209 better understanding of the structure of the HCV envelope, which is responsible for attachment and fu

210 ndem sites (S1 and S2) near the 5 end of the HCV genome, stabilizing it and promoting its synthesis.

211 TNF inhibited completion of the HCV infectious cycle in hepatoma cells and HFLCs in a do

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

213 arrhythmia following coadministration of the HCV-NS5B prodrug sofosbuvir with amiodarone was recently

214 nt receptor for binding to PS exposed on the HCV envelope.

215 Here, we show that the HCV protein, nonstructural protein (NS) 5B, directly bin

216 ated with reduced recruitment of Ago2 to the HCV S1 site.

217 t viremia had virologic relapse in which the HCV present at baseline persisted in the liver or anothe

218 ction rate of PWID who were unaware of their HCV infection was 2.5 per day.

219 We further observed that these HCV-infected hepatocytes express transforming growth fac

220 e a means for large-scale production of this HCV vaccine candidate.

221 lly supported high-need participants through HCV care and treatment, and SVR rates demonstrate the re

222 not HCV adaptive immunity, may contribute to HCV viral control following RG-101 therapy.

223 emonstrate that human macrophages exposed to HCV induce CCL5 secretion, which plays a significant rol

224 collagen expression in monocytes exposed to HCV, and knockdown of TLR7 partially attenuated this exp

225 ted patients with prior virologic failure to HCV DAA-containing therapy.

226 ean additional cost of identifying 1 unaware HCV-infected PWID was US$13 (site range: US$7-US$140).

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

228 and treated patients compared with untreated HCV patients.

229 Here we used HCV-infected cells and liver biopsies to study how HCV m

230 C virus-induced cryoglobulinemia vasculitis (HCV-CV).

231 The Veris HCV Assay demonstrated an analytical performance compara

232 Postpartum hepatitis C viral (HCV) load decline followed by spontaneous clearance has

233 Chronic infections with hepatitis C virus (HCV) and HIV are highly prevalent in the USA and concent

234 Patients co-infected with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) are at high

235 chronically infected with hepatitis C virus (HCV) and who do not have a sustained virologic response

236 solicitation), evaluated hepatitis C virus (HCV) antibody testing, diagnosis, and costs for each of

237 Hepatitis C virus (HCV) cure rates have been similar in patients with and w

238 Hepatitis C virus (HCV) has dominated the field of hepatology for the past

239 miR-122, a pro-viral hepatitis C virus (HCV) host factor, binds and recruits Ago2 to tandem site

240 ls has been advocated for Hepatitis C Virus (HCV) in people who inject drugs (PWID), but treatment is

241 The association between hepatitis C virus (HCV) infection and end-stage renal disease (ESRD) remain

242 outcomes associated with hepatitis C virus (HCV) infection are rare and critical for assessing the p

243 Whether chronic hepatitis C virus (HCV) infection decreases humoral and cell-mediated immun

244 Chronic hepatitis C virus (HCV) infection is associated with impairment of cognitiv

245 ral treatment for chronic hepatitis C virus (HCV) infection is determined by measuring HCV RNA at spe

246 Hepatitis C virus (HCV) infection is prevalent in the renal transplant popu

247 Hepatitis C virus (HCV) infection is the most common chronic blood-borne in

248 of curative treatment for hepatitis C virus (HCV) infection, because of cost, treatment is often deni

249 nd AP2, are essential for hepatitis C virus (HCV) infection, but the underlying mechanism and relevan

250 All patients with chronic hepatitis C virus (HCV) infections can and should be treated.

251 global control of HIV and hepatitis C virus (HCV) is low levels of awareness of infection among key p

252 Hepatitis C virus (HCV) is one of the leading causes of liver diseases and

253 Chronic infection with hepatitis C virus (HCV) is one of the main causes of hepatocellular carcino

254 r a vaccine to combat the hepatitis C virus (HCV) pandemic, and induction of broadly neutralizing mon

255 t of chronically infected hepatitis C virus (HCV) patients involves direct-acting antivirals (DAA).

256 Hepatitis C virus (HCV) requires multiple receptors for its attachment to a

257 th record-based prompt on hepatitis C virus (HCV) screening rates in baby boomers in primary care and

258 There is a need for hepatitis C virus (HCV) therapies with excellent efficacy across genotypes

259 including human pathogens hepatitis C virus (HCV), Severe acute respiratory syndrome (SARS), coxsacki

260 unodeficiency virus (HIV)/hepatitis C virus (HCV)-coinfected patients treated with interferon (IFN) a

261 Hepatitis C virus (HCV)-mediated chronic liver disease is a serious health

262 The antiviral effects of hepatitis C virus (HCV)-specific CD8 T cells have been shown in an HCV repl

263 or efficient infection by hepatitis C virus (HCV).

264 recombinant strain HCV1 (hepatitis C virus [HCV] genotype 1a) gpE1/gpE2 (E1E2) vaccine candidate was

265 We treated 6 human immunodeficiency virus/HCV coinfected kidney transplant recipients with ledipas

266 , the magnitude and functionality of ex vivo HCV-specific T-cell responses did not increase following

267 A majority (80%) were HCV treatment-naive, and 84% were infected through perin

268 While HCV-specific CD8 T-cell activation with cytolytic and an

269 ients (52.9% with HCV genotype 1; 66.7% with HCV non-genotype 1).

270 as achieved by 60.5% of patients (52.9% with HCV genotype 1; 66.7% with HCV non-genotype 1).

271 opioid agonist therapy were associated with HCV incidence in cities with the highest incidence.

272 Chronic inflammation associated with HCV infection is implicated in cirrhosis and HCC, but th

273 ion and the oxidative stress associated with HCV infection.

274 ing while receiving regimens associated with HCV reactivation.

275 h rates of SVR12 in patients coinfected with HCV and HIV-1.

276 ntinuum of Care for patients identified with HCV in 2 urban EDs, and consider the results in the cont

277 hirty-two chronic HCV patients infected with HCV genotypes 1, 3, and 4 received a single subcutaneous

278 countries who were chronically infected with HCV genotypes 1-6 (HCV RNA >/=10 000 IU/mL) with or with

279 an hepatocytes, we found that infection with HCV leads to activation of nuclear factor-kappaB, result

280 nrolled patients aged 18 years or older with HCV genotype 1, 2, 4, 5, or 6 infection and compensated

281 icacious and well tolerated in patients with HCV genotype 1 infection and prior failure of DAA-contai

282 support use of this therapy in patients with HCV genotype 1 infection and stage 4-5 chronic kidney di

283 irin is safe and effective for patients with HCV genotype 1 or 4 infections.

284 Patients with HCV genotype 1 tended to have a higher risk of developin

285 In patients with HCV genotype 3, Y93H was associated with resistance to d

286 and safe treatment option for patients with HCV genotype 4 infection in preliver and postliver trans

287 rleukin 18, and was reduced in patients with HCV infection in response to T-cell receptor-mediated bu

288 2 phase 3, open-label trials, patients with HCV infection who had not been treated previously with a

289 mpared with healthy donors and patients with HCV infection without CV, patients with HCV-CV, before D

290 is a retrospective study of 46 patients with HCV recurrence posttransplant.

291 pact between ECHO and non-ECHO patients with HCV were then compared.

292 Our two cases show that patients with HCV-associated HCC can attain excellent responses to sor

293 with HCV infection without CV, patients with HCV-CV, before DAA therapy, had a lower percentage of CD

294 prospective clinical trial of patients with HCV-CV, DAA-based therapy restored disturbances in perip

295 t states of immune activation (patients with HCV-infection and interferon-alpha, patients with major

296 The association of lipid rafts with HCV-induced autophagosomes was confirmed by Western blot

297 Even within HCV genotype 1, no single bNAb effectively neutralizes a

298 The Xpert HCV Viral Load assay performs well compared to a market-

299 external quality assessment panel, the Xpert HCV Viral Load assay results (quantified in log10 IU per

300 These were tested with the Xpert HCV Viral Load assay, and results were compared to quant