ライフサイエンスコーパス: HCV infection

1 outcome even in genotype 1 or non-genotype 1 HCV infection.

2 eas SDC-3 and SDC-4 knockouts did not affect HCV infection.

3 with stage 4 or 5 chronic kidney disease and HCV infection.

4 comparing patients with and without chronic HCV infection.

5 A2A, IFNB, IFNL1, and IFNL2 before or during HCV infection.

6 component of the lipid metabolism modulating HCV infection.

7 a promising preventive vaccine candidate for HCV infection.

8 lant recipients with chronic genotype 1 or 4 HCV infection.

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

10 ly effective treatment for the management of HCV infection.

11 stalk between macrophages and HSCs following HCV infection.

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

13 s in the continuum of care for patients with HCV infection.

14 ed risks may be less likely to be tested for HCV infection.

15 l DAAs for treatment of persons with chronic HCV infection.

16 dministration (FDA) for treatment of chronic HCV infection.

17 y lowered HCV cell attachment and subsequent HCV infection.

18 HCV, whereas SMAD6 overexpression increased HCV infection.

19 l therapy was not required for patients with HCV infection.

20 and favorable tolerability in patients with HCV infection.

21 xpression and signaling are modulated during HCV infection.

22 ngs could improve treatment of patients with HCV infection.

23 antiviral drugs for the treatment of chronic HCV infection.

24 care services who have a high prevalence of HCV infection.

25 black and non-black patients with genotype 1 HCV infection.

26 Of these, 204 (31.3%) had undocumented HCV infection.

27 (HCV) is the most common route of pediatric HCV infection.

28 virin for 6 weeks in individuals with recent HCV infection.

29 ferentiation and M2 MPhi polarization during HCV infection.

30 be a novel therapeutic approach to treating HCV infection.

31 to endogenous virus in patients with chronic HCV infection.

32 logical markers used to diagnose and monitor HCV infection.

33 egulation between type I and III IFNs during HCV infection.

34 he early prediction of treatment efficacy in HCV infection.

35 ost is urgently needed for global control of HCV infection.

36 in the pathogenesis of liver disease during HCV infection.

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

38 ir in renal transplant patients with chronic HCV infection.

39 iral load reduction in patients with chronic HCV infection.

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

41 s blocked HCV cell attachment and subsequent HCV infection.

42 ion and the oxidative stress associated with HCV infection.

43 tease and was developed for treating chronic HCV infection.

44 who had not received previous treatment for HCV infection.

45 -IFN)-based therapy in patients with chronic HCV infection.

46 additional metabolic complication of HBV and HCV infection.

47 erted effort to reduce the overall burden of HCV infection.

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

49 hose who have chronic kidney disease without HCV infection.

50 s before, during, and after DAA treatment of HCV infection.

51 activation of Nrf2 signaling during chronic HCV infection.

52 ured cells and in treatment of patients with HCV infection.

53 tients with inherited bleeding disorders and HCV infection.

54 ction after liver transplantation had occult HCV infections.

55 e pathogenesis of chronic hepatitis C virus (HCV) infection.

56 of care for patients with hepatitis C virus (HCV) infection.

57 sed increasingly to treat hepatitis C virus (HCV) infection.

58 for children with chronic hepatitis C virus (HCV) infection.

59 in patients with chronic hepatitis C virus (HCV) infection.

60 ributes to persistence of hepatitis C viral (HCV) infection.

61 GS-9857, in patients with hepatitis C virus (HCV) infection.

62 rited blood disorders and hepatitis C virus (HCV) infection.

63 cirrhosis, of whom 48 (33%) had genotype 1a HCV infection, 39 (27%) had genotype 1b infection, 34 (2

64 ion of PERK axis of ER-stress during chronic HCV infection activates oncogenic Nrf2 signaling that pr

65 Hepatitis C virus (HCV) infection affects over 130 million individuals worl

66 -acting antiviral (DAA) agents for recurrent HCV infection after liver transplantation had occult HCV

67 pective study of 134 patients with recurrent HCV infection after liver transplantation who were treat

68 aminotransferases, despite SVR12 to DAAs for HCV infection after liver transplantation.

69 s that can cure a chronic hepatitis C virus (HCV) infection after 8-12 weeks of daily, well-tolerated

70 ns to treat patients with hepatitis C virus (HCV) infection after liver transplantation include the u

71 Treatment of chronic hepatitis C virus (HCV) infection after renal allograft transplantation has

72 e I IFN increased expression of myosins over HCV infection alone.

73 Whether HCV infection also impacts the B-cell compartment and th

74 ctively eradicate chronic hepatitis C virus (HCV) infection, although HCV genotype 3a is less respons

75 s associated with chronic hepatitis C virus (HCV) infection, although the mechanism is poorly underst

76 These data suggest a recent increase in HCV infection among reproductive-aged women and may info

77 c of sexually transmitted hepatitis C virus (HCV) infection among human immunodeficiency virus (HIV)-

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

79 Patients with both HCV infection and advanced chronic kidney disease have l

80 preclinical candidates for the treatment of HCV infection and as molecular probes to study HCV patho

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

82 Additionally, HCV infection and cell attachment were inhibited by PS b

83 d SDC-2 resulted in remarkable reductions of HCV infection and cell attachment, whereas SDC-3 and SDC

84 V attachment and postattachment receptors in HCV infection and cell-to-cell spread remains controvers

85 not, in a prospective study of patients with HCV infection and compensated cirrhosis included in the

86 We evaluated the association of chronic HCV infection and coronary atherosclerosis among partici

87 ells in the liver compartment during chronic HCV infection and defined the cellular and molecular mec

88 estimate the prospective association between HCV infection and diabetes.

89 , and life expectancy among individuals with HCV infection and for the general population.

90 causally linked to immune activation during HCV infection and HCV-HIV coinfection.

91 e then evaluated the associations of chronic HCV infection and HIV infection with measures of plaque

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

93 significant decrease in the percentage with HCV infection and increases in percentages of patients w

94 racteristics of reproductive-aged women with HCV infection and of their offspring.

95 d phenothiazines and pimozide also inhibited HCV infection and preferentially targeted HCV genotype 2

96 led HIV-infected MSM with recent and chronic HCV infection and quantified HCV from rectal fluid obtai

97 this article, we discuss the epidemiology of HCV infection and reinfection, HCV-related liver disease

98 One hundred fifty-nine adults with HCV infection and sickle cell anemia, thalassemia, or he

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

100 entasvir in patients with hepatitis C virus (HCV) infection and compensated cirrhosis.

101 outcomes of patients with hepatitis C virus (HCV) infection and compensated cirrhosis.

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

103 in patients with chronic hepatitis C virus (HCV) infection and stage 4-5 chronic kidney disease resu

104 epatitis B virus (HBV) or hepatitis C virus (HCV) infection and the development of diabetes in a coho

105 of patients with chronic hepatitis C virus (HCV) infection and their fate after antiviral therapy.

106 Outcomes of hepatitis C virus (HCV) infection and treatment depend on viral and host ge

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

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

109 patients were estimated to have undiagnosed HCV infection, and screening identified 532 (14.4%) HCV

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

111 40%-60% of patients with hepatitis C virus (HCV) infection, and overt cryoglobulinemia vasculitis (C

112 To investigate whether chronic HBV and HCV infection are associated with increased incidence of

113 ts with chronic kidney disease who also have HCV infection are at higher risk for progression to end-

114 soluble markers of immune activation during HCV infection are partially reversible within 6 months o

115 eting the early stages of Hepatitis C virus (HCV) infection are hampered by the lack of structural in

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

117 eficiency virus (HIV) and hepatitis C virus (HCV) infections are associated with increased risk of ca

118 Outbreaks of hepatitis C virus (HCV) infections are associated with unsafe injection pra

119 of mortality data, listing acute or chronic HCV infection as a cause of death, from the National Vit

120 hat patients with chronic hepatitis C virus (HCV) infection associated HCC survive longer than those

121 valence of HCV antibody-positive and chronic HCV infection at accession among younger recently deploy

122 ffective way to find and treat patients with HCV infection at scale using existing primary care provi

123 to be able to detect new hepatitis C virus (HCV) infections at a high rate, but it is unknown the ex

124 s performed between 1998 and 2003, recipient HCV infection, balance of risk score >18, and pre-LT ren

125 evidence for enhanced beta-oxidation during HCV infection because HCV-infected SCID/Alb-uPA mice acc

126 DBS could help improve access to care for HCV infection because they are suitable for use in large

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

128 and liver samples from patients with chronic HCV infection before, during, and after antiviral therap

129 During hepatitis C virus (HCV) infection, broadly neutralizing antibody (bNAb) res

130 Estimates of HCV infection burden are essential to guide policy and p

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

132 ted by Quest, 0.76% (CI, 0.69% to 0.83%) had HCV infection, but the percentage was 3.2-fold higher am

133 ral blood samples from patients with chronic HCV infection, but were detected in liver tissues.

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

135 ted patients with chronic hepatitis C virus (HCV) infection, but this still leaves a large number of

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

137 hese 14 patients, 9 were assessed for occult HCV infection by reverse transcription quantitative poly

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

139 Minimally effective treatment of HCV infection can prevent the development of CKD, althou

140 Because ED patients identified with HCV infection can progress to treatment and cure with ra

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

142 e scenarios could prevent 5500 to 12,700 new HCV infections caused by released inmates, wherein about

143 t to dissect out the contribution of chronic HCV infection (common in PWID) from the effects of injec

144 enome analysis in chronic hepatitis C virus (HCV) infection confirms the innate and adaptive arms of

145 A in regulation of host BCR signaling during HCV infection, contributing to a better understanding of

146 r human and chimpanzees, recovery from acute HCV infection correlates with host CD4+ and CD8+ T cell

147 Tunicamycin treatment or HCV infection could induce cellular autophagy, however,

148 Acute hepatitis C virus (HCV) infection culminates in viral persistence in the ma

149 r an efficient control of hepatitis C virus (HCV) infection, cytotoxic T cells (CTL) are pivotal, but

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

151 TNF inhibits HCV infection despite increased HCV envelope glycoprotei

152 atment capacity and increasing the number of HCV infections diagnosed, total HCV prevalence could fal

153 ed virologic response (SVR), and the role of HCV infection diagnostic tests has had to evolve in orde

154 d spontaneously resolving hepatitis C virus (HCV) infection during the acute phase.

155 imately three quarters of acute hepatitis C (HCV) infections evolve to a chronic state, while one qua

156 ength subtype 1a and 3a sequences from early HCV infections from the International Collaborative of I

157 We have shown previously that HCV infection generates an epithelial-mesenchymal transi

158 High proportions of patients with HCV infections genotypes 1-4 (ranging from 75% to 93%) i

159 HRQL data showed that HCV infection had negative effects on overall physical a

160 Liver tissues from patients with chronic HCV infection had significantly higher levels of SMAD6,

161 However, their importance in HCV infection has not previously been examined experimen

162 Hepatitis C virus (HCV) infection has been associated with increased non-li

163 Chronic hepatitis C viral (HCV) infection has been associated with non-Hodgkin's ly

164 In the United States, hepatitis C virus (HCV) infection has increased among young persons who inj

165 tiviral (DAA) therapy for hepatitis C virus (HCV) infection has resulted in high rates of disease cur

166 Treatments of chronic HCV infection have improved dramatically, albeit with re

167 AA) therapies for chronic hepatitis C virus (HCV) infection have demonstrated high rates of sustained

168 Patients with chronic hepatitis C (HCV) infection have high prevalence of vitamin D deficie

169 MS: Patients with chronic hepatitis C virus (HCV) infection have high rates of sustained virologic re

170 3), and Mac2 binding protein (Mac2BP) during HCV infection, HIV infection, and HCV-HIV coinfection, a

171 95% confidence interval [CI], 0.25-0.62) or HCV infection (HR, 0.51; 95% CI, 0.29-0.93).

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

173 Eradication of HCV infection improved cognitive performance but did not

174 t sE2 vaccination confers protection against HCV infection in a genetically humanized mouse model.

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

176 avir, plus ribavirin in treatment of chronic HCV infection in Egypt.

177 ion of memory B-cell function and persistent HCV infection in HCV-infected hosts.

178 ur study identifies a novel pathway in which HCV infection in hepatocytes exacerbates Tfr cell respon

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

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

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

182 ese findings indicate the presence of occult HCV infection in some patients with abnormal levels of s

183 crease the threat of transfusion-transmitted HCV infection in the battlefield blood supply and may le

184 Applicant screening will reduce chronic HCV infection in the force, result in a small system cos

185 ssociated with liver fibrosis during chronic HCV infection in the livers of both humanized mice and p

186 ve-aged women with acute and past or present HCV infection in the NNDSS doubled, from 15 550 in 2006

187 h those of study participants without HBV or HCV infection in the same age range (n=1289).

188 More significantly, the impairment of HCV infection in the TIM-1 knockout cells could be resto

189 d substantially reduce the burden of chronic HCV infection in the United States, but high budgetary c

190 ating the utility of this model for studying HCV infection in vivo At least 150 million individuals a

191 ective in identifying previously undiagnosed HCV infections in primary care settings.

192 to determine the probability of identifying HCV infections in primary care using targeted BC testing

193 would augment identification of undocumented HCV infections in this ED 2-fold, relative to risk-based

194 ibavirin to treat chronic hepatitis C virus (HCV) infection in kidney transplant recipients is limite

195 ibavirin to treat chronic hepatitis C virus (HCV) infection in kidney transplant recipients is limite

196 enotypic regimen to treat hepatitis C virus (HCV) infection in patients coinfected with human immunod

197 medications, treatment of hepatitis C virus (HCV) infection in renal transplant recipients is possibl

198 effective at eradicating hepatitis C virus (HCV) infection in the general population and in HCV-mono

199 Consistently, HCV infection increases glutamine use and dependence.

200 ted its inhibitory effect on tunicamycin- or HCV infection-induced autophagy.

201 Together, our data show that HCV infection induces sCD55 expression in HCV-infected c

202 study, we have shown that hepatitis C virus (HCV) infection induces epithelial-mesenchymal transition

203 ed in blood samples from patients with acute HCV infection; inducible T-cell co-stimulator expression

204 The results support a model of HCV infection influencing the binding of transcription f

205 Thus, SVR in chronic HCV infection is associated with a strong IFNalpha-induc

206 This study reveals that chronic HCV infection is associated with an increased risk of de

207 The current available therapy for HCV infection is based on interferon-alpha, ribavirin an

208 HCV infection is highly prevalent in EDs.

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

210 nstrating that TIM-1-mediated enhancement of HCV infection is PS dependent.

211 echanism of liver disease progression during HCV infection is still unclear, although inflammation is

212 against viral infection, however its role in HCV infection is still unknown.

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

214 nt player in subverting the host response to HCV infection is the viral nonstructural protein NS5A, w

215 Limitations: Only a fraction of HCV infections is detected and reported to the NNDSS.

216 Hepatitis C virus (HCV) infection is a common risk factor for the developme

217 ACKGROUND & AIMS: Chronic hepatitis C virus (HCV) infection is a major burden on individuals and heal

218 Hepatitis C virus (HCV) infection is a major cause of liver cirrhosis and h

219 Hepatitis C virus (HCV) infection is a major risk factor for the developmen

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

221 g antiviral treatment for hepatitis C virus (HCV) infection is costly and does not protect from re-in

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

223 Chronic hepatitis C virus (HCV) infection is more prevalent among patients who have

224 Hepatitis C virus (HCV) infection is not uncommon in cancer patients.

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

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

227 A vaccine that prevents hepatitis C virus (HCV) infection is urgently needed to support an emerging

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

229 mechanism of how chronic hepatitis C virus (HCV) infection leads to such a high rate of hepatocellul

230 Thus, chronic HCV infection massively disturbs the B-cell compartment

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

232 irus (HIV) and/or chronic hepatitis C virus (HCV) infection may be prescribed statins as treatment fo

233 the CHF risk or if HIV or hepatitis C virus (HCV) infection modifies this association.

234 lantation for HCC, proportions of those with HCV infection, nonalcoholic fatty liver disease, or ALD

235 We investigated the effects of TNF on HCV infection of and spread among Huh-7 hepatoma cells a

236 In addition, HCV infection of cells increased the expression of SMAD6

237 Using HCV infection of human hepatocytes and cells with autono

238 Among participants without HBV or HCV infection, only 6 developed HCC or died from liver-r

239 ither had received no previous treatment for HCV infection or had received previous treatment with in

240 HCV infection progresses in a slow chronic fashion elici

241 patitis B virus (HBV) and hepatitis C virus (HCV) infection promote NHL in HIV-infected patients is u

242 transmission cluster of sexually transmitted HCV infections, providing insight into the distinct evol

243 Applying the Quest HCV infection rate to annual live births from 2011 to 20

244 nic mechanisms of chronic hepatitis C virus (HCV) infection remain to be elucidated and pose a major

245 efense against pathogens, but their roles in HCV infection remains unclear.

246 and 1859 children (aged 2 to 13 years) with HCV infection reported to the NNDSS; 2.1 million reprodu

247 While natural hepatitis C virus (HCV) infection results in highly diverse quasispecies of

248 ndent effects of city and calendar period on HCV infection risk.

249 Women with HIV/HCV infection should be counseled against heavy alcohol

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

251 that patients with acute hepatitis C virus (HCV) infection should be treated with a combination of s

252 individuals clear their primary hepatitis C (HCV) infections spontaneously, clearance (spontaneous or

253 tlist members and transplant recipients with HCV infection, stratified by indication for transplantat

254 In this study, we found that HCV infection suppressed the host innate immune response

255 in blood and liver samples of patients with HCV infection than of controls (median, 1.31% vs 2.32% f

256 icantly higher in patients with a relapse of HCV infection than patients who responded to treatment (

257 s advancing the VA's aggressive treatment of HCV infection that are germane to non-VA settings includ

258 up registered clinical trials of adults with HCV infection that evaluated at least 8 weeks of an FDA-

259 Interestingly, during HCV infection, the activation of SREBPs occurs under nor

260 ve drugs for treatment of hepatitis C virus (HCV) infection, there has been an increase in the incide

261 ce model, suggesting that these NAbs inhibit HCV infection through independent mechanisms.

262 undergoing liver transplantation for chronic HCV infection to be decreasing and fewer patients to hav

263 >56.1 IU/L), to the relationships of HBV and HCV infection to cataract.

264 hed into the rectum in HIV-infected men with HCV infection to directly infect an inserted penis or be

265 ampaign to educate MSM about these routes of HCV infection to reverse the HCV epidemic among HIV-infe

266 of hepatitis B (HBV) and hepatitis C virus (HCV) infection to age-related cataract, and to assess wh

267 position of patients with Hepatitis C virus (HCV) infection to hepatocellular carcinoma (HCC) involve

268 ma (HCC) in patients with hepatitis C virus (HCV) infection treated with direct-acting antivirals (DA

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

270 Chronic HCV infection was defined by detectable HCV viral load.

271 HBV and HCV infection was significantly associated with nuclear

272 Inhibition of HCV infection was studied using infectious HCV models in

273 Historically, acute hepatitis C virus (HCV) infection was treated with shorter durations of int

274 In phase 3 trials of patients with HCV infection, we did not establish that sofosbuvir-velp

275 iviral agents for chronic hepatitis C virus (HCV) infection, we examined the antiviral efficacy and s

276 t of PWID with or without hepatitis C virus (HCV) infection, we sought to dissect out the contributio

277 The hazard ratios for NHL with HBV and HCV infection were 1.33 (95% CI, 0.69 to 2.56) and 0.67

278 ively, compared to HBV uninfection; ORs with HCV infection were 1.35 (95CI = 1.18-1.55) and 1.40 (95C

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

280 chronic HBV infection and 7506 [14.3%] with HCV infection) were included, of whom 40 219 (77%) later

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

282 2 phase 3, open-label trials, patients with HCV infection who had not been treated previously with a

283 fe and highly effective in participants with HCV infection who had previously failed NS5A inhibitor-c

284 Patients with chronic HCV infection who were not in treatment and healthy cont

285 university hospitals diagnosed with chronic HCV infection who were treated with a PEG-IFN and ribavi

286 People with hepatitis C virus (HCV) infection who have failed treatment with an all-ora

287 000 women (CI, 27 400 to 30 900 women) with HCV infection, who gave birth to 1700 infants (CI, 1200

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

289 The significant relationships of HCV infection with nuclear and any cataract were formed

290 ny cataract outcome, but the associations of HCV infection with nuclear and any cataract were not med

291 HCV patients, we examined the association of HCV infection with the incidence of CKD.

292 ntagonises miR-122, in patients with chronic HCV infection with various genotypes.

293 Treatment of genotype 1 hepatitis C virus (HCV) infection with combination directly acting antivira

294 lant recipients with chronic genotype 1 or 4 HCV infection, with or without compensated cirrhosis, an

295 lant recipients with chronic genotype 1 or 4 HCV infection, with or without compensated cirrhosis, an

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

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

298 om 12 healthy donors and 12 individuals with HCV infection without CV.

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

300 ult patients with chronic hepatitis C virus (HCV) infection without cirrhosis or with compensated cir