ライフサイエンスコーパス: HCV infection

1 ownregulation of viral-induced RAD21 reduces HCV infection.

2 ion to innate immune pressure during chronic HCV infection.

3 ction, and 177 (4.8%) harbored a replicating HCV infection.

4 avenue for host-targeting strategies against HCV infection.

5 al for designing animal experiments to model HCV infection.

6 ected donors into recipients who do not have HCV infection.

7 iral regimens have transformed treatment for HCV infection.

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

9 c (Group B, n = 22) patients with genotype 4 HCV infection.

10 ated HCV neutralization in acute and chronic HCV infection.

11 ung transplants from donors who did not have HCV infection.

12 critical step in the development of chronic HCV infection.

13 150,000 persons age >= 18 years with active HCV infection.

14 nding of immune response to and clearance of HCV infection.

15 trafficking pathway during acute and chronic HCV infection.

16 nsplantation, prevented the establishment of HCV infection.

17 y is normally inactivated by NS3-NS4A during HCV infection.

18 espective of HCV genotype, to adults without HCV infection.

19 3 activation and interferon induction during HCV infection.

20 ucleotide substitution rate estimated during HCV infection.

21 diabetes increased only among patients with HCV infection.

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

23 in adolescents aged 12 years and older with HCV infection.

24 12-month injection behaviors associated with HCV infection.

25 in selected recipients both with and without HCV infection.

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

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

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

29 ferentiation and M2 MPhi polarization during HCV infection.

30 in the pathogenesis of liver disease during HCV infection.

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

32 ir in renal transplant patients with chronic HCV infection.

33 iral load reduction in patients with chronic HCV infection.

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

35 f the viremic population was aware of having HCV infection.

36 d virus-specific CD4+ T cell response during HCV infection.

37 HCV-RNA and identified 13 (0.4%) with a new HCV infection.

38 150 000 persons aged >=18 years with active HCV infection.

39 for monitoring the therapy and management of HCV infection.

40 for 6 weeks in people with acute and recent HCV infection.

41 mal B cell function is a hallmark of chronic HCV infection.

42 plant candidates with or without preexisting HCV infection.

43 ell immunity might contribute to controlling HCV infection.

44 (DAAs) to MSM identified with a replicating HCV infection.

45 code proteins that influence DENV, ZIKV, and HCV infection.

46 es of the opioid epidemic, including chronic HCV infection.

47 the minimum treatment duration required for HCV infection.

48 endations for the optimal treatment of acute HCV infections.

49 LCMV Clone 13, and in patients with chronic HCV infections.

50 oping HCC among patients with chronic HBV or HCV infections.

51 s have greatly reduced the burden of HBV and HCV infections.

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

53 major cause of pediatric hepatitis C virus (HCV) infection.

54 nsider the elimination of hepatitis C virus (HCV) infection.

55 ide are estimated to have hepatitis C virus (HCV) infection.

56 effective at eradicating hepatitis C virus (HCV) infection.

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

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

59 Squibb for key drugs for hepatitis C virus (HCV) infection.

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

61 chronically infected with hepatitis C virus (HCV) infection.

62 kidneys from donors with hepatitis C virus (HCV) infection.

63 epatitis B virus (HBV) or hepatitis C virus (HCV) infections.

64 ibuted to a sharp rise in hepatitis C virus (HCV) infections.

65 80%) MSM and identified 177 with replicating HCV infections (4.8%); 150 (85%) of which started DAA tr

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

67 ts achieved an SVR (22.4%) (94 patients with HCV infection, 98 patients with HBV infection, and 8 pat

68 (51.9%) did not receive treatment for their HCV infection after complete response to prior HCC thera

69 who did not receive DAA treatment for their HCV infection after complete response to prior HCC thera

70 exually transmitted acute hepatitis C virus (HCV) infections (AHIs) have been mainly described in hum

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

72 otransferase (AST) value, Hepatitis C virus (HCV) infection, alcohol abuse, CD4/CD8 ratio and an incr

73 s on how to best screen for and manage acute HCV infections, along with broad access to rapid HCV the

74 that SOF-based regimens in the treatment of HCV infection among hemodialysis patients are both effec

75 18, we diagnosed 15 likely sexually acquired HCV infections among 14 MSM using PrEP.

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

77 Hepatitis C virus (HCV) infection among maintenance hemodialysis patients i

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

79 Sexually acquired hepatitis C virus (HCV) infections among human immunodeficiency virus (HIV)

80 Increasing numbers of hepatitis C virus (HCV) infections among men who have sex with men (MSM) ar

81 associated with an increase in hepatitis C (HCV) infections among women of childbearing age in the U

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

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

84 The association between HCV infection and CCA has been examined in a number of e

85 ric g-computation to estimate the effects of HCV infection and DAA treatment on mortality had partici

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

87 ks after completion of antiviral therapy for HCV infection and graft survival at 6 months after trans

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

89 We examined correlates of HCV infection and HIV-HCV co-infection using bivariate a

90 ole of innate immunity in protection against HCV infection and immune evasion is only partially under

91 ntive and therapeutic strategies for chronic HCV infection and its serious comorbidities.

92 ck of a convenient animal model for study in HCV infection and liver pathogenesis.

93 that have been used to study risk of HBV and HCV infection and patient outcomes.

94 we show that VAPA and VAPB are redundant for HCV infection and that dimerization is not required for

95 We found that HCV infection and the BMP/SMAD pathway are mutually anta

96 effective setting both for treating chronic HCV infections and for preventing new infections among P

97 hington, that captured the spread of HIV and HCV infections and incarceration and treatment systems a

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

99 n associated with chronic hepatitis C virus (HCV) infection and is a key prognostic indicator for pro

100 spontaneous clearance of hepatitis C virus (HCV) infection and response to interferon-based treatmen

101 individuals with chronic hepatitis C viral (HCV) infection and without cirrhosis, glecaprevir/pibren

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

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

104 rapid HCV suppression, prevention of chronic HCV infection, and excellent early allograft function in

105 of the opioid crisis, curative treatment for HCV infection, and mortality among the HCV-infected popu

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

107 This drug eliminates most chronic HCV infections, and resistance-associated substitutions

108 dentify adults with NASH, hepatitis C virus (HCV) infection, and alcohol-related liver disease (ALD)

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

110 two million new cases of hepatitis C virus (HCV) infections annually underscore the urgent need for

111 tation is the primary method by which active HCV infections are identified and the response to direct

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

113 Kidneys from donors with hepatitis C virus (HCV) infection are traditionally considered to be at ris

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

115 proved drug used to treat hepatitis C virus (HCV) infections-as a potent antiviral with a novel mecha

116 Chronic hepatitis C virus (HCV) infection-associated liver disease is a global heal

117 ir-sofosbuvir in Rwandan adults with chronic HCV infection at a single study site (Rwanda Military Ho

118 ects were free of any CVD event diagnosis of HCV infection at baseline.

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

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

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

122 s and the progression of HCC associated with HCV infection but not for assessing the degree of hepati

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

124 fe treatment for Asian patients with chronic HCV infection, but might have lower efficacy in those in

125 mmune-mediated control of hepatitis C virus (HCV) infection, but the relative contribution of neutral

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

127 ess to treatment, and increase screening for HCV infection by considering six scenarios: no change ma

128 inhibition of innate immune pathways during HCV infection by exploiting the ability of LRPPRC to inh

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

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

131 Organization aims for a 90% reduction in new HCV infections by 2030.

132 ions are needed to prevent sexually acquired HCV infections by MSM using PrEP.

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

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

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

136 Chronic hepatitis C virus (HCV) infection causes decreased expression of the iron h

137 ecific CD4+ T cells during acute and chronic HCV infection compared to patients with spontaneously re

138 11-fold, respectively, more likely to clear HCV infection compared with individuals carrying none or

139 ith cirrhosis before an SVR to treatment for HCV infection continue to have a high risk for HCC (>2%/

140 atients who had never received treatment for HCV infection (controls).

141 h year of previously diagnosed and untreated HCV infections could reduce the HCV incidence by 61% (95

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

143 in 2015, with an estimated 1.75 million new HCV infections diagnosed in 2015.

144 lion people in the United States had current HCV infection during 2013-2016; compared to past estimat

145 are denied treatment for hepatitis C virus (HCV) infection, even if they are receiving opioid agonis

146 The rate of newly diagnosed HCV infections exceeded the rate of newly diagnosed HIV

147 tiviral (DAA) therapy for hepatitis C virus (HCV) infection for patients with a history of hepatocell

148 t drugs contribute substantially to incident HCV infections globally.

149 tment assessments, and management of chronic HCV infection has been presented in this article.

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

151 antiviral agents to treat hepatitis C virus (HCV) infection has raised the possibility of substantial

152 Cases of acute HCV infection have increased approximately 3.8-fold over

153 immune responses against hepatitis C virus (HCV) infection have been studied in great detail, the ro

154 ssed factors associated with past or present HCV infection (HCV antibody [anti-HCV] positive) among y

155 osterone in a cohort of 327 men with chronic HCV infection (human immunodeficiency virus [HIV] coinfe

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

157 S-independent, signaling pathway that limits HCV infection.IMPORTANCE The HCV NS3-NS4A protease compl

158 RBV cotreatment of HCV-infection improved pSTAT4-dependent IFNgamma-product

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

160 y, natural history, and treatment of chronic HCV infection in adolescents and children, and we highli

161 ion, diagnosis, treatment, and management of HCV infection in adult CKD populations.

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

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

164 Finally, we discuss the hypothetical role of HCV infection in CCA development by induction of epithel

165 he estimated global prevalence and burden of HCV infection in children aged 1-19 years is 0.15%, corr

166 xtensive update of KDIGO's 2008 guideline on HCV infection in CKD.

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

168 norvegicus (RHV-rn1) mirrors key aspects of HCV infection in humans, including chronicity, hepatitis

169 The seroprevalence of HBV and HCV infection in Malaysia is low and intermediate, respe

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

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

172 ment selection for the management of chronic HCV infection in resource-limited settings.

173 cting antivirals (DAAs) in the management of HCV infection in the CKD population.

174 d in greater ease and confidence in managing HCV infection in transplant recipients that in turn has

175 We classified HCV infections in HIV-positive MSM as either domesticall

176 g 8 weeks of ledipasvir/sofosbuvir for acute HCV infections in men with HIV infections, reports a 100

177 pasvir/sofosbuvir for the treatment of acute HCV infections in participants with chronic human immuno

178 to estimate the current and future burden of HCV infections in this high-risk population.

179 ortant public health strategies for reducing HCV infections in this high-risk population.

180 Chronic hepatitis C virus (HCV) infection in Asia is characterized by specific dist

181 luation, and treatment of hepatitis C virus (HCV) infection in chronic kidney disease (CKD) is an ext

182 Treatment uptake for hepatitis C virus (HCV) infection in people who inject drugs (PWID) and pat

183 Most persons with chronic hepatitis C virus (HCV) infection in the United States are undiagnosed or l

184 rapy is now available for hepatitis C virus (HCV) infection in the United States, it is not clear whe

185 ease in organ donors with hepatitis C virus (HCV) infection in the United States.

186 he development of chronic hepatitis C virus (HCV) infection in uninfected recipients of HCV-infected

187 proportion of undiagnosed hepatitis C virus (HCV) infections in high-risk populations, such as human

188 HCV infection increased the level of Arl8b 3-fold and re

189 ality among patients with hepatitis C virus (HCV) infection increased from 2007 through 2013 and then

190 Consistently, HCV infection increases glutamine use and dependence.

191 During mitosis, HCV infection induces hypercondensation of chromosomes a

192 mediated regulation of CD4+ T cells in early HCV infection, irrespective of outcome, with persistent

193 HCV infection is associated with an increased risk of ca

194 However, HCV infection is highly underdiagnosed; therefore, a glo

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

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

197 We conclude that HCV infection is rapidly cleared from liver with DAA lea

198 HCV infection is usually asymptomatic during childhood,

199 ofile suitable for potential use in treating HCV infections is disclosed here.

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

201 Hepatitis C virus (HCV) infection is a global public health problem because

202 Chronic hepatitis C virus (HCV) infection is a leading cause of cirrhosis worldwide

203 Hepatitis C virus (HCV) infection is a major cause of chronic liver disease

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

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

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

207 Chronic hepatitis C virus (HCV) infection is characterized by persistent high-level

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

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

210 Hepatitis C virus (HCV) infection is highly prevalent among people who inje

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

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

213 Hepatitis C virus (HCV) infection is the leading cause of chronic hepatitis

214 Hepatitis C virus (HCV) infection is the main cause of hepatocellular carci

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

216 Hepatitis C virus (HCV) infection is the most commonly reported bloodborne

217 used for the treatment of hepatitis C virus (HCV) infections, is a potent antiviral against EV-D68 by

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

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

220 Untreated, chronic hepatitis C virus (HCV) infection may lead to progressive liver damage, whi

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

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

223 Veterans database for patients with chronic HCV infection (n = 242,680) and identified patients who

224 nsive strategy to control hepatitis C virus (HCV) infection needs a vaccine.

225 nd CCA and recent publications of studies of HCV infection of cholangiocytes and CCA cell lines as we

226 We previously observed that HCV infection of hepatocytes transcriptionally down-regu

227 HCV infection of MLH co-culture resulted in upregulation

228 Carrying out HCV infections of control and eIF3e-silenced Huh-7.5 cel

229 udy aimed to determine the effect of chronic HCV infection on the expression of the major regulators

230 viral (DAA) therapies for hepatitis C virus (HCV) infection on hepatocellular carcinoma (HCC) recurre

231 ng antibodies can prevent hepatitis C virus (HCV) infection, one of the leading causes of cirrhosis a

232 dentified 24 individuals (14%) with incident HCV infection; one-third of them had a negative HCV anti

233 in Washington, DC, 100 patients with chronic HCV infection, opioid use disorder, and ongoing injectio

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

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

236 ared to patients with spontaneously resolved HCV infection (p < 0,0001).

237 0 antigen and presence of hepatitis C virus (HCV) infection predicted early (year 1) GFR deterioratio

238 In HIV burden networks, high HCV infection prevalence may occur in MSM without HIV.

239 estimated-defined here as the percentage of HCV infections prevented if additional HCV transmission

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

241 Hepatitis C virus (HCV) infection promotes metabolic disorders, and the sev

242 nes for the management of hepatitis C virus (HCV) infections provide varying recommendations for the

243 The county-level HCV infection rate is 4 times higher in minority countie

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

245 of virus-specific CD4+ T cells in persisting HCV infection remain unclear.

246 he way for HCV elimination, most people with HCV infection remain undiagnosed and untreated globally,

247 rams on the rate of new HIV and Hepatitis C (HCV) infections remains unknown as high mortality can ex

248 While some HCV infections resolve spontaneously, viral persistence

249 In conclusion, HCV infection results in the generation of HCV-specific

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

251 the diagnosis, management, and monitoring of HCV infection specific to the Asian region is a major un

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

253 Together, our results suggest that HCV infection suppresses miR-181c in hepatocytes, result

254 During active HCV infection, testosterone deficiency may be masked due

255 s on the diagnosis and management of chronic HCV infection that reflects local conditions.

256 with the percentage of a country's prevalent HCV infections that are among people who inject drugs.

257 Among patients with HCV infection, the age-standardized mortality for extrah

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

259 carcinoma and extrahepatic manifestations of HCV infection; there are also data to indicate that an S

260 Prevention of HCV infection through blood transfusion, HCV treatment a

261 th acute, chronic and spontaneously resolved HCV infection to assess the expression pattern of the co

262 longitudinally sampled from acute to chronic HCV infection to investigate the underlying viral popula

263 mpare overall survival between patients with HCV infection treated with DAAs and patients who did not

264 ogy of liver cells due to hepatitis C virus (HCV) infection using this model.

265 Risk factors for hepatitis C virus (HCV) infection vary, and there were an estimated 1.75 mi

266 n healthy volunteers who are not at risk for HCV infection; viral vectors encoding nonstructural prot

267 In hepatitis C virus (HCV) infection, virus-specific CD8+ T cells are recruite

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

269 The 10-year mortality risk difference for HCV infection was 4.3% (95% CI 0.4-8.9%) and the risk ra

270 n the short term, all-oral DAA treatment for HCV infection was associated with a decreased risk of de

271 ohort of HCV-infected veterans, treatment of HCV infection was associated with a significant decrease

272 Acute HCV infection was diagnosed in 32% (15/47) ,with all pat

273 Acute HCV infection was diagnosed in 32% (15/47) with all pati

274 en of cardiovascular disease associated with HCV infection was responsible for 1.5 million DALYs, wit

275 HCV infection was significantly associated with injectio

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

277 kthroughs in treatment of hepatitis C virus (HCV) infection, we have limited understanding of how vir

278 for treatment of chronic hepatitis C virus (HCV) infection, we looked at the impact of DAA use and 1

279 Independent predictors of HCV infection were identified using Cox regression model

280 ug users in 2017, and 8% (5-12) of prevalent HCV infections were among people who currently inject dr

281 Cohort Study and diagnosed with replicating HCV infections, were sequenced.

282 ssion results in a significant inhibition of HCV infection, which is associated with an increased act

283 ly increases the diagnostic effectiveness of HCV infections, while allowing the identification of und

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

285 In patients without HCV infection who received a heart or lung transplant fr

286 sons aged 18 years and older with genotype 1 HCV infection who were willing to receive HCV therapy on

287 Patients with current or prior HCV infection will engage in alcohol treatment when enco

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

289 etes in individuals successfully treated for HCV infection with DAA agents.

290 CA is one of the most affected regions by HCV infection with Uzbekistan enduring one of the highes

291 s are limited for patients with hepatitis C (HCV) infection with treatment failure after sofosbuvir p

292 fibrosis, but only 49.8% were aware of their HCV infection, with higher disease awareness in those wi

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

294 epatitis B virus (HBV) or hepatitis C virus (HCV) infection, with or without a sustained response to

295 eginning in 2018, to 100% of newly diagnosed HCV infections within 3 months of diagnosis and 25% each

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

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

298 s (MAbs) from a single person who cleared an HCV infection without treatment, and we identify 3 new s

299 an estimated 43% (95% CrI 25-67) of incident HCV infections would be prevented from 2018 to 2030, var

300 population of people with hepatitis C virus (HCV) infection, yet little is known about HCV among peop