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1 rictions for people co-infected with HIV and hepatitis C virus.
2 compounds showed antiviral activity against hepatitis C virus.
3 be avoided in black patients with genotype 1 hepatitis C virus.
4 a performed well in patients with cACLD with hepatitis C virus and alcoholic and nonalcoholic steatoh
5 We demonstrate that, in sharp contrast to hepatitis C virus and human immunodeficiency virus patie
8 ople have been estimated to be infected with hepatitis C virus, and many more are at risk for infecti
11 enter prospective study of 226 patients with hepatitis C virus-associated cirrhosis and CSPH who had
12 lticenter prospective study of patients with hepatitis C virus-associated cirrhosis, an SVR to all-or
14 r 24 weeks in 9 human immunodeficiency virus/hepatitis C virus-coinfected patients who relapsed after
15 or ultrasensitive and selective detection of hepatitis C virus core antigen (HCV) have been investiga
18 SV) 1 and 2, human immunodeficiency virus 1, hepatitis C virus, enterovirus 70, and variant Creutzfel
19 This issue provides a clinical overview of hepatitis C virus, focusing on transmission, prevention,
20 available North American sequences from five hepatitis C virus genes (E1, E2, NS2, NS4B, NS5B), with
21 MC647055/ritonavir + JNJ-56914845 in chronic hepatitis C virus genotype (GT)1-infected treatment-naiv
22 confidence interval, 86%-100%) patients with hepatitis C virus genotype 1 infection, 13 of 14 (93%; 9
25 eened 45 316 publicly available sequences of hepatitis C virus genotype 1a for location and genotype,
29 caprevir/pibrentasvir (G/P) in patients with hepatitis C virus genotype 3 infection with prior treatm
33 steatosis (HS) is common in individuals with hepatitis C virus (HCV) and human immunodeficiency virus
34 Patients who are chronically infected with hepatitis C virus (HCV) and who do not have a sustained
35 [BPA], and patient solicitation), evaluated hepatitis C virus (HCV) antibody testing, diagnosis, and
36 afety and efficacy in treating patients with hepatitis C virus (HCV) awaiting liver transplant (LT).
39 urrent standard of care for the treatment of hepatitis C virus (HCV) consists of interferon-free dire
40 lines were genetically engineered to display Hepatitis C virus (HCV) core antigen linked to gold bind
46 we longitudinally sampled and sequenced the hepatitis C virus (HCV) envelope genome region (1,680 nu
53 S5A, which is involved in replication of the hepatitis C virus (HCV) genome, presumably via membranou
54 r + DSV) +/- ribavirin (RBV) is approved for hepatitis C virus (HCV) genotype 1 (GT1) treatment in HI
55 n the United States for treatment of chronic hepatitis C virus (HCV) genotype 1 and 4 infections, as
57 BACKGROUND & AIMS: Patients with chronic hepatitis C virus (HCV) genotype 2 have high rates of re
59 pproved treatment regimens for patients with hepatitis C virus (HCV) genotypes (GTs) 2 and 3 contain
65 atients chronically infected with genotype 3 hepatitis C virus (HCV) have faster disease progression
66 is study examined the interactions among the hepatitis C virus (HCV) helicase and RLR helicases in li
68 changes that occur upon prolonged passage of hepatitis C virus (HCV) in human hepatoma cells in an ex
69 tly-acting antivirals has been advocated for Hepatitis C Virus (HCV) in people who inject drugs (PWID
70 dynamics, and phenotypic diversification of hepatitis C virus (HCV) in the course of 200 passages in
71 We determined temporal trends (1985-2011) in hepatitis C virus (HCV) incidence and associated behavio
73 ing antiviral agents that can cure a chronic hepatitis C virus (HCV) infection after 8-12 weeks of da
74 recommended regimens to treat patients with hepatitis C virus (HCV) infection after liver transplant
76 known of an epidemic of sexually transmitted hepatitis C virus (HCV) infection among human immunodefi
77 response (SVR) on outcomes of patients with hepatitis C virus (HCV) infection and compensated cirrho
78 lecaprevir and pibrentasvir in patients with hepatitis C virus (HCV) infection and compensated cirrho
80 egimen for 12 weeks in patients with chronic hepatitis C virus (HCV) infection and stage 4-5 chronic
81 ociations between hepatitis B virus (HBV) or hepatitis C virus (HCV) infection and the development of
82 AIT cells in livers of patients with chronic hepatitis C virus (HCV) infection and their fate after a
84 pment of drugs targeting the early stages of Hepatitis C virus (HCV) infection are hampered by the la
85 tive studies of the outcomes associated with hepatitis C virus (HCV) infection are rare and critical
86 have demonstrated that patients with chronic hepatitis C virus (HCV) infection associated HCC survive
87 nbiased genome-to-genome analysis in chronic hepatitis C virus (HCV) infection confirms the innate an
89 with persistent and spontaneously resolving hepatitis C virus (HCV) infection during the acute phase
92 Direct-acting antiviral (DAA) therapy for hepatitis C virus (HCV) infection has resulted in high r
93 acting antiviral (DAA) therapies for chronic hepatitis C virus (HCV) infection have demonstrated high
94 BACKGROUND & AIMS: Patients with chronic hepatitis C virus (HCV) infection have high rates of sus
95 of interferon and ribavirin to treat chronic hepatitis C virus (HCV) infection in kidney transplant r
96 of interferon and ribavirin to treat chronic hepatitis C virus (HCV) infection in kidney transplant r
97 ffective, and pan-genotypic regimen to treat hepatitis C virus (HCV) infection in patients coinfected
98 ng antiviral (DAA) medications, treatment of hepatitis C virus (HCV) infection in renal transplant re
99 asvir-sofosbuvir is effective at eradicating hepatitis C virus (HCV) infection in the general populat
100 In a previous study, we have shown that hepatitis C virus (HCV) infection induces epithelial-mes
107 efficacy of antiviral treatment for chronic hepatitis C virus (HCV) infection is determined by measu
113 immunodeficiency virus (HIV) and/or chronic hepatitis C virus (HCV) infection may be prescribed stat
114 s stage influences the CHF risk or if HIV or hepatitis C virus (HCV) infection modifies this associat
115 Whether chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infection promote NHL in HIV-inf
116 The immuno-pathogenic mechanisms of chronic hepatitis C virus (HCV) infection remain to be elucidate
117 lines now recommend that patients with acute hepatitis C virus (HCV) infection should be treated with
118 e the relationships of hepatitis B (HBV) and hepatitis C virus (HCV) infection to age-related catarac
120 atocellular carcinoma (HCC) in patients with hepatitis C virus (HCV) infection treated with direct-ac
124 lete regimen for adult patients with chronic hepatitis C virus (HCV) infection without cirrhosis or w
125 ivirals (DAAs) effectively eradicate chronic hepatitis C virus (HCV) infection, although HCV genotype
127 ins are detected in 40%-60% of patients with hepatitis C virus (HCV) infection, and overt cryoglobuli
128 e the availability of curative treatment for hepatitis C virus (HCV) infection, because of cost, trea
129 ptor proteins AP1 and AP2, are essential for hepatitis C virus (HCV) infection, but the underlying me
130 h cure rate in treated patients with chronic hepatitis C virus (HCV) infection, but this still leaves
132 ent of more effective drugs for treatment of hepatitis C virus (HCV) infection, there has been an inc
141 artments (EDs) seem to be able to detect new hepatitis C virus (HCV) infections at a high rate, but i
149 itious targets for global control of HIV and hepatitis C virus (HCV) is low levels of awareness of in
156 formed by glycoproteins E1 and E2 within the hepatitis C virus (HCV) lipid envelope is a potential va
158 nt pan-genotype and macrocyclic inhibitor of hepatitis C virus (HCV) NS3/4A protease and was develope
162 enib with alternative therapies according to hepatitis C virus (HCV) or hepatitis B virus (HBV) statu
163 rotein synthesis to directly incorporate the hepatitis C virus (HCV) p7 protein into supported lipid
164 s an urgent need for a vaccine to combat the hepatitis C virus (HCV) pandemic, and induction of broad
165 rd-of-care treatment of chronically infected hepatitis C virus (HCV) patients involves direct-acting
166 inhibitors, particularly those of HIV-1 and hepatitis C virus (HCV) protease, revealed a plethora of
168 to assess human immunodeficiency virus (HIV)/hepatitis C virus (HCV) real-world treatment outcomes.
169 pite recent advances in therapeutic options, hepatitis C virus (HCV) remains a severe global disease
171 , exhibit potent inhibitory activity against hepatitis C virus (HCV) replication in genotype 1b Con 1
172 croRNAs (miRNAs) have been shown to regulate hepatitis C virus (HCV) replication, yet a systematic in
176 polymerase that catalyzes replication of the hepatitis C virus (HCV) RNA genome and therefore is cent
177 The affordable and reliable detection of Hepatitis C Virus (HCV) RNA is a cornerstone in the mana
180 an electronic health record-based prompt on hepatitis C virus (HCV) screening rates in baby boomers
181 ntive Services Task Force recommend one-time hepatitis C virus (HCV) testing for persons born during
182 ntrol and Prevention (CDC) recommends 1-time hepatitis C virus (HCV) testing in the 1945-1965 birth c
187 out substitutions that mediate resistance of hepatitis C virus (HCV) to direct-acting antivirals (DAA
188 ral direct-acting antivirals has altered the hepatitis C virus (HCV) treatment paradigm for both pre-
190 ivirals (DAAs) have changed the landscape of hepatitis C virus (HCV) treatment, but chronic hepatitis
192 e models has been an obstacle for developing hepatitis C virus (HCV) vaccines and affordable antivira
196 ect drugs (PWID); and the prevalence of HIV, hepatitis C virus (HCV), and hepatitis B virus (HBV) amo
197 ected by human immunodeficiency virus (HIV), hepatitis C virus (HCV), and hepatitis B virus (HBV).
198 for detection of cirrhosis in patients with hepatitis C virus (HCV), hepatitis B virus (HBV), NAFLD,
199 th decompensated cirrhosis (DC) secondary to hepatitis C virus (HCV), is associated with improved hep
200 RNA (+RNA) viruses including human pathogens hepatitis C virus (HCV), Severe acute respiratory syndro
201 burden posed by hepatitis B virus (HBV) and hepatitis C virus (HCV), to learn from each other's expe
202 with human immunodeficiency virus (HIV) and hepatitis C virus (HCV), we assessed fibrosis progressio
203 cohort of human immunodeficiency virus (HIV)/hepatitis C virus (HCV)-coinfected patients treated with
204 was cloned from T cells that expanded when a hepatitis C virus (HCV)-infected HLA-A2(-) individual re
205 A) is the nation's largest care provider for hepatitis C virus (HCV)-infected patients and is uniquel
206 k of chronic kidney disease (CKD) in chronic hepatitis C virus (HCV)-infected patients and the incide
213 k of acute myocardial infarction (AMI) among hepatitis C virus (HCV)-positive versus HCV-negative per
215 Guidelines recommend that patients with hepatitis C virus (HCV)-related liver disease be treated
229 ly observed in individuals infected with the hepatitis C virus (HCV); however, the underlying molecul
232 igh rates of sustained virological response (hepatitis C virus [HCV] RNA <15 IU/mL) at post-treatment
233 serostatus (+ or -: hepatitis B core [HBc], hepatitis C virus [HCV], Epstein-Barr virus [EBV], or cy
234 st a wide variety of viruses, including HIV, hepatitis C virus, hepatitis B virus, enterovirus 71, in
235 as well as profound antiviral effect against hepatitis C virus, human rhinovirus, and coxsackievirus
236 or without ribavirin as treatment of chronic hepatitis C virus in solid organ transplant recipients a
237 AA) therapies are effective in patients with hepatitis C virus-induced cryoglobulinemia vasculitis (H
238 hepatitis B virus (HBV) has been reported in hepatitis C virus-infected individuals receiving direct-
240 HIV-negative patients with cancer (n = 53), hepatitis C virus-infected patients (n = 17), and health
242 ir (LDV/SOF) can be considered in genotype 1 hepatitis C virus-infected patients who are treatment-na
243 treatment policies in a real-life cohort of hepatitis C virus-infected policy 1, "universal," treat
244 his retrospective evaluation included 62,290 hepatitis C virus-infected veterans completing oral DAA
245 n (54.1%, P = 0.001), had lower incidence of hepatitis C virus infection (4.9%, P = 0.001) and longer
246 old-especially those born in the peak era of hepatitis C virus infection and among whites/Caucasians.
247 preclinical candidates for the treatment of hepatitis C virus infection and as probes to study hepat
248 called mixed cryoglobulinemia and is seen in hepatitis C virus infection and systemic diseases such a
250 antiviral drugs for the treatment of chronic hepatitis C virus infection have reduced mortality and t
251 s after DAA therapy in patients with chronic hepatitis C virus infection in the context of the immune
254 report a case series of three patients with hepatitis C virus infection who all presented with sever
255 djusted for age, race or ethnicity, smoking, hepatitis C virus infection, alcohol use disorders, drug
256 and well tolerated in patients with chronic hepatitis C virus infection, including those with compen
257 ) to interferon-based treatments for chronic hepatitis C virus infection, whereas Asian race was asso
258 New Zealand of 197 patients with genotype 1 hepatitis C virus infection, with or without compensated
261 us infection; 29.1% (95% CI: 23.6-34.5%) for hepatitis C virus infection; 33.9% (95% CI: 24.3-43.5%)
262 through the control of hepatitis B virus and hepatitis C virus infections by vaccination and treatmen
264 ture-based design of HCV vaccines.IMPORTANCE Hepatitis C virus is a leading cause of liver disease an
266 stimulation during persistent infection with hepatitis C virus is associated with continuous activati
268 listed women differed in age (58 vs 57), non-hepatitis C virus listing diagnoses (69% vs 56%), hepati
269 29382 young persons currently infected with hepatitis C virus lived >10 miles from a syringe service
270 itis C virus-positive (50.9-57.9 years) than hepatitis C virus-negative (51.3-54.3 years) registrants
272 avage of four novel substrate motifs for the hepatitis C virus NS3/4 protease using an in vivo assay.
274 tis C virus infection and as probes to study hepatitis C virus pathogenesis and host-virus interactio
275 We conducted a retrospective cohort study of hepatitis C virus patients who were treated with DAA in
276 ood and tissue donors, persons infected with hepatitis C virus, persons with elevated alanine aminotr
278 th cold ischemic time >12 hours, livers from hepatitis C virus positive donors, livers from donation
279 5.7 years, with a more prominent increase in hepatitis C virus-positive (50.9-57.9 years) than hepati
280 ed from 2002 to 2014, driven by aging of the hepatitis C virus-positive cohort and increased prevalen
284 further show that kinesin knockdown inhibits hepatitis-C virus replication in hepatocytes, likely bec
286 ssion, all from an active IVDU donor who was hepatitis C virus seronegative at time of donation, but
289 ify the transmission dynamics that drive the hepatitis C virus subtypes 4a (HCV4a) and 4d (HCV4d) epi
291 nce of some countries not following the 2016 hepatitis C virus treatment guidelines by the European A
292 rejection (n = 2 KT, 4 LT) occurred, during hepatitis C virus treatment in 4 and after cessation of
296 involved in the assembly and release of the hepatitis C virus, was determined from proteins expresse
297 the setting of viral hepatitis, particularly hepatitis C virus, where sustained viral response has be
298 ral direct-acting antiviral drugs (DAAs) for hepatitis C virus, which have response rates of 95% or m
299 ategy for patients chronically infected with hepatitis C virus who experience virologic failure after
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