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1                                              DAA at 20% coverage had an ICER of $27,251/QALY.
2                                              DAA cure does not promote resurrection of exhausted CD4(
3                                              DAA therapy restores a normal adaptive NK phenotype and
4                                              DAA therapy significantly reduces the incidence and risk
5                                              DAA treatment (hazard ratio [HR] 0.53, 95% CI .46-.63) a
6                                              DAA treatment restored ADCC ability and reduced programm
7                                              DAA-treated persons had longer diabetes-free survival ra
8                                              DAAs have recently been available long enough to estimat
9                                              DAAs were effective when implemented through the Rwandan
10                     BEST PRACTICE ADVICE 11: DAA therapy should not be withheld from patients with co
11    Among patients with cirrhosis (n = 2157), DAA therapy was associated with a 72% and a 62% lower in
12                                    Among 537 DAA-treated patients who experienced a virological failu
13 60) and after (AOR 0.63; 95% CI, 0.55, 0.71) DAA therapy was available.
14                                            A DAA-induced SVR reduces a patient's risk of cirrhosis an
15 s the hepatic and extrahepatic benefits of a DAA-induced sustained virologic response (SVR).
16  studied HCV infected persons initiated on a DAA regimen between October 2014 and March 2017 at two c
17 n (hazard ratio 0.78; 95% CI 0.71-0.85) or a DAA regimen (hazard ratio 0.57; 95% CI 0.51-0.65) was as
18 rferon and ribavirin regimen (n = 4436) or a DAA-containing regimen (n = 12,667).
19 d ribavirin regimen (PEG/RBV, n = 4764) or a DAA-containing regimen (n = 21 279), after excluding tho
20 5% CI 14.7-18.0) in the group treated with a DAA regimen, and 30.4 (95% CI 29.2-31.7) in the control
21                   We developed a long-acting DAA system (LA-DAAS) capable of prolonged dosing and exp
22 unctions termed decay-accelerating activity (DAA) and cofactor activity (CFA).
23      Whether VD replacement during and after DAA therapy can improve hepatic fibrosis remains unclear
24 cell phenotype and function before and after DAA treatment in 59 patients chronically infected with H
25 TT, genotype did not change during and after DAA treatment.
26 present the highest-risk group for HCC after DAA-induced sustained virologic response.
27 a median follow-up of 43 (3-57) months after DAA start, 36 of 452 (8%) patients developed de novo HCC
28 HCC in HCV genotype-3 infected persons after DAA therapy is not well known.
29 l and mental component summary scales) after DAA treatment compared with before treatment.
30                  LS at the time of SVR after DAA therapy predicts the clinical outcome of HIV/HCV-coi
31                  LS at the time of SVR after DAA therapy predicts the clinical outcome of people livi
32 tension (CSPH; HVPG >=10 mmHg) and SVR after DAA therapy showed that disappearance of CSPH (primary e
33 show a reduction in HCC risk over time after DAA-induced sustained virologic response.
34 laprevir is a direct-acting antiviral agent (DAA) that targets the NS3/4A protease of hepatitis C vir
35 a (HCC) after direct-acting antiviral agent (DAA) treatment.
36  between HCV direct-acting antiviral agents (DAA) and HIV antiretrovirals.
37 (PWID), focusing on direct antiviral agents (DAA) and medication-assisted treatment combined with syr
38          New direct-acting antiviral agents (DAA) offer an unprecedented opportunity to cure HCV.
39  of newer, directly acting antiviral agents (DAA) upon this risk are unknown.
40 PWID), focusing on direct anti-viral agents (DAA) and medication-assisted treatment combined with syr
41 w regarding the use of direct-acting agents (DAAs) in chronic hepatitis C [2].
42 red treatment with HCV direct-acting agents (DAAs) to MSM identified with a replicating HCV infection
43 ome and that direct-acting antiviral agents (DAAs) have been demonstrated to improve clinical as well
44  (SVR) after direct acting antiviral agents (DAAs) holds promise for reducing hepatocellular cancer (
45  When considering health-sector costs alone, DAA alone was the most cost-effective intervention.
46                                        Among DAA-treated patients, 43 deaths occurred during 941 pers
47 th PEG/RBV, and 9.89 (95% CI 8.7-11.1) among DAA-treated persons (P < .001).
48 himera with robust CFA (for C3b and C4b) and DAA (for classical and alternative pathway C3 convertase
49 d AST normalized rapidly between pre-DAA and DAA, whereas only mean ALT continued to decrease until p
50  However, the effect of HCV co-infection and DAA treatment on mortality after initiating antiretrovir
51 to estimate the effects of HCV infection and DAA treatment on mortality had participants initiated AR
52 combination with other DAAs in DAA-naive and DAA-experienced patients infected with any subtype of HC
53 ion, and those treated with both PEG/RBV and DAA regimens.
54 regard to HCC incidence, HCC recurrence, and DAA efficacy, and to summarize best practice advice rega
55  achieved a sustained virologic response and DAA therapy was well tolerated.
56 e studies supporting the benefits of SVR and DAA therapies, including a decline in patients added to
57  Pharmacokinetics of the antiretrovirals and DAAs were characterized when administered alone and in c
58 95% CI, 0.2%-1.7%) (P < .05 for change), and DAAs were detectable in liver.
59 ting ART according to modern guidelines, and DAAs are effective at reducing mortality in this populat
60 ther treatment with direct-acting antiviral (DAA) agents affects risk of CVD.
61 ving treatment with direct-acting antiviral (DAA) agents, from 2014 through 2017.
62  less responsive to direct-acting antiviral (DAA) drug treatment than other genotype 4 subtypes.
63 en evaluated in the direct-acting antiviral (DAA) era.
64                 New direct-acting antiviral (DAA) regimens are available.
65                     Direct-acting antiviral (DAA) regimens are safe and effective at eradicating hepa
66                     Direct-acting antiviral (DAA) therapies are effective in achieving sustained viro
67 after completion of direct-acting antiviral (DAA) therapy (SVR(12) ).
68 interaction between direct-acting antiviral (DAA) therapy for hepatitis and hepatocellular carcinoma
69 ing the benefits of direct-acting antiviral (DAA) therapy for hepatitis C virus (HCV) infection for p
70                     Direct-acting antiviral (DAA) therapy for hepatitis C virus (HCV) is highly effec
71 estricted access to direct-acting antiviral (DAA) therapy from 2016.
72 estricted access to direct-acting antiviral (DAA) therapy from 2016.
73                     Direct-acting antiviral (DAA) therapy has altered the frequency and outcome of li
74      The success of direct-acting antiviral (DAA) therapy has led to near-universal cure for patients
75                     Direct-acting antiviral (DAA) therapy has transformed the management of human imm
76                     Direct-acting antiviral (DAA) therapy is highly effective in people who inject dr
77                     Direct acting antiviral (DAA) therapy is highly effective in PWID; however, rates
78 titis C virus (HCV) direct-acting antiviral (DAA) therapy.
79 parameters early in direct-acting antiviral (DAA) therapy.
80 ents treated with directly acting antiviral (DAA) therapy.
81 s for initiation of direct-acting antiviral (DAA) treatment and sustained virological response (SVR).
82 t teleconsultation, direct-acting antiviral (DAA) treatment, and sustained virologic response (SVR).
83               While direct-acting antiviral (DAA) treatments are effective, limited uptake of therapy
84  different rates of direct-acting antiviral (DAA) use.
85 response (SVR) with direct-acting antiviral (DAA).
86 29,033 treated with direct-acting antiviral [DAA] agents and 19,102 treated with interferon-based reg
87 data on the use of direct-acting antivirals (DAA) on the risk of death and tumoral recurrence in pati
88 HCV) with all-oral direct-acting antivirals (DAA) therapy is now entering into its fourth year; howev
89 r eradication with direct-acting antivirals (DAA) would increase 25-hydroxyVD [25(OH)VD] levels.
90 ter treatment with direct-acting antivirals (DAA).
91 rosis treated with direct-acting antivirals (DAA).
92 y sofosbuvir-based direct-acting antivirals (DAAs) and addition of RBV improves NK cell function in l
93                    Direct-acting antivirals (DAAs) are becoming accessible in sub-Saharan Africa.
94        The cost of direct-acting antivirals (DAAs) for hepatitis C virus (HCV) prompted many payers t
95 the development of direct-acting antivirals (DAAs) has generated international interest in the global
96      The advent of direct-acting antivirals (DAAs) has transformed the landscape of hepatitis C virus
97      High costs of direct-acting antivirals (DAAs) have led health-care insurers to limit access worl
98  efficacious, oral direct-acting antivirals (DAAs) have ushered in a new era of hepatitis C treatment
99 dvocate the use of direct-acting antivirals (DAAs) in all patients.
100 C virus (HCV) with direct-acting antivirals (DAAs) in hepatitis B virus (HBV) coinfection can result
101 he introduction of direct-acting antivirals (DAAs) in the management of HCV infection in the CKD popu
102 cirrhosis cured by direct-acting antivirals (DAAs) is still undefined.
103      High costs of direct acting antivirals (DAAs) led healthcare insurers to limit access worldwide.
104                    Direct-acting antivirals (DAAs) show excellent results in controlling viremia, alt
105                    Direct-acting antivirals (DAAs) targeting hepatitis C virus (HCV) have revolutioni
106 increase access to direct-acting antivirals (DAAs), especially among people who inject drugs (PWID).
107 l eradication with direct acting antivirals (DAAs).
108 V in prisons using direct-acting antivirals (DAAs).
109            We conclude that sofosbuvir-based DAA therapy is safe and highly effective in HCV-HIV pati
110 ive, open-label study using sofosbuvir-based DAA therapy to treat HIV/HCV-coinfected participants pre
111    We also estimated the association between DAA therapy and risk of early HCC recurrence (defined as
112  was used to examine the association between DAA therapy and time to recurrence after a complete resp
113  We compared HCC recurrence patterns between DAA-treated and untreated HCV-infected patients who had
114 n clinical outcomes remains unavailable, but DAA regimens were associated with SVR rates greater than
115 eatment baseline and subsequent selection by DAA treatment of both NS5A and NS5B S282 RASs.
116 target would likely be achieved by combining DAA scale-up with a 40% reduction in HCV transmission am
117 cted MSM in Berlin likely requires combining DAA scale-up with moderately effective behavioral interv
118  patients achieved SVR(12) , 1 has completed DAA therapy, and 2 remain on treatment.
119 T recipients had either started or completed DAA therapy.
120                    Of 30 patients completing DAA therapy with active illicit opioid use at intake, 14
121 follow-up before completion; 1 is continuing DAA treatment.
122 ding criminal justice system-related costs), DAA 20% with MAT+ 80% was most effective and was cost sa
123 ding criminal justice system-related costs), DAA at 20% with MAT+ at 80% was the most effective inter
124  with criminal justice system-related costs, DAA and MAT+ implemented together became the most cost-e
125  with criminal justice system-related costs, DAA and MAT+ implemented together become the most cost-e
126                             At 20% coverage, DAAs had an incremental cost-effectiveness ratio (ICER)
127 ated high adherence to once- and twice-daily DAA therapy among people with recent IDU or currently re
128 (OAT) and compared once-daily to twice-daily DAA therapy.
129 ith liver resection or ablation should defer DAA therapy until after HCC treatment is completed.
130 iral treatment received after HCC diagnosis: DAA, interferon (IFN), or no antiviral.
131       The mean LDL increased markedly during DAA therapy (pre-DAA, 86.6 to DAA, 107.4 mg/dL; P < .000
132 cipients and 17 HCV-infected patients during DAA-treatment.
133 ecay-accelerating factor (DAF) that exhibits DAA and membrane cofactor protein (MCP) that exhibits CF
134 agonist treatment (OAT) during and following DAA-based treatment.
135 viors remained stable or decreased following DAA-based HCV treatment.
136 mmon among people with ongoing IDU following DAA therapy on OAT, as well as those who were not confid
137 mmon among people with ongoing IDU following DAA therapy on OAT, as well as those who were not confid
138 se associated with HCV reinfection following DAA therapy among PWID on opioid agonist therapy (OAT) a
139 epatitis C virus (HCV) reinfection following DAA therapy among PWID on opioid agonist therapy (OAT) a
140                      The risk difference for DAA treatment was -3.8% (95% CI -9.2-0.9%) and the risk
141 ein, we have parsed the functional units for DAA and CFA by constructing chimeras of the decay-accele
142                                We formulated DAAs in drug-polymer pills and studied the release kinet
143 ty-nine treatment studies (n = 10 181) found DAA regimens associated with pooled SVR rates greater th
144 start DAA therapy, 82 (40.0%) initiated free DAA therapy, 74 (36.1%) completed therapy (27.8% to 60.0
145 h complete response to HCC therapy; however, DAA therapy can be deferred 4-6 months to confirm respon
146                                           In DAA-treated and untreated patients, most recurrences wer
147                                           In DAA-treated patients with cirrhosis and FIB-4 scores >=3
148 xilaprevir in combination with other DAAs in DAA-naive and DAA-experienced patients infected with any
149 ncluding treatment response, were similar in DAA-treated and untreated patients.
150                      Of those, 698 initiated DAA treatment on the basis of medical record abstraction
151 ional HCV program for patients who initiated DAAs between November 2015 and March 2017.
152 ceive surveillance imaging before initiating DAA treatment.
153                       We believe that the LA-DAA system can provide a cost-effective and patient-cent
154 oxy measures for evaluating population-level DAA treatment and SVR outcomes.
155                                      Post-LT DAA was not related to increased risk of recurrence (haz
156  multivariable regression, the use of pre-LT DAA was not associated to risk of recurrence (hazard rat
157 vival was 93.4%, 84.8%, 73.9% for the pre-LT DAA, pre-LT IFN, and antiviral naive groups, respectivel
158 7.8% to 60.0% by practice), and 70 (94.6% of DAA completers) achieved SVR.
159                         In a large cohort of DAA-treated patients with cirrhotic HCV, GRS was associa
160                              Combinations of DAA 20% with MAT+ at 20%, 40%, and 80% coverage had ICER
161                              Combinations of DAA at 20% with MAT+ at 20%, 40%, and 80% coverage had I
162 emained in OUD treatment after completion of DAA treatment.
163 oral ribavirin) to investigate the effect of DAA use.
164 valuating benefits and cost-effectiveness of DAA therapy in patients with active intermediate or adva
165  of this work was to estimate the effects of DAA access policies on 10-year all-cause mortality among
166 witch PhENAQ, we investigated the effects of DAA and DAQ on rhythmic local field potentials (LFPs) oc
167 re phase 4 trials evaluating the efficacy of DAA among people with past 6-month injecting drug use or
168 atients before and after the introduction of DAA.
169                       A larger proportion of DAA-treated than untreated patients received potentially
170                                Eight RCTs of DAA therapy vs placebo or an outdated antiviral regimen,
171 mented with targeted searches for studies of DAA treatment and with abstracts from nephrology, hepato
172 er fibrosis (F3) or cirrhosis at the time of DAA treatment represent the highest-risk group for HCC a
173            BEST PRACTICE ADVICE 8: Timing of DAA therapy for patients with HCC who are listed for liv
174 ice regarding HCC surveillance and timing of DAA therapy.
175        The high efficacy and tolerability of DAA therapy has also created a rationale for utilizing H
176 which should serve to increase the uptake of DAA-based HCV treatment.
177 ly viral kinetics, to reduce the duration of DAAs therapy.
178     This study examined the effectiveness of DAAs in patients treated through the Rwandan national he
179 , while no study has explored the effects of DAAs on this NK subset.
180 cremental cost-effectiveness ratio (ICER) of DAAs at a price USD 41,046 per treatment was USD 9,080 p
181                  Tunable release kinetics of DAAs was enabled for 1 mo with drug-polymer pills in vit
182 on control, PWID harm reduction, offering of DAAs at diagnosis, and outreach screening to increase th
183                     However, if the price of DAAs is reduced by 55-85% (USD 6,730 to 17,720), HCV tre
184 h newly diagnosed HCV, 30% received all-oral DAA therapy (DAA group) and 70% were not treated (untrea
185      Conclusion: In the short term, all-oral DAA treatment for HCV infection was associated with a de
186 population-level effectiveness of these oral DAAs, hepatitis C treatment by a wide range of providers
187 se of voxilaprevir in combination with other DAAs in DAA-naive and DAA-experienced patients infected
188 ed whereas memory B cells were expanded post DAA therapy.
189 V-specific cytokines were also improved post DAA.
190 henotypic and functional reconstitution post DAA therapy.
191 nt survival was 73.1% pre-DAA and 86.2% post-DAA (P < .001).
192 gible (HCV: n = 499 pre-DAA and n = 322 post-DAA; non-HCV: n = 547 pre-DAA and n = 744 post-DAA).
193 A; non-HCV: n = 547 pre-DAA and n = 744 post-DAA).
194 ft survival was 69.8% pre-DAA and 83.8% post-DAA (P < .001).
195 s were defined: pre-DAA (2009-2012) and post-DAA (2014-2017).
196 uary 1, 2011, to December 31, 2013) and post-DAA (January 1, 2014, to February 28, 2017) cohorts were
197 ors of HCV treatment in the pre-DAA and post-DAA periods in four large, diverse health care settings
198 2,879/13,240) of those with chronic HCV post-DAA were treated compared with 3.5% (574/16,304) in the
199                            The positive post-DAA era effect was observed only in HCV patients with fi
200                         Conclusion: The post-DAA era has seen increased utilization of HCV-viremic do
201                      When adjusted, the post-DAA era represented an independent positive predictive f
202  HCV patients, receiving a re-LT in the post-DAA era was associated with improved patient and graft s
203 and patient survival after re-LT in the post-DAA era.
204 ts treated for HCV has increased in the post-DAA period, especially among those with liver-related co
205 7, 3.94) were more likely to be treated post-DAA.
206      One-year patient survival was 73.1% pre-DAA and 86.2% post-DAA (P < .001).
207 -LT patients were eligible (HCV: n = 499 pre-DAA and n = 322 post-DAA; non-HCV: n = 547 pre-DAA and n
208 A and n = 322 post-DAA; non-HCV: n = 547 pre-DAA and n = 744 post-DAA).
209        One-year graft survival was 69.8% pre-DAA and 83.8% post-DAA (P < .001).
210 n ALT and AST normalized rapidly between pre-DAA and DAA, whereas only mean ALT continued to decrease
211                   Two eras were defined: pre-DAA (2009-2012) and post-DAA (2014-2017).
212       Predictors of HCV treatment in the pre-DAA (January 1, 2011, to December 31, 2013) and post-DAA
213 t and predictors of HCV treatment in the pre-DAA and post-DAA periods in four large, diverse health c
214 d compared with 3.5% (574/16,304) in the pre-DAA period.
215 L increased markedly during DAA therapy (pre-DAA, 86.6 to DAA, 107.4 mg/dL; P < .0001), but then it d
216  care in Japan could examine ways to procure DAAs at a price where they would be cost-saving.
217  to determine the effectiveness of providing DAAs in primary care, compared with hospital-based speci
218 follow-up among patients who did not receive DAA therapy (crude rate ratio, 0.23; 95% confidence inte
219 d with DAAs and patients who did not receive DAA treatment for their HCV infection after complete res
220 sites in Australia or New Zealand to receive DAAs at their primary care site or local hospital (stand
221 s with HCV-related HCC, 383 (48.1%) received DAA therapy and 414 (51.9%) did not receive treatment fo
222 ith HCV-associated HCC, 304 (38.3%) received DAA therapy and 489 (61.7%) were untreated.
223                           Patients receiving DAA therapy had an overall survival of 71.8 months vs 11
224 r location, cancer treatment type, receiving DAA treatment and achieving SVR12 had independent influe
225 CI, 38%-59%) of coinfected persons receiving DAAs.
226                          Decisions regarding DAA treatment in these patients should be considered in
227  After removing fibrosis stage restrictions, DAA initiations increased by 1.8-fold (95% CI 1.3, 2.4)
228  After removing fibrosis stage restrictions, DAA initiations increased by 1.8-fold (95% confidence in
229                                  Restrictive DAA access policies may decrease survival compared to tr
230                                   Similarly, DAA therapy was associated with a 57% and a 58% lower in
231 eview, 119 (58.0%) were recommended to start DAA therapy, 82 (40.0%) initiated free DAA therapy, 74 (
232 nfections (4.8%); 150 (85%) of which started DAA treatment and 149 (99.3%) were cured.
233                 Fifty-eight patients started DAAs.
234   In this multicenter intent-to-treat study, DAA therapy was not found to be a risk factor for mortal
235                                   Successful DAA-therapy did not affect CD107a-degranulation, but dec
236  response (SVR), however, whether successful DAA treatment reconstitute T follicular helper (T(FH))-B
237                                This suggests DAA therapy and achieving SVR12 is associated with incre
238 tion in a cohort of coinfected people taking DAAs.
239 ADVICE 10: There are no conclusive data that DAA therapy is associated with increased or decreased ri
240 that a quantitative mechanism built from the DAA hypothesis is able to maintain polymorphism in the M
241 tients, the use of HCV-viremic grafts in the DAA era appears to be efficacious and well tolerated.
242 st HCV reinfection in MSM was similar in the DAA era compared to the interferon era with a hazard rat
243           For patients with cirrhosis in the DAA group, the mean adjusted liver-related costs ($1749
244  (PPVs) by comparing the algorithms with the DAA initiation and SVR results from the registry.
245 osed HCV, 30% received all-oral DAA therapy (DAA group) and 70% were not treated (untreated group).
246 lirubinemia during direct antiviral therapy (DAAs) therapy for HCV despite achieving sustained virolo
247 arkedly during DAA therapy (pre-DAA, 86.6 to DAA, 107.4 mg/dL; P < .0001), but then it decreased to 9
248 ho inject drugs face significant barriers to DAA access.
249   The LA-DAAS was cost-effective compared to DAA therapy alone in all groups considered (base case in
250 -effectiveness analysis comparing LA-DAAS to DAA alone in various patient groups, including people wh
251 atients with sustained virologic response to DAA therapy (hazard ratio, 0.29; 95% CI, 0.18-0.47), but
252  differed by sustained virologic response to DAA therapy; risk of death was reduced in patients with
253                    A number of approaches to DAAs have produced landmark clinical studies over the pa
254  polymorphisms associated with resistance to DAAs in other genotypes.
255 n of variants with reduced susceptibility to DAAs, including NS3/4A protease inhibitors such as voxil
256 accessing direct-acting antiviral treatment (DAA) for hepatitis C virus (HCV) infection.
257 nts with complete response to HCC treatment, DAA therapy was not associated with increased overall or
258 ts should be identified and receive a triple DAA combination regimen as first-line treatment.
259 o estimate 10-year all-cause mortality under DAA access policies that included treating (i) all peopl
260                               Unfortunately, DAAs remain expensive, so treatment of all HCV-infected
261                          Following universal DAA access, annual HCV treatment uptake in those eligibl
262 cted adults in Australia following universal DAA access.
263 cted adults in Australia following universal DAA access.
264 igh uptake and effectiveness of unrestricted DAA therapy in Australia have permitted rapid treatment
265                                   Scaling up DAA treatment rates, beginning in 2018, to 100% of newly
266 If the proportion of eligible patients using DAAs dropped from 65% per year in 2016 to 20% per year i
267 f eligible (HCV RNA positive) patients using DAAs stays at 65% per year between 2016 and 2025, with h
268 exerts its effect primarily on RGCs, whereas DAA induces light-dependent spiking primarily through am
269 ge groups and to estimate the price at which DAAs become cost-saving in Japan.
270 he number diagnosed; and a scenario in which DAAs are not introduced (ie, treatment is only with pegy
271                                        While DAA 20% with MAT+ 80% was more expensive (e.g., less cos
272                                        While DAA at 20% with MAT+ at 80% was more expensive (eg, less
273                      Factors associated with DAA uptake were analysed.
274                      Factors associated with DAA uptake were analyzed.
275 L by post-SVR year 1 (P < .001 compared with DAA; P = .0013 compared with SVR).
276 ared to historical controls (consistent with DAA trials at the time of the study design); secondary o
277                         RBV cotreatment with DAA-therapy for HCV increased CD56Bright NK cell IFNgamm
278  successfully treated for HCV infection with DAA agents.
279 infection is rapidly cleared from liver with DAA leaving <2% HCV-infected hepatocytes at Day 7.
280 ecrease in sustained virologic response with DAA therapy.
281 o recurrence after a complete response, with DAA therapy analyzed as a time-varying exposure.
282        Our results demonstrate that SVR with DAA therapy is effective in the reconstitution of phenot
283 with advanced fibrosis, who achieve SVR with DAA, HIV-coinfection seems to be associated with a lower
284 duals were included if they met: 1) SVR with DAA-based combination; 2) Liver stiffness (LS) >=9.5 kPa
285 riteria were included: (i) Achieved SVR with DAA-including regimen; (ii) LS >= 9.5 kPa before therapy
286 criteria were included: i) Achieved SVR with DAA-including regimen; ii) LS >=9.5 kPa before therapy a
287  100 person-year among patients treated with DAA, IFN, and antiviral naive, respectively (P < 0.001).
288                      Curative treatment with DAA attenuated the liver stiffness and inflammation but
289 ions of people with HIV/HCV coinfection with DAAs at random.
290 ence of treating all coinfected persons with DAAs compared with no treatment was -3.7% (95% confidenc
291 C virus (HCV) patients who achieved SVR with DAAs from 129 Veterans Health Administration hospitals b
292                   Patients were treated with DAAs according to the physicians' preference.
293 nclusion: Patients successfully treated with DAAs and at risk of HCC did not regress after 3.6 years
294 een patients with HCV infection treated with DAAs and patients who did not receive DAA treatment for
295  when liver stiffness >=12 kPa) treated with DAAs.
296 regulator), and HCC in patients treated with DAAs.
297 atients with cirrhosis before treatment with DAAs (n = 9784), those with pre-SVR fibrosis-4 (FIB-4) s
298                Scaling-up HCV treatment with DAAs for the entire Spanish prison population, irrespect
299  cost saving) than MAT+ at 80% alone without DAA, it offered a favorable value compared to MAT+ at 80
300 ess cost-saving) than MAT+ 80% alone without DAA, it offered favorable value compared to MAT+ 80% alo

 
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