ライフサイエンスコーパス: antiviral therapy

1 able serum HCV RNA 12 weeks after the end of antiviral therapy).

2 and chronic HBV infections and responses to antiviral therapy.

3 T interactions may be a promising avenue for antiviral therapy.

4 ion, with or without a sustained response to antiviral therapy.

5 tic replication, which could be targeted for antiviral therapy.

6 at the SLII domain is a potential target for antiviral therapy.

7 ovides a novel target for the development of antiviral therapy.

8 e pathway can provide a potential target for antiviral therapy.

9 istant viruses during core protein-targeting antiviral therapy.

10 42% had cirrhosis, and 54% had failed prior antiviral therapy.

11 d nuclear HBV DNA under conditions mimicking antiviral therapy.

12 fore, we propose it to be a novel target for antiviral therapy.

13 C virus (HCV) infection and their fate after antiviral therapy.

14 h reactivation can occur despite suppressive antiviral therapy.

15 lation did not change during the 12 weeks of antiviral therapy.

16 sessed and followed up through the course of antiviral therapy.

17 dividuals, and to enable linkage to care and antiviral therapy.

18 e been sought as novel molecular targets for antiviral therapy.

19 supports improved intermediate outcomes with antiviral therapy.

20 rvoir in infected individuals on suppressive antiviral therapy.

21 oncomitantly received nucleos(t)ide analogue antiviral therapy.

22 ubjects developed HBeAg seroconversion after antiviral therapy.

23 re longitudinally monitored before and after antiviral therapy.

24 ars) with chronic HBV infection treated with antiviral therapy.

25 ns is paramount in optimizing the success of antiviral therapy.

26 on, suggesting it may be a future target for antiviral therapy.

27 G should again only be used with concomitant antiviral therapy.

28 ppress viral replication and a potential pan-antiviral therapy.

29 ial during pregnancy for the sole purpose of antiviral therapy.

30 mplications and could benefit from immediate antiviral therapy.

31 2 weeks of appropriately dosed and delivered antiviral therapy.

32 omen with chronic HBV infection treated with antiviral therapy.

33 f ZIKV and implicate AXL as a new target for antiviral therapy.

34 osed with chronic HBV infection who received antiviral therapy.

35 ore neurologic sequelae and may benefit from antiviral therapy.

36 G opsonizing activity and can be reversed by antiviral therapy.

37 s infection and may be effective targets for antiviral therapy.

38 nce, and those at risk of noncompliance with antiviral therapy.

39 r, there is currently no approved vaccine or antiviral therapy.

40 liver fibrosis as well as responsiveness to antiviral therapy.

41 se functionalities, represent a milestone in antiviral therapy.

42 s) causes mortality rates of 10%-20% despite antiviral therapy.

43 rawal due to adverse events vs placebo or no antiviral therapy.

44 as CMV viremia and/or disease necessitating antiviral therapy.

45 ture clinical indications for this potential antiviral therapy.

46 stance detected at the time of initiation of antiviral therapy.

47 ithin 2 weeks after initiating direct-acting antiviral therapy.

48 piratory syndrome coronavirus 2 (SARS-CoV-2) antiviral therapy.

49 and examined the population-level impact of antiviral therapy.

50 ably the strongest potential as a target for antiviral therapy.

51 voirs respond poorly to current vaccines and antiviral therapy.

52 atients who achieved a sustained response to antiviral therapy.

53 risk of progression to CS-CMVi that require antiviral therapy.

54 assess the prospects of using decoy RNAs in antiviral therapy.

55 KO hamster model for evaluation of promising antiviral therapies.

56 ding survival, and reduce the need for toxic antiviral therapies.

57 ging field that is destined to suggest novel antiviral therapies.

58 ng drug-resistant variants emerging with new antiviral therapies.

59 that may ultimately enable escape-resistant antiviral therapies.

60 the chronopharmacology of antibacterial and antiviral therapies.

61 has hampered the development of appropriate antiviral therapies.

62 lication will guide the development of novel antiviral therapies.

63 d the effective monitoring of the associated antiviral therapies.

64 currently no licensed filovirus vaccines or antiviral therapies.

65 ion reveals potential avenues for developing antiviral therapies.

66 os(t)ide analogues are 2 classes of approved antiviral therapies.

67 % and few short-term harms relative to older antiviral therapies.

68 inically validated targets for direct-acting antiviral therapies.

69 wide, highlighting an urgent need to develop antiviral therapies.

70 n, and their ability to evolve resistance to antiviral therapies.

71 d targetable host factors for broad-spectrum antiviral therapies.

72 ng of the viral life cycle to develop better antiviral therapies.

73 ications for the development of vaccines and antiviral therapies.

74 ent varied but included immunomodulating and antiviral therapies.

75 not attain the new, expensive, direct-acting antiviral therapies.

76 efenses is important for developing improved antiviral therapies.

77 w avenues that can be explored for potential antiviral therapies.

78 an adapt to changing environments and thwart antiviral therapies.

79 at promise for the development of bunyavirus antiviral therapies.

80 fusion, revealing a potential new target for antiviral therapies.

81 interventions in the absence of a vaccine or antiviral therapies.

82 edge that may guide development of effective antiviral therapies.

83 targets for the development of vaccines and antiviral therapies.

84 frequently, highlighting the need for novel antiviral therapies.

85 Cohort A: After 3 years of antiviral therapy, 33% and 30% had detectable HBcrAg and

86 Cohort A: After 3 years of antiviral therapy, 33% and 30% had detectable HBcrAg and

87 n specialty care were more likely to receive antiviral therapy (50% versus 24% for specialty care ver

88 ough it was lower than those recommended for antiviral therapy (78.2%).

89 Even after years of fully effective antiviral therapy, a persistent reservoir of virus-infec

90 BV to determine HBV monitoring and long-term antiviral therapy after completion of anticancer therapy

91 e critical for the future design of curative antiviral therapies against chronic hepatitis B.

92 There are no vaccines or antiviral therapies against HAstV disease.

93 IE could facilitate the development of novel antiviral therapies against viral diseases.

94 basal QTc values, basal heart rate and dual antiviral therapy, age(OR 1.06, 95% C.I. 1.00-1.13, p<0.

95 Oral antiviral therapy alone without hepatitis B immune globu

96 ently limited data regarding the use of oral antiviral therapy alone without hepatitis B immune globu

97 that can be reduced, but not solved, through antiviral therapy alone.

98 orovirus protease represents a key target in antiviral therapies, an improved understanding of its fu

99 ons for the combined use of CoRAs and FIs in antiviral therapies and point to a multifaceted role for

100 In the absence of effective antiviral therapies and vaccines, these viruses pose ser

101 ical responses, animal models, and potential antiviral therapies and vaccines.

102 We measured hsa-miRNAs before and after antiviral therapy and correlated hsa-miRNA expression le

103 improved virological response (VR) rates to antiviral therapy and decreased progression of liver fib

104 e stability of HBV cccDNA in the presence of antiviral therapy and during cell division induced by im

105 ge, baseline viral load, vaccination status, antiviral therapy and emergence of drug resistance on vi

106 iral biology and offers new targets both for antiviral therapy and for oncolytic vector design.IMPORT

107 rpose PS function in assembly for both novel antiviral therapy and gene/drug/vaccine applications.

108 achieving an intermediate outcome following antiviral therapy and improved clinical outcomes but wer

109 hort of veterans with hepatitis B infection; antiviral therapy and liver imaging were independently a

110 in the clinic ranging from antibacterial and antiviral therapy and prophylaxis to anticancer therapeu

111 detected at early stages, can be cured with antiviral therapy and reduced administration of immunosu

112 se findings emphasize the need for effective antiviral therapy and/or preventive measures such as vac

113 e the improved design of RV vaccines, better antiviral therapies, and expression vectors.

114 ensive supportive treatment and experimental antiviral therapies, and had been discharged with undete

115 no licensed alphavirus vaccines or effective antiviral therapies, and more molecular information on v

116 ge, baseline viral load, vaccination status, antiviral therapy, and emergence of drug resistance on v

117 in infected hepatocytes even after long-term antiviral therapy, and its integration, though no longer

118 , it should be administered with concomitant antiviral therapy, and that evidence concerning preempti

119 ously resolved low-grade CMV DNAemia without antiviral therapy; and (3) Noncontrollers (NC; n = 21):

120 t prophylaxis with CMVIG in combination with antiviral therapy appears effective in D+/R- heart trans

121 Since there is currently no vaccine or antiviral therapy approved for humans, there is an urgen

122 etting of impaired cellular immunity, and no antiviral therapies are available, so survival depends o

123 n in affected areas, no licensed vaccines or antiviral therapies are available.

124 for enterovirus EV71 infection for which no antiviral therapies are available.

125 Though highly effective direct-acting antiviral therapies are costly, the price of a cure is a

126 Since specific antiviral therapies are not available for the treatment

127 Studies on antiviral therapy are undergoing to elucidate the optima

128 the absence of licensed vaccines or specific antiviral therapies, are recognized to pose significant

129 to persist in individuals during combination antiviral therapy (ART).

130 As such, these enzymes are prime targets for antiviral therapy, as has recently been demonstrated for

131 cial for maximizing the benefit of available antiviral therapy, as treatment efficacy rapidly decreas

132 virus (HCV) screening found interferon-based antiviral therapy associated with increased likelihood o

133 eduction in immunosuppression and preemptive antiviral therapy, at the discretion of the attending te

134 manized mice and patients, and direct-acting antiviral therapy attenuated M2 macrophage activation an

135 remains a serious concern even with approved antiviral therapies available.

136 a highly infectious virus with no vaccine or antiviral therapy available to control the pandemic; the

137 ter informed consent, all patients underwent antiviral therapy (AVT) with sofosbuvir/ledipasvir and c

138 , such that we could not model the impact of antiviral therapy based on stratification by specific cl

139 Interferon-alpha therapy may be an effective antiviral therapy beneficial in chronic HBV-infected chi

140 such patients might not require pre-emptive antiviral therapy, but should be followed up on a monthl

141 Antibodies have a long history in antiviral therapy, but until recently, they have not bee

142 Current antiviral therapies can prevent mortality if infection i

143 administration of pangenotypic direct-acting antiviral therapy can safely prevent the development of

144 spective cohort, we report on the success of antiviral therapy combined with a short course (in hospi

145 CTs with posttreatment follow-up <12 months, antiviral therapy compared to placebo improved alanine a

146 Based on 18 trials (n = 2972), antiviral therapy compared with placebo or no treatment

147 ence of early CMV reactivation (and BM-toxic antiviral therapy), cotransplantation of host Treg cell

148 In advance of effective antiviral therapies, countries have applied different pu

149 No vaccine or effective antiviral therapy currently exists to control RSV or HMP

150 ant unconjugated bilirubinemia during direct antiviral therapy (DAAs) therapy for HCV despite achievi

151 ove that provided by current ART or proposed antiviral therapies directed at limiting Nef, Vpr, or Vp

152 get for immunomodulation in conjunction with antiviral therapy during chronic viral infection.

153 he efficacy and maternal and fetal safety of antiviral therapy during pregnancy.

154 nfection and for assessment of the effect of antiviral therapy, especially when fecal samples are not

155 reduces the risk of HCC development, even if antiviral therapy fails to completely eliminate HCC risk

156 Thus, BocaSR may be a target for antiviral therapies for HBoV and may also have utility i

157 With newer, direct-acting antiviral therapies for HCV, our objective was to determ

158 With the advent of highly efficient antiviral therapies for hepatitis C virus (HCV) infectio

159 We review the status of direct-acting antiviral therapies for hepatitis C virus infection and

160 re are currently no FDA-licensed vaccines or antiviral therapies for VEEV.

161 Administration of antiviral therapy for 48 weeks reversed aberrant IgG-Fc

162 of cCMV screening were assumed to come from antiviral therapy for affected newborns to reduce hearin

163 Combination intravitreal and systemic antiviral therapy for ARN can be effective in improving

164 Antiviral therapy for chronic hepatitis B (CHB) is effec

165 approach, preemptive therapy (initiation of antiviral therapy for early asymptomatic CMV viremia det

166 systematically assessed before starting the antiviral therapy for early detection and the improvemen

167 Clinicians should start antiviral therapy for HBsAg-positive/anti-HBc-positive p

168 ity-based screening and early treatment with antiviral therapy for HBV in The Gambia.

169 Antiviral therapy for HBV infection was associated with

170 gic response at 12 weeks after completion of antiviral therapy for HCV infection and graft survival a

171 Sofosbuvir-based antiviral therapy for HCV recurrence after liver transpl

172 also been included in interferon-free direct antiviral therapy for HCV, modulate host immune response

173 reventive Services Task Force (USPSTF) found antiviral therapy for hepatitis B virus (HBV) infection

174 nce is a critical problem limiting effective antiviral therapy for HIV/AIDS.

175 In recent years, short-term antiviral therapy for pregnant women in the third trimes

176 acy of combination intravitreal and systemic antiviral therapy for the treatment of acute retinal nec

177 e supporting the use of intravenous and oral antiviral therapy for the treatment of ARN.

178 pathology records of patients dispensed CHB antiviral therapy from 4 major hospitals in Melbourne be

179 The remarkable effectivity of current antiviral therapies has led to consider the elimination

180 3, 4, or 6 infections whose prior course of antiviral therapy has failed, and the feasibility of sho

181 , higher whole blood VL before initiation of antiviral therapy has no clinically meaningful predictiv

182 highly effective and tolerable direct-acting antiviral therapy has paved the way for HCV elimination,

183 Although antiviral therapies have improved the long-term outcomes

184 Currently available direct-acting antiviral therapies have reduced efficacy in patients wi

185 emia to below the limit of detection without antiviral therapy have been termed elite controllers (EC

186 Antiviral therapy (hazard ratio = 0.85, 95% confidence i

187 espite combination systemic and intravitreal antiviral therapy; however, none of the 19 patients demo

188 e been suggested to be potential targets for antiviral therapies, identification of these molecules i

189 Ongoing trials are testing antiviral therapies, immune modulators, and anticoagulan

190 maceuticals, with implications for potential antiviral therapies.IMPORTANCE Enteroviruses are signifi

191 r of HBV production and could be a target of antiviral therapy.IMPORTANCE HBV infection is a worldwid

192 rn sericulture but also shed light on future antiviral therapy.IMPORTANCE Pathogen genome targeting h

193 es and may provide an alternative target for antiviral therapy.IMPORTANCE Varicella-zoster virus (VZV

194 nic HBV infection, antivirals compared to no antiviral therapy improve HBV DNA suppression and freque

195 s with posttreatment follow-up >/=12 months, antiviral therapy improved cumulative HBeAg clearance/lo

196 Antiviral therapy improves HBV suppression and reduces M

197 itis B immune globulin and vaccination, oral antiviral therapies in highly viremic mothers can furthe

198 tudies of shortened courses of direct-acting antiviral therapies in persons with HIV infections, incl

199 d/or HBsAg are critical endpoints for future antiviral therapy in chronic HBV.

200 r questions about stopping versus continuing antiviral therapy in hepatitis B e antigen-negative pati

201 stions about discontinuing versus continuing antiviral therapy in hepatitis B e antigen-positive pati

202 ating HSV encephalitis is clear, the role of antiviral therapy in HSV meningitis remains controversia

203 Prophylactic antiviral therapy in immunocompetent cytomegalovirus ser

204 ic outcomes were significantly improved with antiviral therapy in immunocompromised patients with her

205 s B e antigen (HBeAg) status and response to antiviral therapy in patients with chronic hepatitis B (

206 lity evidence supported the effectiveness of antiviral therapy in patients with immune active chronic

207 size evidence regarding the effectiveness of antiviral therapy in the management of chronic HBV infec

208 safe use of in vitro expanded CMV-CTLs as an antiviral therapy in transplant patients with refractory

209 patients with chronic HBV infection require antiviral therapy in Vietnam.

210 nts of rational strategies for the design of antiviral therapies, including monoclonal antibodies (mA

211 and safety of sofosbuvir-based direct-acting antiviral therapy, individually tailored according to th

212 revalence of recommended laboratory testing, antiviral therapy initiation, and liver imaging among a

213 d RNA [(+)RNA] viruses, the major target for antiviral therapies is genomic RNA replication, which oc

214 The discovery of new antiviral therapies is imperative to address this challe

215 Antiviral therapy is a first line of defence against new

216 However, no specific antiviral therapy is available at present.

217 Initial oral or intravenous antiviral therapy is effective in treating ARN.

218 Effective antiviral therapy is essential for achieving sustained v

219 e diagnostics and pangenotypic direct-acting antiviral therapy is essential to achieve the WHO 2030 e

220 Scale-up of direct-acting antiviral therapy is expected to abate hepatitis C virus

221 short course of HBIG combined with long-term antiviral therapy is highly effective in preventing HBV

222 Since numerous viruses cause URTI, antiviral therapy is impractical.

223 duction of the risk of developing HCC during antiviral therapy is largely dependent upon the maintena

224 identified and the response to direct-acting antiviral therapy is monitored.

225 Direct-acting antiviral therapy is now curative, but it is estimated t

226 rapy and that can lead to rebound viremia if antiviral therapy is removed is critical for testing int

227 and dilated cardiomyopathy, but an effective antiviral therapy is still not available.

228 for maintaining a functional HIV-1 cure when antiviral therapy is stopped.

229 ir accumulation over time in patients before antiviral therapy is underexplored, in large part becaus

230 equential long-acting slow-effective release antiviral therapy (LASER ART) and CRISPR-Cas9 demonstrat

231 of magnitude among individual cells and that antiviral therapy leads to a reduction in nuclear DNA in

232 patocytes, even in the presence of available antiviral therapies, lies in the accumulation of covalen

233 One class of antiviral therapies may lie in known pregnancy-acceptabl

234 response to heterologous antigens, and that antiviral therapy may ameliorate this.

235 Antiviral therapy may be considered in pregnant women wi

236 adhere to frequent, consistent follow-up so antiviral therapy may begin at the earliest sign of reac

237 ation of intravitreal foscarnet and systemic antiviral therapy may have greater therapeutic efficacy

238 Based on 16 trials (n = 4809), antiviral therapy might be associated with improved clin

239 Antiviral therapy might provide protective benefits on a

240 ere randomly assigned to receive combination antiviral therapy (n=316) or monotherapy (n=317).

241 Combination direct-acting antiviral therapy of 8-24 weeks is highly effective for

242 IFNalpha-based antiviral therapy of hepatitis delta was independently a

243 There are no effective antiviral therapies or licensed vaccines for this virus,

244 c health threat worldwide, yet there are few antiviral therapies or prophylaxes targeting these patho

245 Additionally, no specific antiviral therapies or vaccines currently exist for huma

246 Without effective antiviral therapies or vaccines, these viruses pose seri

247 patients in C-SURFER who received immediate antiviral therapy or who received placebo before therapy

248 R 1.07, 95% C.I. 1.02-1.13, p<0.01) and dual antiviral therapy(OR 12.46, 95% C.I. 2.09-74.20, p<0.1)

249 o the introduction of varicella vaccination, antiviral therapy, or change in the prevalence of immuno

250 After antiviral therapy, patients had increased numbers of T-r

251 te, of human convalescent plasma, and of two antiviral therapies (poly I:C and remdesivir).

252 Antiviral therapy reduced MTCT, as defined by infant hep

253 The patient received different antiviral therapy regimens (pegylated interferon alpha 2

254 stant CMV infection or who are intolerant to antiviral therapy require alternative strategies.

255 been linked with a differential response to antiviral therapy, risk of steatosis and fibrosis, as we

256 The newly approved antiviral therapies sofosbuvir and simeprevir, with sign

257 There are currently no antiviral therapies specific for SARS-CoV-2, the virus r

258 eloping severe disease; however, no approved antiviral therapies specific to HAdV exist.

259 e advent of safe and effective direct-acting antiviral therapy, such that most patients can be cured

260 h detectable viremia who received preemptive antiviral therapy, suggesting that the adaptive NK cell

261 can cause serious human disease, but current antiviral therapies target lytic but not latent infectio

262 er understanding for the design of candidate antiviral therapies targeting drug-abusing individuals.

263 ective hepatitis C virus (HCV) direct-acting antiviral therapies that do not require modification of

264 Currently, there are no antiviral therapies that have been specifically approved

265 Antiviral therapies that impede virus entry are attracti

266 al of RED-SMU1 destabilizing molecules as an antiviral therapy that could be active against a wide ra

267 a specificities to generate a cost-effective antiviral therapy that provides broad coverage against a

268 versal hepatitis B vaccination and effective antiviral therapy, the estimated overall seroprevalence

269 eveloped concomitant ALT flare with oral HBV antiviral therapy; the risk was 1.7 per 100 person years

270 liminate HIV-1 in individuals on suppressive antiviral therapy, those approaches will need to elimina

271 M(Pro) is an attractive target for antiviral therapies to combat the coronavirus-2019 disea

272 ave potential implications for the timing of antiviral therapy to achieve better virus control.

273 ortunately, there are currently no effective antiviral therapy to contain HCoV-NL63 infection.

274 and identify the patients who require timely antiviral therapy to prevent the development of detrimen

275 minate the virus from the liver, but current antiviral therapies typically fail to do so.

276 Antiviral therapy using newer nucleos(t)ide analogues wi

277 plified WHO criteria) to select patients for antiviral therapy using the national guidelines as a ref

278 ntigen (HBsAg) rapid test and subsequent HBV antiviral therapy versus current practice, in which ther

279 HBV infection had to be receiving effective antiviral therapy (viral load <100 IU/mL); antiviral the

280 cterized according to age; sex; comorbidity; antiviral therapy; viral load, expressed as cycle thresh

281 = 24 686) found inconsistent associations of antiviral therapy vs no therapy with risk of hepatocellu

282 The first episode of CMV viremia requiring antiviral therapy was assessed in 282 patients (147 CMV

283 An SVR after antiviral therapy was associated with decreased adjusted

284 Antiviral therapy was associated with higher risk of wit

285 An SVR after antiviral therapy was associated with improved clinical

286 Antiviral therapy was associated with improvement in sur

287 An sustained response to antiviral therapy was defined as undetectable level of H

288 Prolonged antiviral therapy was given to 226 (80.1%) of 282 patien

289 e antiviral therapy (viral load <100 IU/mL); antiviral therapy was not required for patients with HCV

290 Based on 12 trials (n = 4127), first-line antiviral therapies were at least as likely as nonprefer

291 sis, HCV-specific graft loss and response of antiviral therapy were examined.

292 veloped pQTc; age, basal heart rate and dual antiviral therapy were found as independent predictor of

293 odes (18 = brincidofovir; 23 = cidofovir) of antiviral therapy were observed in 27 patients.

294 ho were followed for at least 1 year without antiviral therapy, were enrolled.

295 imicking chronic infections with and without antiviral therapy, which prevents de novo viral replicat

296 Several studies demonstrated that antiviral therapy with NUCs could reduce the risk of HCC

297 ve observational cohort study, direct-acting antiviral therapy with SOF/ledipasvir, ombitasvir/parita

298 onic HCV infection before, during, and after antiviral therapy with sofosbuvir and velpatasvir, we fo

299 ay fail to respond to commercially available antiviral therapies, with or without demonstrating genot

300 als that could lead to intrinsic combination-antiviral therapies within a single molecule-evolutionar