ライフサイエンスコーパス: oseltamivir

1 K, and NA-I222R caused reduced inhibition by oseltamivir.

2 ional safety signals after administration of oseltamivir.

3 on and found to be sensitive to nystatin and oseltamivir.

4 e current frontline neuraminidase inhibitor, oseltamivir.

5 ntly used NA inhibitors, as exemplified with oseltamivir.

6 tant or sensitive to the antiviral inhibitor oseltamivir.

7 at accommodates the pentyloxy substituent of oseltamivir.

8 ed random mutations conferring resistance to oseltamivir.

9 icipants were assigned to placebo and 598 to oseltamivir.

10 ally (H275Y) and phenotypically resistant to oseltamivir.

11 tics, including drugs such as irinotecan and oseltamivir.

12 ered in combination with the antiviral agent oseltamivir.

13 stance to two antiviral drugs, zanamivir and oseltamivir.

14 H274Y conferred highly reduced inhibition by oseltamivir.

15 eplacement therapies (19%); 38% had received oseltamivir.

16 mmunosuppressed, aged >65 years, or received oseltamivir.

17 1 with the lowest hydrolytic activity toward oseltamivir.

18 edding for over 5 weeks despite therapy with oseltamivir.

19 ll culture with increasing concentrations of oseltamivir.

20 resistant to adamantanes and susceptible to oseltamivir.

21 istance barrier, and synergistic effect with oseltamivir.

22 strain of IAV in the presence and absence of oseltamivir.

23 ith a therapeutic window superior to that of oseltamivir.

24 mpared to an irrelevant control mAb R347 and oseltamivir.

25 by dispensing of the neuraminidase inhibitor oseltamivir.

26 Oseltamivir 1 mg/kg/dose twice daily in infants <38 week

27 se (RR 0.37, 95% CI 0.17-0.81; p=0.013; 0.6% oseltamivir, 1.7% placebo, risk difference -1.1%, 95% CI

28 placebo (2292 household members) and 598 to oseltamivir (2402 household members).

29 tion of symptoms was similar in both groups (oseltamivir 3 days [IQR 2-5], placebo 3 days [1-5]; p=0.

30 Oseltamivir 3 mg/kg/dose once daily in premature infants

31 us isolation on days 2 (placebo 374 [66%] vs oseltamivir 321 [56%]; difference 15.2%, 95% CI 9.5-20.8

32 ; (iv) exhibit large volumes of synergy with oseltamivir (36 and 331 muM(2) % at 95% confidence); and

33 bility of 31% (rats), which is comparable to oseltamivir (36%).

34 were vaccinated intramuscularly or received oseltamivir (5 mg/kg twice daily) prophylactically befor

35 The NAI oseltamivir (5, 20, or 80 mg/kg/day) was administered to

36 rated randomisation system to receive either oseltamivir (75 mg), amantadine (100 mg), and ribavirin

37 We assessed whether combinations of oseltamivir (a neuraminidase inhibitor) and T-705 (a non

38 Current antiviral therapies include oseltamivir, a neuraminidase inhibitor that prevents the

39 Oseltamivir, a widely used anti-influenza drug, is hydro

40 nfirmed H5N1 infection who were treated with oseltamivir, according to viral clade, age, respiratory

41 al susceptibility to the anti-influenza drug oseltamivir acid, whereas PDFSA was used for in situ ima

42 tions and, specifically, why the efficacy of oseltamivir against the double mutant IRHY was significa

43 2%) over that of the neuraminidase inhibitor oseltamivir alone (50%).

44 A comparison with oseltamivir alone and combination of MEDI8852 and oselta

45 MEDI8852 or oseltamivir alone early in infection was equally effecti

46 s might be more effective than administering oseltamivir alone in the treatment of influenza.

47 nd MEDI8852 plus oseltamivir was better than oseltamivir alone.

48 ulticentre phase 2 trial of a combination of oseltamivir, amantadine, and ribavirin versus oseltamivi

49 ns of influenza virus that were resistant to oseltamivir, an FDA-approved therapeutic treatment for i

50 pandemic preparations involve stock- piling oseltamivir, an oral neuraminidase inhibitor (NAI), so r

51 A series of oseltamivir analogues bearing an N-substituted guanidine

52 median times to alleviation were 97.5 h for oseltamivir and 122.7 h for placebo groups (difference -

53 he effects of the influenza virus inhibitors oseltamivir and amantadine on the kinetics of in vivo in

54 Rates of oseltamivir and antibiotic prescriptions were significan

55 Therapy with oral oseltamivir and inhaled zanamivir may provide a net bene

56 Direct comparison of oral oseltamivir and inhaled zanamivir suggests no important

57 ogically past term, n=4) resulted in similar oseltamivir and oseltamivir carboxylate exposure.

58 ouble E119D/H275Y mutation further increased oseltamivir and peramivir 50% inhibitory concentrations

59 NA-R292K substitution is highly resistant to oseltamivir and peramivir and partially resistant to zan

60 aminidase gene conferring resistance to both oseltamivir and peramivir without any loss in fitness, t

61 NA-R292K led to highly reduced inhibition by oseltamivir and peramivir, while NA-E119V, NA-I222K, and

62 lethal H5N1 infection in ferrets compared to oseltamivir and R347, and MEDI8852 plus oseltamivir was

63 l H3N2v viruses examined were susceptible to oseltamivir and zanamivir and resistant to adamantane an

64 ) mutant of H1N1-2009 NA reduced efficacy of oseltamivir and zanamivir by 45 and 10 times, (1) respec

65 treatment of an immunocompromised child with oseltamivir and zanamivir for A(H1N1)pdm09 virus infecti

66 nal change upon binding of the NA inhibitors oseltamivir and zanamivir in the wild-type and the IR an

67 ruses and the target for the influenza drugs oseltamivir and zanamivir.

68 uals testing positive for influenza viruses (oseltamivir), and it is potentially beneficial to identi

69 samples of H1N1 influenza A and detected an oseltamivir (antiviral therapy) resistance mutation in t

70 benefits of the neuraminidase (NA) inhibitor oseltamivir are dampened by the emergence of drug resist

71 Thus, patients naive to oseltamivir are most likely to be susceptible when this

72 Antivirals (eg, oseltamivir) are important for mitigating influenza epid

73 Oseltamivir at 20 and 80 mg/kg protected 80% and 88% of

74 Only 1 patient had received oseltamivir before specimen collection.

75 Oseltamivir binds weakly with the open conformation of N

76 21N and Y276F, each reduce susceptibility to oseltamivir by increasing NA activity without altering d

77 However, the usefulness of oseltamivir can be compromised by the emergence and spre

78 Plasma steady-state trough oseltamivir carboxylate (OC) concentration was measured

79 Oseltamivir carboxylate (oseltamivir's active metabolite

80 sistant variants in the presence of the NAIs oseltamivir carboxylate and zanamivir in MDCK cells.

81 oximately 84 and 51 times lower affinity for oseltamivir carboxylate and zanamivir, respectively, com

82 38 weeks postmenstrual age (n=8) resulted in oseltamivir carboxylate exposure comparable to previousl

83 rm, n=4) resulted in similar oseltamivir and oseltamivir carboxylate exposure.

84 unit dose for this age group (ie, 30 mg) had oseltamivir carboxylate exposures below the target range

85 , and 4 in N8) conferred resistance to NAIs (oseltamivir carboxylate, zanamivir, or peramivir) as det

86 al effect of WJ379 was also synergistic with oseltamivir carboxylate.

87 The crystal structure of the I221L NA and oseltamivir complex showed that the leucine side chain p

88 Predictions of oseltamivir consumption from detected levels were compar

89 Several 5-guanidino- and 5-amidino-based oseltamivir derivatives were synthesized and profiled fo

90 population diversity or differentiation, and oseltamivir did not alter the selective environment.

91 However, prophylactic oseltamivir did not prevent H5N1 virus replication in th

92 The appropriate twice-daily oral oseltamivir dose for infants </=8 months of age is 3.0 m

93 An oseltamivir dose of 3.0 mg/kg produced drug exposures wi

94 ed between 3-4 and 120-154 people were using oseltamivir during the study period in the two WWTP catc

95 The emergency of resistance to oseltamivir during treatment was rare overall (<1%) and

96 For individuals treated with oseltamivir, early initiation of treatment substantially

97 alter illness severity but may have reduced oseltamivir effectiveness.

98 In this double-blind oseltamivir efficacy trial, we identified index patients

99 Antiviral treatment with oseltamivir enhanced survival of obese mice.

100 However, the appropriate dose of oseltamivir for children <2 years of age is unknown.

101 8, or 72 hours postinfection was superior to oseltamivir for H5N1.

102 Trials of oseltamivir for treatment of naturally occurring influen

103 tive than the current standard of treatment, oseltamivir, given twice daily for six days.

104 Household secondary illness was lower in the oseltamivir group (196 [8%] influenza cases) than in the

105 dian duration of symptoms was shorter in the oseltamivir group (3 days, IQR 1-5) than in the placebo

106 r patients with influenza A/H1N1pdm09 in the oseltamivir group developed H275Y resistance mutations.

107 8 days, 95% CI -2.11 to 0.97; p=0.39) in the oseltamivir group.

108 ot differ between the placebo (103 [5%]) and oseltamivir groups (92 [4%]; 0.84, 0.59-1.19, p=0.319);

109 R292K conferred the highest increase in oseltamivir half-maximal inhibitory concentration (IC50)

110 as significantly reduced, to the point where oseltamivir has become an ineffective treatment.

111 Other resources (oseltamivir, hospital beds and human resources) are ineq

112 These samples were analyzed for oseltamivir hydrolysis and CES1 expression.

113 onducted a 2-sample pharmacokinetic study of oseltamivir in 12 premature infants.

114 -specific (MS) RT-PCR detected resistance to oseltamivir in 19 patients postbaseline (17 H1N1pdm2009

115 Our findings show that oseltamivir in adults with influenza accelerates time to

116 ed, double-blind trials of 75 mg twice a day oseltamivir in adults.

117 ollaborative Antiviral Study Group evaluated oseltamivir in infants aged <2 years in an age-de-escala

118 In years 1-3 of IRIS, emergent resistance to oseltamivir in influenza viruses during treatment was un

119 cination is more effective than prophylactic oseltamivir in preventing CNS invasion by H5N1 virus via

120 ymptom dynamics, we explored the efficacy of oseltamivir in reducing both symptoms (symptom efficacy)

121 use, questions remain about the efficacy of oseltamivir in the treatment of influenza.

122 e results provide initial guidance on dosing oseltamivir in this vulnerable population.

123 n 223, that reduce the apparent affinity for oseltamivir in vitro.

124 an the current anti-influenza A therapeutic, oseltamivir, in treating severe influenza infection in m

125 Regarding safety, oseltamivir increased the risk of nausea (RR 1.60, 95% C

126 Delayed initiation of treatment with oseltamivir increases the likelihood of death, with an o

127 tralizing antibodies and an antiviral agent, Oseltamivir, influenza virus can exploit these networks

128 requiring ventilatory support at the time of oseltamivir initiation were more likely to die from the

129 Oseltamivir is especially effective for treating H5N1 in

130 Furthermore, the antiviral drug oseltamivir is less effective for treating influenza B v

131 The results suggest that the efficacy of oseltamivir is reduced significantly because of conforma

132 Oseltamivir is widely used as treatment for influenza vi

133 The neuraminidase (NA) inhibitor, oseltamivir, is a widely used anti-influenza drug.

134 febrile 8 days after completing a course of oseltamivir; isolation was instituted 9 days after sympt

135 He was treated with oral oseltamivir, later combined with intravenous zanamivir.

136 Among patients treated with oseltamivir, length of stay and mortality did not differ

137 suggest that, in high-risk populations, oral oseltamivir may reduce mortality (odds ratio, 0.23 [95%

138 ely insusceptible to the antiviral effect of oseltamivir, might confer an additional fitness advantag

139 nd ribavirin (600 mg) combination therapy or oseltamivir monotherapy twice daily for 5 days, given or

140 seltamivir, amantadine, and ribavirin versus oseltamivir monotherapy with matching placebo for the tr

141 intravenous zanamivir (n=209), or 75 mg oral oseltamivir (n=205) twice a day; 11 patients discontinue

142 and I222K reduced the inhibitory activity of oseltamivir, not only in the NI assay, but also in infec

143 anamivir dosed at 600 mg was not superior to oseltamivir or 300 mg intravenous zanamivir.

144 randomly allocated on a 1:1 basis to receive oseltamivir or placebo twice daily for 5 days.

145 allocated eligible patients (1:1) to receive oseltamivir or placebo twice-daily for 5 days, and we st

146 substitutions associated with resistance to oseltamivir or T-705 were detected.

147 efficiently in NHBE cells in the presence of oseltamivir or zanamivir and that virus with the H274Y N

148 of rg-E119A in NHBE cells in the presence of oseltamivir or zanamivir and the fitness advantage of rg

149 fully treated with neuraminidase inhibitors (oseltamivir or zanamivir); however, the efficacy of thes

150 with or without escalating concentrations of oseltamivir over serial passages.

151 827-, 25-, 286-, and 702-fold for zanamivir, oseltamivir, peramivir, and laninamivir, respectively).

152 Oseltamivir phosphonic acid (tamiphosphor, 3a), its mono

153 hile addition of the neuraminidase inhibitor oseltamivir potentiates neutralization, hemagglutinin in

154 Differences in antibiotic and oseltamivir prescription rates were analyzed.

155 Oseltamivir pressure selected a variant of A/Hong Kong/2

156 a virus-infected mice that were treated with oseltamivir prior to a challenge with S. pneumoniae.

157 No patients with B/I221V infection received oseltamivir prior to specimen collection.

158 AAL-R combined with oseltamivir provided maximum protection against a lethal

159 It is unclear if higher-dose oseltamivir provides benefit beyond the standard dose in

160 cells of viruses with reduced inhibition by oseltamivir (recombinant virus with the E119A mutation g

161 m that would explain the rapidity with which oseltamivir resistance achieved fixation among sH1N1 iso

162 Oseltamivir resistance among 2009 pandemic influenza A (

163 inical specimens from patients who developed oseltamivir resistance and demonstrated the ultrasensiti

164 that only selection of H274Y is required for oseltamivir resistance and that H274Y is not deleterious

165 Between 2007 and 2009, oseltamivir resistance developed among seasonal influenz

166 lly altered by the acquisition of high-level oseltamivir resistance due to the NA-R292K mutation.

167 Virus from 3 subjects developed oseltamivir resistance during antiviral treatment.

168 8 h since illness onset and the frequency of oseltamivir resistance during treatment.

169 The propensity for oseltamivir resistance emergence was assessed in oseltam

170 Oseltamivir resistance in A(H1N1)pdm09 influenza is rare

171 model may correlate with clinically relevant oseltamivir resistance in humans.

172 NA mutations previously known to confer oseltamivir resistance in N1 strains, including H275Y an

173 vide a basis for predicting the evolution of oseltamivir resistance in other influenza strains.

174 lanation for the recent reproducible rise in oseltamivir resistance in seasonal H1N1 IAV strains in h

175 ltamivir sensitivity and greatly potentiates oseltamivir resistance in the context of the H275Y mutat

176 Interestingly, we were unable to detect the oseltamivir resistance mutation in pretreatment samples,

177 VS-HRM) that is able to detect the His275Tyr oseltamivir resistance mutation to 0.5% in a background

178 ever, the IAV genome can evolve rapidly, and oseltamivir resistance mutations have been detected in n

179 The His274-->Tyr274 (H274Y) mutation confers oseltamivir resistance on N1 influenza neuraminidase but

180 utations contribute to the appearance of the oseltamivir resistance substitution H274Y in the neurami

181 No oseltamivir resistance was found.

182 Oseltamivir resistance was later confirmed by pyrosequen

183 the airway for 2 weeks, during which time an oseltamivir resistance-associated R292K mutation rapidly

184 on genomics of IAV during the development of oseltamivir resistance.

185 Y neuraminidase substitution responsible for oseltamivir resistance.

186 esistant and sensitive to the antiviral drug oseltamivir, resistance was propagated through contact t

187 ch higher concentration, suggesting that the oseltamivir-resistance mutation itself caused susceptibi

188 enza A/H1N1 virus strains (A[H1N1]pdm09) are oseltamivir resistant, almost exclusively because of a H

189 We estimated that the oseltamivir-resistant A H1N1 strain that emerged in 2007

190 t widespread community transmission of H275Y oseltamivir-resistant A(H1N1)pdm09 influenza.

191 nic avian influenza (HPAI) virus A/H5N1, and oseltamivir-resistant A/H1N1 strains; (iv) exhibit large

192 cocirculated in the recent seasons: clade 2B oseltamivir-resistant and adamantane-susceptible viruses

193 Here we demonstrate that an oseltamivir-resistant clinical isolate, an A/Brisbane/59

194 Oseltamivir-resistant H1N1 influenza viruses carrying th

195 However, oseltamivir-resistant H1N1 influenza viruses carrying th

196 de, that potently inhibit the NA activity of oseltamivir-resistant H1N1 viruses with the H275Y NA mut

197 ng that caused by highly pathogenic H5N1 and oseltamivir-resistant H1N1 viruses.

198 lication of influenza viruses, including the oseltamivir-resistant H275Y strain, at low nanomolar to

199 Compound 7a is active to the oseltamivir-resistant H275Y strains of H1N1 and H5N1 vir

200 Following emergence of naturally occurring oseltamivir-resistant influenza A(H1N1) viruses, a globa

201 In 2007, an oseltamivir-resistant influenza seasonal A H1N1 strain e

202 With the emergence of oseltamivir-resistant influenza viruses and in view of a

203 Importantly, this included an oseltamivir-resistant isolate.

204 Our data suggest that the oseltamivir-resistant NA (specifically, one or both of t

205 ates, we further show that expression of the oseltamivir-resistant NA in the context of viral protein

206 We hypothesized that the oseltamivir-resistant neuraminidase (NA), in addition to

207 ts oseltamivir-sensitive predecessor and the oseltamivir-resistant pandemic A H1N1 strain that emerge

208 We investigated a cluster of oseltamivir-resistant pH1N1 infections in a hospital war

209 Oseltamivir-resistant pH1N1 infections were found with r

210 omology confirmed nosocomial transmission of oseltamivir-resistant pH1N1.

211 ation of wild-type influenza A(H7N9) and its oseltamivir-resistant R292K variants in mice.

212 Thus, in stark contrast to oseltamivir-resistant seasonal influenza A(H3N2) viruses

213 r of clinical isolates of FluA, including an oseltamivir-resistant strain, and FluB, without showing

214 5Y mutation and that widespread emergence of oseltamivir-resistant strains may now be more likely.

215 ge against neuraminidases from wild-type and oseltamivir-resistant strains.

216 Emergence of oseltamivir-resistant variants was not detected.

217 Three genetically similar oseltamivir-resistant variants were detected outside of

218 Here we show that highly oseltamivir-resistant viruses containing both the S247N

219 tion was collected on patients infected with oseltamivir-resistant viruses.

220 e a future pandemic influenza strain that is oseltamivir-resistant, alternative therapy options are n

221 tients received 150 mg and 75 mg twice-daily oseltamivir, respectively; their enrollment characterist

222 Oseltamivir carboxylate (oseltamivir's active metabolite) was recovered from two

223 terminant of transmission efficiency between oseltamivir-sensitive and -resistant Brisbane/59-like sH

224 lates of influenza A viruses, including both oseltamivir-sensitive and -resistant strains.

225 (95% CrI 17-30) less transmissible than its oseltamivir-sensitive counterpart.

226 than does a highly similar, contemporaneous oseltamivir-sensitive isolate.

227 erval [CrI] 3-5) more transmissible than its oseltamivir-sensitive predecessor and the oseltamivir-re

228 NA in the context of viral proteins from the oseltamivir-sensitive virus (a 7:1 reassortant) is suffi

229 rring N1 neuraminidase mutation that reduces oseltamivir sensitivity and greatly potentiates oseltami

230 MEDI8852, alone or with oseltamivir, shows promise for prophylaxis or therapy of

231 In those with all swab specimens (n=1134), oseltamivir significantly reduced virus isolation on day

232 (B/I221V), associated with reduced in vitro oseltamivir susceptibility were detected in North Caroli

233 ity of 2009 (H1N1) influenza A virus remains oseltamivir susceptible, the threat of resistance due to

234 aste water epidemiology approach to estimate oseltamivir (Tamiflu(R)) compliance.

235 ections of the sialidase inhibitors DANA and oseltamivir (Tamiflu) starting either 1 day or 10 days a

236 s, an influenza virus model of resistance to oseltamivir (Tamiflu) was used.

237 pin III, two cholesterol-binding agents, and oseltamivir (Tamiflu), a viral neuraminidase inhibitor,

238 Oseltamivir (Tamiflu), an oral neuraminidase inhibitor,

239 ent using the neuraminidase (NA) inhibitors, oseltamivir (Tamiflu), and zanamivir (Relenza).

240 located adjacent to a hydrophobic portion of oseltamivir that is chemically distinct from the substra

241 sceptibility of influenza A(H7N9) viruses to oseltamivir, the most prescribed anti-influenza virus dr

242 The selective pressure exerted by different oseltamivir therapy regimens have received little attent

243 e (NA) gene of an H3N2 virus after 5 days of oseltamivir therapy.

244 Among patients who completed oseltamivir, those with B/I221V infection reported a lon

245 robust in vivo synergism when combined with oseltamivir, thus highlighting treatment strategies that

246 Several studies have proven oseltamivir to be efficient in reducing influenza viral

247 y of homologous vaccination and prophylactic oseltamivir to prevent H5N1 virus CNS invasion via the o

248 f treatment with the neuraminidase inhibitor oseltamivir to reduce patient illness and viral shedding

249 e same study, we aimed to assess efficacy of oseltamivir to reduce secondary household illnesses in t

250 tamivir resistance emergence was assessed in oseltamivir-treated animals infected with wild-type viru

251 events, than did populations in control and oseltamivir-treated mice, but no substitutions associate

252 2K, NA-I222R, or NA-R292K) recovered from an oseltamivir-treated patient were tested for NAI suscepti

253 Oseltamivir treatment (5 or 25 mg/kg of body weight/dose

254 for age, having been infected in Egypt, and oseltamivir treatment (P = .02).

255 e found no additional benefit of higher-dose oseltamivir treatment in adults hospitalized with influe

256 In a crowded, low income setting, oseltamivir treatment of index patients resulted in a sm

257 d trial in Dhaka, Bangladesh, we showed that oseltamivir treatment of index patients was able to redu

258 Oseltamivir treatment resulted in a modest reduction in

259 enrolled less than 48 h since illness onset, oseltamivir treatment significantly reduced virus isolat

260 enrolled 48 h or longer since illness onset, oseltamivir treatment significantly reduced virus isolat

261 uenza A (H1N1) virus within a few days after oseltamivir treatment was initiated.

262 However, we did not find any association of oseltamivir treatment with duration of viral shedding by

263 infections (rapid influenza test followed by oseltamivir treatment) and 22% (95% CI 16-27%) more effe

264 an immunocompromised patient after prolonged oseltamivir treatment.

265 tness of the Y275 mutation in the absence of oseltamivir treatment.

266 loped drug resistance de novo in response to oseltamivir treatment.

267 92K mutation was transiently detected during oseltamivir treatment.

268 Study regimen of either 150 mg or 75 mg oseltamivir twice daily for 5 days was allocated by site

269 e clearance, 40-60 mL/minute) received 75 mg oseltamivir twice daily.

270 s zanamivir, or standard-of-care (75 mg oral oseltamivir) twice a day for 5-10 days; patients were fo

271 al rate, without a corresponding increase in oseltamivir usage.

272 ceptibility of two antivirals, Zanamivir and Oseltamivir, using the assay.

273 rter time to alleviation of all symptoms for oseltamivir versus placebo recipients (time ratio 0.79,

274 g (RR 2.43, 95% CI 1.83-3.23; p<0.0001; 8.0% oseltamivir vs 3.3% placebo, risk difference 4.7%, 95% C

275 a (RR 1.60, 95% CI 1.29-1.99; p<0.0001; 9.9% oseltamivir vs 6.2% placebo, risk difference 3.7%, 95% C

276 [RR] 0.56, 95% CI 0.42-0.75; p=0.0001; 4.9% oseltamivir vs 8.7% placebo, risk difference -3.8%, 95%

277 Oseltamivir was administered 7 days after inoculation.

278 tients with the neuraminidase (NA) inhibitor oseltamivir was associated with emergence of viruses car

279 d to oseltamivir and R347, and MEDI8852 plus oseltamivir was better than oseltamivir alone.

280 that the mechanism of resistance of IRHY to oseltamivir was due to the loss of key hydrogen bonds be

281 ng for all risk factors, early initiation of oseltamivir was found to be particularly effective in in

282 Earlier treatment with oseltamivir was generally associated with better outcome

283 amivir alone and combination of MEDI8852 and oseltamivir was included in some studies.

284 uction of proinflammatory mediators, whereas oseltamivir was only partially effective at reducing the

285 ase (NA) conferring high-level resistance to oseltamivir were isolated from an immunocompromised pati

286 ous zanamivir, 600 mg intravenous zanamivir, oseltamivir) were diarrhoea (10 [5%], 15 [7%], 14 [7%]),

287 mice compared to the neuraminidase inhibitor oseltamivir when treatment is started late in infection.

288 mice compared to the neuraminidase inhibitor oseltamivir when treatment is started late in infection.

289 lanation for the high level of resistance to oseltamivir while retaining good fitness of viruses carr

290 R292K conferred highly reduced inhibition by oseltamivir, while E119V and I222K each caused reduced i

291 toms was reduced by 1 day in the group given oseltamivir who were enrolled less than 48 h since sympt

292 a-analysis for all clinical trials comparing oseltamivir with placebo for treatment of seasonal influ

293 ld contacts, we found that the initiation of oseltamivir within 24 hours was associated with shorter

294 performed molecular dynamics simulations of oseltamivir, zanamivir and peramivir bound to H7N9, H7N9

295 ug resistance to the currently approved NAIs oseltamivir, zanamivir, and peramivir by assessing recom

296 associated with reduced inhibition by NAIs (oseltamivir, zanamivir, and peramivir): (i) novel subtyp

297 l epithelial (NHBE) cells in the presence of oseltamivir, zanamivir, or peramivir.

298 tal structure was determined in complex with oseltamivir, zanamivir, or sialic acid, and structural a

299 n standardized NA inhibition (NI) assay with oseltamivir, zanamivir, peramivir, and laninamivir.

300 ighly reduced inhibition by 4 NA inhibitors: oseltamivir, zanamivir, peramivir, and laninamivir.