ライフサイエンスコーパス: oseltamivir

1 ith a therapeutic window superior to that of oseltamivir.

2 by dispensing of the neuraminidase inhibitor oseltamivir.

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

4 ional safety signals after administration of oseltamivir.

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

6 e current frontline neuraminidase inhibitor, oseltamivir.

7 ntly used NA inhibitors, as exemplified with oseltamivir.

8 tant or sensitive to the antiviral inhibitor oseltamivir.

9 at accommodates the pentyloxy substituent of oseltamivir.

10 ed random mutations conferring resistance to oseltamivir.

11 icipants were assigned to placebo and 598 to oseltamivir.

12 ally (H275Y) and phenotypically resistant to oseltamivir.

13 stance to two antiviral drugs, zanamivir and oseltamivir.

14 the intensive care unit, and 15.9% received oseltamivir.

15 ns (2010-2011 to 2017-2018) and treated with oseltamivir.

16 mpared to an irrelevant control mAb R347 and oseltamivir.

17 tics, including drugs such as irinotecan and oseltamivir.

18 ered in combination with the antiviral agent oseltamivir.

19 H274Y conferred highly reduced inhibition by oseltamivir.

20 istance barrier, and synergistic effect with oseltamivir.

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

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

23 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

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

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

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

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

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

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

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

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

32 domized 2:1 to receive pimodivir 600 mg plus oseltamivir 75 mg or placebo plus oseltamivir 75 mg twic

33 ible participants were randomized to receive oseltamivir 75 mg or placebo twice daily for 5 days.

34 00 mg plus oseltamivir 75 mg or placebo plus oseltamivir 75 mg twice daily for 7 days in this phase 2

35 r 300 mg or 600 mg, or pimodivir 600 mg plus oseltamivir 75 mg.

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

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

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

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

43 MEDI8852 or oseltamivir alone early in infection was equally effecti

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

45 nd MEDI8852 plus oseltamivir was better than oseltamivir alone.

46 Sensitivity to oseltamivir also differed between virions.

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

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

49 initiation of viral mRNA synthesis, whereas oseltamivir, an older drug, inhibits release of virus pr

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 a seasons, allocated 1629 to usual care plus oseltamivir and 1637 to usual care, and ascertained the

54 idase and M2 genes that confer resistance to oseltamivir and adamantanes were assessed.

55 Rates of oseltamivir and antibiotic prescriptions were significan

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

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

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

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

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

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

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

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

69 y in blood (85%), and antiviral responses to oseltamivir appeared less pronounced.

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

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

72 leviation of symptoms was 79.0 hours for the oseltamivir arm and 84.0 hours for the placebo arm (P =;

73 nety-nine (45.0%) of 220 participants in the oseltamivir arm had virus detected at day 3 compared wit

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

75 While appearing virologically superior to oseltamivir, baloxavir exhibits a low barrier of resista

76 Only 1 patient had received oseltamivir before specimen collection.

77 The trial was designed and powered to assess oseltamivir benefit overall and in 36 prespecified subgr

78 Oseltamivir binds weakly with the open conformation of N

79 Its adverse event profile is comparable to oseltamivir but is still vulnerable to resistance.

80 21N and Y276F, each reduce susceptibility to oseltamivir by increasing NA activity without altering d

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

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

83 Oseltamivir carboxylate (oseltamivir's active metabolite

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

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

86 38 weeks postmenstrual age (n=8) resulted in oseltamivir carboxylate exposure comparable to previousl

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

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

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

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

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

92 Predictions of oseltamivir consumption from detected levels were compar

93 Oseltamivir decreased viral shedding in this low-risk po

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

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

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

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

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

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

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

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

102 alter illness severity but may have reduced oseltamivir effectiveness.

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

104 Antiviral treatment with oseltamivir enhanced survival of obese mice.

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

106 8, or 72 hours postinfection was superior to oseltamivir for H5N1.

107 Trials of oseltamivir for treatment of naturally occurring influen

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

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

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

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

112 en of vomiting or nausea was observed in the oseltamivir group.

113 8 days, 95% CI -2.11 to 0.97; p=0.39) in the oseltamivir group.

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

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

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

117 Oseltamivir has not been shown to have efficacy, and cor

118 shorter in participants randomly assigned to oseltamivir (hazard ratio 1.29, 95% Bayesian credible in

119 tered alongside standard care (most commonly oseltamivir), hIVIG was not superior to placebo for adul

120 of having flu, and she completed a course of oseltamivir; however, she had continued fatigue, fever,

121 of having flu, and she completed a course of oseltamivir; however, she had continued to experience fa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 Oseltamivir is especially effective for treating H5N1 in

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

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

140 Oseltamivir is widely used as treatment for influenza vi

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

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

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

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

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

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

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

148 rus (34 A/H1N1pdm09; 15 A/H3N2) treated with oseltamivir, most of whom were aged <5 years (n = 39).

149 s (34, A/H1N1pdm09; 15, A/H3N2) treated with oseltamivir, most of whom were aged <5 years (n = 39).

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

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

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

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

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

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

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

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

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

159 A enzyme active site as those of other NAIs, oseltamivir (OS), zanamivir (ZAN), and peramivir, and ma

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

161 ed influenza should be promptly treated with oseltamivir, particularly when A/H3N2 is circulating.

162 827-, 25-, 286-, and 702-fold for zanamivir, oseltamivir, peramivir, and laninamivir, respectively).

163 Oseltamivir phosphate, an antiinfluenza drug, prevented

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

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

166 Differences in antibiotic and oseltamivir prescription rates were analyzed.

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

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

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

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

171 nts with influenza-like illness treated with oseltamivir recovered one day sooner on average than tho

172 replication more rapidly and completely than oseltamivir, reducing the duration of infectiousness.

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

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

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

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

177 8 h since illness onset and the frequency of oseltamivir resistance during treatment.

178 The propensity for oseltamivir resistance emergence was assessed in oseltam

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

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

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

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

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

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

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

186 No oseltamivir resistance was found.

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

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

189 Y neuraminidase substitution responsible for oseltamivir resistance.

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

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

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

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

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

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

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

197 Oseltamivir-resistant H1N1 influenza viruses carrying th

198 However, oseltamivir-resistant H1N1 influenza viruses carrying th

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

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

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

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

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

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

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

206 Importantly, this included an oseltamivir-resistant isolate.

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

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

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

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

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

215 Emergence of oseltamivir-resistant variants was not detected.

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

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

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

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

220 Pimodivir (with or without oseltamivir) resulted in significant virologic improveme

221 d transmissibility, but few data exist about oseltamivir's ability to alter viral shedding.

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 The efficacy of oseltamivir should not be assumed to be equal against al

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

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

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

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

239 nces in virulence and antiviral responses to oseltamivir that may explain the exceptionally high mort

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

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

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

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

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

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

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

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

248 r a larger study of pimodivir in addition to oseltamivir to test whether it results in a clinically s

249 ptive, randomised controlled trial of adding oseltamivir to usual care in patients aged 1 year and ol

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 In a multicenter cohort study including 22 oseltamivir-treated patients with influenza A(H1N1)pdm09

254 We assessed whether early oseltamivir treatment (<=48 hours from symptom onset) de

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

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

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

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

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

260 Oseltamivir treatment resulted in a modest reduction in

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

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

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

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

265 92K mutation was transiently detected during oseltamivir treatment.

266 an immunocompromised patient after prolonged oseltamivir treatment.

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

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

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

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

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

272 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

273 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

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

275 The estimated absolute mean benefit from oseltamivir was 1.02 days (95% [BCrI] 0.74-1.31) overall

276 Oseltamivir was administered 7 days after inoculation.

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

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

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

280 Earlier treatment with oseltamivir was generally associated with better outcome

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

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

283 esponsible for highly reduced sensitivity to oseltamivir, was 23%.

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

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

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

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

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

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

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

291 The association of early oseltamivir with mortality was assessed with log-binomia

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 Pimodivir plus oseltamivir yielded a significantly lower viral load tit

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

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

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

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

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

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