ライフサイエンスコーパス: escape mutant

1 g an immune response and may represent a CTL escape mutant.

2 on acts both as a CTL and protease inhibitor escape mutant.

3 n of the hepatic allograft with the YMDD HBV escape mutant.

4 ld have public health relevance as a vaccine escape mutant.

5 he same peptide retained potency against ENF-escape mutants.

6 uppressed viral replication and generated no escape mutants.

7 ations of a neutralizing antibody to isolate escape mutants.

8 ll responses and limits recognition of viral escape mutants.

9 umventing or limiting the emergence of viral escape mutants.

10 at these plasma Nef variants represent novel escape mutants.

11 topes and minimizes the likely generation of escape mutants.

12 d results in cumulative toxicities and viral-escape mutants.

13 mals without the emergence of drug-resistant escape mutants.

14 n, which in turn could have selected for new escape mutants.

15 an unbiased approach to isolate and analyze escape mutants.

16 nd may limit the emergence of neutralization-escape mutants.

17 ed B6 mice suppressed the development of CTL escape mutants.

18 ereby reducing the probability of generating escape mutants.

19 e emergence and competitive advantage of CTL escape mutants.

20 susceptible to the problem of drug-resistant escape mutants.

21 e ability of the response to recognize virus escape mutants.

22 that such variants represent neutralization escape mutants.

23 evolution of antiviral resistance or vaccine-escape mutants.

24 shown to reduce drastically the selection of escape mutants.

25 immune pressure leading to the selection of escape mutants.

26 be more widely useful and less vulnerable to escape mutants.

27 nanobody fusions suppressed the emergence of escape mutants.

28 identifying a drug's mechanism of action and escape mutants.

29 ompletely inhibited the replication of these escape mutants.

30 rry the benefit of mitigating risks of viral escape mutants.

31 r the emergence of drug-resistance or immune-escape mutants.

32 munodeficient hosts failed to generate viral escape mutants.

33 public health risk linked with generation of escape mutants.

34 ding domain (RBD) and generated 50 different escape mutants.

35 g the likelihood of selecting neutralisation-escape mutants.

36 synergistically and limits the emergence of escape mutants.

37 everal Ags may limit the generation of viral escape mutants.

38 ficacy can be undermined by the emergence of escape mutants.

39 DNA within the host genome, which can harbor escape mutants.

40 an and zoonotic SARS-CoVs and neutralization escape mutants.

41 clonal Abs (mAbs) to sequentially select IAV escape mutants.

42 antiviral-resistant variants and host immune escape mutants.

43 ll immunity against commonly occurring virus escape mutants.

44 esistance and increasing the risk of vaccine escape mutants.

45 Attempts to generate an escape mutant against L7Ae-mediated inhibition resulted

46 This study demonstrates that the immune escape mutants also (i) gained greater replication abili

47 Development of escape mutants also strongly correlated with neutralizin

48 the interaction as previously determined by escape mutant analysis and site-directed mutation, is lo

49 Epitope-mapping studies using neutralization escape mutant analysis, deuterium exchange mass spectrom

50 We also report an escape mutant analysis, which allows the mapping of hete

51 evolve and catch up with the dominant HIV-1 escape mutant and persist long-term in most cases.

52 show increased tolerance to potential virus escape mutants and an emerging variant of concern.

53 ance monitoring is essential to detect assay escape mutants and ensure universal detection of evolvin

54 her epitope characterization by selection of escape mutants and epitope mapping by flow cytometry ana

55 of resolving infection without selecting for escape mutants and is applicable to other virus-host int

56 Information on SARS-CoV-2 escape mutants and mutations affecting the antiviral act

57 The structure also rationalizes inhibitor escape mutants and mutations observed in live-attenuated

58 e present study, we generated neutralization escape mutants and studied the effect of these neutraliz

59 ity-matured HC-1 antibodies yielded no viral escape mutants and, with the affinity-matured IgG1, need

60 pe does not preclude the selection of T cell escape mutants, and epitope-specific T cells are still p

61 ibody responses to secondary infections with escape mutants are dominated by specificities to the ori

62 a lymphocytic choriomeningitis virus-derived escape mutant as demonstrated by the sustained activatio

63 development of cytotoxic T lymphocyte (CTL) escape mutants, as compared to the lung memory NP-specif

64 These clones were not found to be escape mutants, as their replicative ability was severel

65 Escape mutant assays identified five amino acid residues

66 1H3 selects an escape mutant at amino acid 273 on EBOV GP.

67 cape mutants that predicts the prevalence of escape mutants at the population level.

68 An escape mutant (B2PD.3), derived with the mAb used to gen

69 probability that the population develops an escape mutant before extinction, is encoded in the risk

70 temporary human influenza viruses identified escape mutants before they caused an epidemic in 2014-20

71 different prevalences of monoclonal antibody-escape mutants between the two subgroups.

72 at Wyeth/IL-15/5Flu does not generate T cell escape mutants but increases stochastic events for virus

73 ergence and immune presentation of viral CTL escape mutants but rather arise de novo following primin

74 roved potency of inhibitory peptides against escape mutants by increasing enthalpic release of energy

75 ing therapeutic strategy, but neutralization escape mutants can develop.

76 The escape mutant, CC101.19, continued to use CCR5 for entry

77 dynamics profiles of the A92E and G94D CypA escape mutants closely resemble that of wild-type CA ass

78 tent activity without the emergence of viral escape mutants, co-administration of different bNAbs is

79 Of note, the serum escape mutant completely lost the ability to bind to hum

80 The escape mutants contain multiple nef mutations that impai

81 Typically, these escape mutants contained 3-4 base substitutions, but dif

82 Additionally, a second subset of escape mutants contained amino acid deletions within the

83 suggested that cytotoxic T-lymphocyte (CTL) escape mutants contributed to virus amplification and th

84 However, viral escape mutants could compromise efficacy.

85 pecificity for the spectrum of preferred CTL escape mutants, could prove effective.

86 in different MERS-CoV isolates and antibody escape mutants, cross-neutralization of divergent MERS-C

87 Interestingly, the neutralization escape mutant derived from growing DH012 in the presence

88 the higher dose and that while GCV resistant escape mutants did arise, a significant fraction of the

89 of specific CTLs to the frequency of Tat SL8 escape mutants during acute SIV infection allowed us to

90 anticipates the possible evolution of viral escape mutants during the use of therapies targeting thi

91 The immune-escape mutants emerge frequently, displacing or co-circu

92 ics of immune escape, we found that multiple escape mutants emerge simultaneously during the escape,

93 lobal threat to human health particularly as escape mutants emerge.

94 An escape mutant emerged which was approximately 100-fold m

95 However, ZIKV escape mutants emerged in vitro and in vivo in the prese

96 linical improvement and did not induce viral escape mutants, encouraging the future use of remdesivir

97 r basis for selection and recognition of the escape mutant epitope by TCR and KIR2DL2.

98 orating the receptor-blocking hypothesis, T2 escape mutants evolve resistance to PinQ anti-phage defe

99 tance rapidly emerged, no feedback-disruptor escape mutants evolved in long-term cultures.

100 We determined that the V-to-A CTL escape mutant failed to induce a Db GP33-43-specific CTL

101 c barrier to the generation and selection of escape mutants following exposure to host-targeted imino

102 Our results showed the serum escape mutant formed large plaques in Madin-Darby canine

103 potential limitation on the viability of PV escape mutants from antibody neutralization.

104 Selecting escape mutants from parental versus sequential variants

105 rther characterization of the neutralization escape mutant generated using this MAb showed that three

106 ould also consider the potential risk of the escape mutants generated by mAb treatment to public heal

107 Here, we describe escape mutants generated by serial passage of A/Netherla

108 oV-2 and its variants of concern, as well as escape mutants generated by the parental monoclonal anti

109 opted by the immune system to neutralize the escape mutants generated during pathogenic insult.

110 ncy of the appearance of monoclonal antibody escape mutants generated when the virus is pressured to

111 carditic H3 variant of CVB3 and the antibody escape mutant H310A1.

112 ious experiments have identified an antibody escape mutant (H310A1) of a myocarditic variant of CVB3

113 was His to Tyr at amino acid 44; additional escape mutants had a His-to-Arg mutation at amino acid 4

114 Despite great effort, a full map of escape mutants has not been delineated for an anti-HIV a

115 inhibitory compounds, indicating that the F escape mutants have a reduced conformational stability a

116 Hepatitis B virus immune escape mutants have been associated with vaccine failure

117 Although palivizumab escape mutants have been generated in the laboratory, th

118 Seasonal vaccines are often ineffective and escape mutants have been reported to all treatments for

119 Previous studies of natural neutralization escape mutants have predominantly focused on gp120 and g

120 These allosteric escape mutants have the activated conformation in the ab

121 s, including the isolation of neutralization escape mutants, hydrogen/deuterium exchange mass spectro

122 Genome analysis of these phage escape mutants identified a total of 15 mutated genes.

123 k-derived decomplementing factors, then OspA escape mutants, if infectious, could seriously diminish

124 Selection for escape mutant immunodeficiency viruses by cytotoxic T ly

125 Next-generation sequencing of a putative RHV escape mutant in a vaccinated rat identified mutations i

126 ic dose of the antibody used to generate the escape mutant in vitro.

127 However, HF5 quickly selected pH1N1 virus escape mutants in both prophylactic and therapeutic trea

128 Serotype-specific neutralization escape mutants in dengue virus E proteins are all locate

129 ssible routes for the evolution of fit viral escape mutants in HIV-1YU-2-infected humanized mice, wit

130 dramatic invasions of cytotoxic T lymphocyte escape mutants in human influenza A.

131 of drug-resistant mutants and immunological-escape mutants in patients.

132 ape; new pandemic variants, as well as viral escape mutants in seasonal influenza, compromise the bui

133 from SARS-CoV-2 challenge, albeit selecting escape mutants in some animals.

134 A trend of more escape mutants in the GP1 and GP2 domains was observed f

135 s appeared to determine the stability of the escape mutants in the infant over time.

136 We generated palivizumab and motavizumab escape mutants in vitro and examined the development of

137 While it was possible to generate escape mutants in vitro, they were neutralized by the an

138 ffinity also led to the suppression of viral escape mutants in vitro.

139 Structural analysis of our observed escape mutants indicates changes toward the less-preferr

140 g antibody classes that can neutralize viral escape mutants is critical for universal influenza virus

141 lying that a diverse population of potential escape mutants is present during immune selection.

142 ated ability to suppress generation of HIV-1 escape mutants is significantly lower than the activity

143 oned the env genes from the the parental and escape mutant isolates and made chimeric infectious mole

144 ments reveal a high barrier for emergence of escape mutants, making it a good candidate for clinical

145 tically stable virus antigens, suggests that escape mutants may be a serious problem when CTL therapy

146 acids undergoing escape, and growth rates of escape mutants, may affect when escape occurs.

147 d the potential for immune selection of PorA-escape mutants.Methods.

148 An RSV escape mutant, MP4, has been shown to resist PZ prophyla

149 had broad neutralizing capabilities, and its escape mutant N149D had reduced viral stability and huma

150 h enhanced bnAb lineage envelope binding and escape mutant neutralization-traits associated with incr

151 e inhibition of that mutant but not of other escape mutants nor of the ancestral, unevolved phage.

152 re have been no significant strain shifts or escape mutants noted since the introduction of rotavirus

153 Finally, we investigated an escape mutant of the dominant GP33-41 epitope that elici

154 ity, rates of virus evolution, and potential escape mutants of A/H2N2.

155 sible role of outer surface protein A (OspA) escape mutants of Borrelia burgdorferi in decreasing the

156 Here, we show that escape mutants of GBS expressing one-repeat alpha C prot

157 Cytotoxic T lymphocytes select for virus escape mutants of HIV and SIV, and this limits the effec

158 protein would be less likely to promote the escape mutants of SARS-CoV-2 as frequently as did those

159 The emergence of new escape mutants of the severe acute respiratory syndrome

160 ctedly, given the complete dependence of the escape mutant on CCR5 for entry, monomeric gp120 protein

161 a HLA-B27 restricted cytotoxic T lymphocyte escape mutant on the nucleoprotein that emerged in the 1

162 n site-specific mutants, monoclonal antibody escape mutants, or field isolates.

163 erating enhanced protection against pathogen escape mutants, or novel specificities after vaccination

164 he present study, we report the isolation of escape mutant phage that are able to replicate more effi

165 , leading to high potential for evolution of escape mutant populations.

166 with the wild-type virus revealed that some escape mutants possessing an amino acid substitution oth

167 The development of escape mutants potentially limits the efficacy of this n

168 ins a large number of cytotoxic T lymphocyte escape mutants, presenting another challenge to HIV cure

169 Competitive analysis of the escape mutants provides insights into the basis of siRNA

170 nts using single shRNAs, multiple SARS-CoV-2 escape mutants quickly emerged from infected cells withi

171 The in vitro selection of an HCV escape mutant recapitulates the ongoing evolution of ant

172 e responses, the longer-term impact of viral escape mutants remains unclear, as these variants can al

173 In chronic infection, HIV-1 escape mutants repopulate the plasma, and V3 and CD4bs n

174 To assess whether and how escape mutants resistant to IgG1b12 can be generated, we

175 of a new, perfect, antisense RNA against an escape mutant resulted in the inhibition of that mutant

176 luenza A virus and attempts to select for an escape mutant resulted in variants that conformed to hos

177 a panel of monoclonal antibody hemagglutinin escape mutants revealed a positive correlation between r

178 The genotypic analysis of escape mutants revealed a unique putative epitope region

179 In vitro selection of antibody escape mutants revealed that 53C10 recognizes a novel no

180 ural and biochemical analyses and engineered escape mutants revealed that these inhibitors restrict a

181 Vaccine escape mutants selected by NA exposure were frequent and

182 Sequence changes in escape mutants selected by these antibodies occur in two

183 A/NWS/33(HA)-A/Mem/31/98(NA) (H1N2) and nine escape mutants selected by these monoclonal antibodies.

184 The escape mutants selected in infected patients can be tran

185 Neutralization escape mutants selected with MAb A6.2.1 contained a leuc

186 The in vitro immune escape mutant selection method used in this study could

187 Based on our escape mutant sequence analysis, previously predicted do

188 three positions, two of which overlap known escape mutant sites.

189 However, there is a risk of selecting viral escape mutants, so a new combination is needed using dif

190 these were mapped in distinct epitopes using escape mutants, structure analyses, and competition assa

191 Sequence analysis of the evolution of the escape mutants suggested that the most relevant changes

192 tibodies decrease the in vitro generation of escape mutants, suggesting their potential in mitigating

193 and also has less risk of selection of PorA-escape mutants than a conventional OMV vaccine.

194 thought to have a higher genetic barrier to escape mutants than directly acting antivirals, yet ther

195 A DENV-4 escape mutant that contained a Lys174-Glu substitution i

196 An escape mutant that leads to a slightly longer infection

197 Escape mutants that alleviate this burden can rapidly ev

198 Evidence of HBsAg escape mutants that are undetected by commercial assays

199 dies, we previously identified H9N2 antibody escape mutants that contained deletions of amino acids i

200 First, CBH-2 escape mutants that contained mutations at D431G or A439

201 pressed, preventing the evolution of antigen escape mutants that drive resistance to CAR T cell thera

202 , these neutralizing antibodies selected for escape mutants that harbored substitutions and deletions

203 iduals; however, the virus often rebounds by escape mutants that have evolved resistance.

204 alize the TF virus but also can select virus escape mutants that in turn select affinity-matured neut

205 essure in patients to drive the evolution of escape mutants that lead to sustained chromatin occupanc

206 hat aims to decrease the potential for virus escape mutants that might arise in response to selective

207 genic drift, the rapid emergence of antibody escape mutants that precludes durable vaccination.

208 olution and between-host transmission of CTL escape mutants that predicts the prevalence of escape mu

209 A-B*57, are associated with the selection of escape mutants that reduce viral replicative capacity.

210 ification, we selected a population of viral escape mutants that resist stringent neutralization with

211 envelope region (loop D) and selected virus escape mutants that resulted in both enhanced bnAb linea

212 udies with past influenza viruses identified escape mutants that were antigenically similar to varian

213 not against the emergence of neutralization escape mutants that were found to be already present in

214 accinated mice challenged with WT vs. H28-A2 escape mutants, the selective advantage conferred by gly

215 been demonstrated in previous studies of CTL escape mutants, this is the first illustration of signif

216 HN proteins, and the characterization of an escape mutant to localize the binding site of AVS-I to t

217 Furthermore, a neutralization escape mutant to one of the antibodies (b12) selected in

218 fic host conditions are required for epitope escape mutants to display increased virulence, and the N

219 immune pressure that quickly selects epitope escape mutants to gp33-41.

220 anisms of CTL and reveal the possibility for escape mutants to prevail in the hostile environment of

221 No escape mutants to serotype 3-specific MAbs could be gene

222 We find here that allosteric escape mutants to the most broadly neutralizing antibodi

223 ession on the potential development of virus escape mutants using a permissive T-cell line cultured u

224 e present study, we generated neutralization-escape mutants, using 6 different monoclonal antibodies,

225 have broad strain recognition, and the only escape mutants, V339I and D348E, are located on the C'D'

226 hemagglutinin antigenic sites by generating escape mutant variants against the neutralizing antibodi

227 Both in vitro and in vivo, individual RSV PZ escape mutants varied in their susceptibility to PZ.

228 T cells selected for epitope-specific viral escape mutants via a perforin-dependent pathway.

229 Epitope mapping of the neutralizing mAbs via escape mutant virus generation revealed a shared binding

230 We observed that each individual escape mutant virus was able to avoid neutralization by

231 We generated an escape mutant virus with resistance to an N peptide and

232 o viral RNA in virions of wild-type, but not escape mutant, virus.

233 Three of four escape mutant viruses had increased lethality in the DBA

234 sion machinery, and the selection of COV1-65 escape mutant viruses identified critical residues Y886H

235 ure on the HA stalk can lead to expansion of escape mutant viruses in study participants challenged w

236 Interestingly, in mice the neutralization escape mutant viruses showed either attenuation (Urbani

237 To investigate the potential threat of serum escape mutant viruses to humans and poultry, the impact

238 Competitive growth of the escape mutant viruses with the wild-type virus revealed

239 ess HIV-1 replication, but also select HIV-1 escape mutant viruses.

240 inin interacting with the MAbs, we generated escape mutant viruses.

241 hich suggests that the rate of generation of escape mutants was a significant factor in the efficacy

242 ic sequencing, no evidence of neutralization-escape mutants was detected.CONCLUSIONIn adults hospital

243 However, the diversity of escape mutants was highly restricted since only two type

244 pe, revealed that attenuation of the epitope escape mutants was not due to the loss of a pathogenic i

245 ndicated that the net selective advantage of escape mutants was slight, further underscoring the impo

246 lay epitope mapping assay and neutralization escape mutant, we show that mAb11 recognizes the fusion

247 re a response to emergence of neutralization escape mutants, we cloned expressed and characterized en

248 ctra of wild-type and the A92E and G94D CypA escape mutants, we demonstrate that assembled CA is dyna

249 be subject to sequence variations leading to escape mutants, we examined sequence variations of one I

250 he antibodies in vivo, as mice infected with escape mutants were 100% protected after only a single t

251 The mutations present in five of the escape mutants were determined by DNA sequencing.

252 tope achieved fitness-balanced escape, these escape mutants were each maintained in the viral populat

253 Furthermore, AbiA escape mutants were found to be insensitive to AbiJ, whi

254 Two escape mutants were identified; one had all 7 bp deleted

255 Escape mutants were not generated after treatment with a

256 ls [PBMCs]; not significant [NS]), and viral escape mutants were observed in both KY9 and KK10, resul

257 g mutations within the S510 epitope (epitope escape mutants) were associated with persistent virus an

258 azeb protects against the rapid emergence of escape mutants, whereas monotherapies even against conse

259 scFv before inoculation into mice grew into escape mutants, whereas spirochetes incubated with an ir

260 ed in previous studies, we isolated 66 phage escape mutants which had become insensitive to 13 distin

261 229 features a high barrier for selection of escape mutants, which are rare and associated with reduc

262 The establishment of tumor escape mutants, which can be driven by innate and/or ada

263 ses while decreasing the prevalence of viral escape mutants, which could cause the therapeutic to no

264 rotein on 80R versus ACE2 binding, including escape mutants, which should facilitate the design of im

265 gens might play a role in generating vaccine-escape mutants, while substitutions at positions S195D a

266 our results indicate that chimeric/deletion escape mutants will be killed as well.

267 Escape mutants with a change at 198 have reduced NA acti

268 tment with P28 alone led to the emergence of escape mutants with mutations in the P28 target region.

269 Selection of escape mutants with mutations within the target sequence

270 HIV escape mutants with reduced sensitivity to ALLINIs commo

271 ically to increase immune escape, (2) immune-escape mutants with replication deficiencies relative to

272 ail and used to select a total of 26 unique 'escape' mutants with substitutions across nine different

273 ressure can lead to the development of viral escape mutants, with consequent loss of immune control.

274 hesis that natural selection has favored CTL escape mutants within an infected host.

275 rus infection and that this response selects escape mutants within the epitope.

276 nd the replacement of wild-type virus by CTL escape mutants within the latent reservoir.