ライフサイエンスコーパス: escape mutation

1 lymphocyte responses and frequency of viral escape mutation.

2 ventually be overwhelmed by viral growth and escape mutation.

3 R could lead to better protection from viral escape mutation.

4 ell response, with a>=50% loss defined as an escape mutation.

5 al logs; sequence analysis revealed no viral escape mutation.

6 rgeting the same surface often have distinct escape mutations.

7 se with enhanced fitness due to reversion of escape mutations.

8 , the virus typically evolves several immune escape mutations.

9 notype determination and detection of immune escape mutations.

10 lineages following selection after acquiring escape mutations.

11 licative defects imparted by the deleterious escape mutations.

12 lly arise concomitantly with Gag(181-189)CM9 escape mutations.

13 region that does not tolerate neutralization escape mutations.

14 with the positions of the previously mapped escape mutations.

15 ical epitopes to determine the importance of escape mutations.

16 residue (tryptophan at position 4) prone to escape mutations.

17 ell responses through the development of CD8 escape mutations.

18 as indicated by the rapid emergence of viral escape mutations.

19 with the rapid development of neutralization escape mutations.

20 l or de novo responses against epitopes with escape mutations.

21 indicative of reversions of transmitted CD8 escape mutations.

22 ll epitopes leads to the rapid appearance of escape mutations.

23 o replicative fitness of viruses bearing the escape mutations.

24 fection were maintained and there were no Th escape mutations.

25 ial passages in cultured cells to select for escape mutations.

26 6), respectively, and could represent immune escape mutations.

27 d impact on the emergence and persistence of escape mutations.

28 ng immune pressure as an important driver of escape mutations.

29 yielding HIV strains with antibody- and drug-escape mutations.

30 p mutational scanning, to catalogue antibody escape mutations.

31 eir ability to predict biologically relevant escape mutations.

32 imarily as a result of neutralizing antibody escape mutations.

33 also occurs in the presence of selected CTL escape mutations.

34 ects should be considered when analyzing HIV escape mutations.

35 ral effector functions or selected for viral escape mutations.

36 s performed, to monitor for the emergence of escape mutations.

37 ell epitopes that functionally act as immune escape mutations.

38 e basis of analysis of mutants with antibody escape mutations.

39 aints limit the available sites tolerable to escape mutations.

40 ed to target epitopes that do not accumulate escape mutations.

41 wever, immune control is undermined by viral escape mutations.

42 target epitopes and the development of viral escape mutations.

43 %) of T cell epitopes harbored no detectable escape mutations.

44 ed to target epitopes that do not accumulate escape mutations.

45 bilization in the absence of Gag(181-189)CM9 escape mutations.

46 g to the same RBD surface but have different escape mutations.

47 ase the genetic barrier for the emergence of escape mutations.

48 sure on viral diversity and potential immune-escape mutations.

49 To examine how escape mutations affect the presentation and recognition

50 Escape mutations affected 47% of supertype epitopes, whi

51 ed how interference between these concurrent escape mutations affects their escape rates in systems w

52 The escape mutations all mapped to the same phage genome seg

53 Furthermore, the progeny accumulated CRISPR escape mutations, allowing rapid evolution of mutant pha

54 tenuation through Gag-specific CD8(+) T-cell escape mutations, among other factors, in the control of

55 sistent decay of CTL responses after epitope escape mutation and provide insight into potential mecha

56 ly, 1-18 is not susceptible to typical CD4bs escape mutations and effectively overcomes HIV-1 resista

57 g, and protein structural analyses to define escape mutations and mechanisms of neutralization escape

58 rug interaction surfaces less susceptible to escape mutations and potentiate the power of polypharmac

59 bed in terms of the cost-benefit tradeoff of escape mutations and predicts a trajectory in the cost-b

60 died viral evolution and the dynamics of CTL escape mutations and reversion of these mutations after

61 hway was characterized by acquisition of CTL escape mutations and the other by selection for wild-typ

62 Defining escape mutations and their dynamics will be useful in th

63 esting they may not be easily susceptible to escape mutations, and exhibit a lower binding:neutralizi

64 Most escape mutations appeared during acute infection and rem

65 NMD-escape mutations are additionally found to associate wit

66 Escape mutations are believed to be important contributo

67 etroviral drug-resistance mutations, epitope escape mutations are inconsistently observed.

68 We therefore infer that escape mutations are likely to be associated with weak f

69 observed pattern of escape, in which several escape mutations are observed transiently in an epitope.

70 low anti-HBs titer and the presence of HBsAg escape mutations are possible hypotheses to explain this

71 These escape mutations are rare and drug-specific, and some co

72 ve previously shown that while CD8(+) T-cell escape mutations are rarely seen in proviral Gag sequenc

73 cross four independent melanoma cohorts, NMD-escape mutations are significantly associated with clini

74 Neutralization escape mutations are widely distributed over the VP8* su

75 rictive for primary SIVsm isolates, although escape mutations arise late in infection.

76 CTL) epitopes impair T cell recognition, but escape mutations arising in flanking regions that alter

77 er the course of infection, an unusual viral escape mutation arose within the p6(Pol) epitope through

78 er, in a subset of HLA-B27(+) subjects, rare escape mutations arose at the HLA-B27 anchor residue, R(

79 tion in RC was significantly greater for CTL escape mutations associated with protective HLA class I

80 nhibit each other in vitro and select for an escape mutation at the same position on the EBOV glycopr

81 CTL epitopes accrue escape mutations at different rates in vivo.

82 ralization in their human hosts by acquiring escape mutations at epitopes of prevalent antibodies.

83 Rare alternative escape mutations at R(264) have been observed, but facto

84 We demonstrate that while escape mutations at residue 2633 (position 5) of the epi

85 complex forces limit the accumulation of CD8 escape mutations at the population level.

86 xogenous CypA escape protein, which contains escape mutations at the small RNA interference recogniti

87 viral load kinetics or magnitude or in viral escape mutations, but was associated with the evolution

88 However, it is now clear that CTL escape mutations can also confer a fitness cost, and the

89 on transmission to new hosts, these original escape mutations can be lost.

90 The observation that CTL escape mutations can carry an associated fitness cost in

91 rved sites on influenza proteins where viral escape mutations can result in large fitness costs [1].

92 oviral treatment or the emergence of epitope escape mutations, causes HIV-specific CD8 T cell respons

93 V entry blockers are in clinical trials, but escape mutations challenge their potential.

94 The escape mutations cluster on several surfaces of the RBD

95 of virions bearing GP that contain the Q508 escape mutation common to a number of virus-neutralizing

96 gnificantly reduced number of drug-resistant escape mutations compared to contemporary clinically-eva

97 odeficiency virus type 1 (HIV-1), leading to escape mutations compromising virologic control.

98 rimary HIV-1-specific T cells rapidly select escape mutations concurrent with falling virus load in a

99 ve cell therapy treated melanoma cohort, NMD-escape mutation count is the most significant biomarker

100 In recent years, methods that use escape mutation data to estimate rates of HIV escape hav

101 uman leukocyte antigen (HLA)-mediated immune-escape mutations defined by older analysis methods.

102 However, escape mutation depends on the net balance of selective

103 In cases in which multiple escape mutations developed within a targeted epitope, a

104 on of these upstream mutations with the rare escape mutations dramatically restored viral replication

105 Some studies reveal that the later these escape mutations emerge, the more slowly they go to fixa

106 es/ml for almost a decade until a nonbinding escape mutation emerged within the immunodominant CTL ep

107 of these studies included: (i) SIV Gag K165R escape mutations emerged in both plasma and cerebrospina

108 Envelope escape mutations emerged in rebound virus of mAb-treated

109 We ask how the rates at which an escape mutation emerges in a host who bears the restrict

110 Collectively, our findings indicate that escape mutation events have already occurred for half of

111 Reversion of escape mutations following HAART initiation was extremel

112 Escape mutations for most antibodies are present in some

113 de-off is limited by the small number of CTL escape mutations for which a fitness cost has been quant

114 otype determination, and detection of immune escape mutations from a single contiguous HBV sequence.

115 lication capacities, in part associated with escape mutations from cytotoxic-T-lymphocyte (CTL) respo

116 have been made to experimentally define the escape mutations from specific antibodies in specific vi

117 We then asked whether such CTL escape mutations had an impact equivalent to that seen f

118 Importantly, the majority of escape mutations had negative impacts on hDPP4 receptor

119 The selection of escape mutations has a major impact on immune control of

120 n viral persistence and development of viral escape mutations has been postulated.

121 ng human immunodeficiency virus (HIV) immune escape mutations has implications for understanding the

122 Although escape mutations have also been characterized in major h

123 CTL escape mutations have been identified in several chronic

124 Thus, escape mutations identified as HLA associated systematic

125 s, MAbs 8F8, 8M2, and 2G1 each elicited H2N2 escape mutations immediately adjacent to the receptor-bi

126 eplication competent and contained the T242N escape mutation in Gag, which is known to decrease viral

127 An early CD8(+) T-cell escape mutation in the dominant HLA-B57-restricted Gag e

128 t restore replication fitness reduced by the escape mutation in the epitope and by itself had little

129 YY9-specific CD8(+) T cells demonstrated an escape mutation in this epitope <3 wk postinfection, con

130 cial for controlling a variant virus with an escape mutation in this epitope.

131 -mediated DNA damage enriches for cells with escape mutations in a core CRISPR-p53 interactome, which

132 We first observed that escape mutations in a heterogeneous simian immunodeficie

133 A closer examination of CD8 escape mutations in additional persons with chronic dise

134 s-specific CD8+ T cells likely helps prevent escape mutations in chronic viral infections.

135 many-though not all-HIV-1 polymerase immune escape mutations in circulation over time.

136 help was associated with emergence of viral escape mutations in class I major histocompatibility com

137 These data suggest that CTL escape mutations in epitopes associated with suppression

138 Our results suggest that escape mutations in epitopes bound by "protective" MHC-I

139 CTL escape mutations in Gag and Nef were seen in the donors,

140 CD8 responses capable of selecting for viral escape mutations in highly conserved regions of the viru

141 re is a striking all or none pattern for CTL escape mutations in HIV-1 Gag epitopes.

142 ss I-restricted cytotoxic T-lymphocyte (CTL) escape mutations in HIV-1 that persist upon transmission

143 This revealed a loss of some escape mutations in HLA class I epitopes during pregnanc

144 t and impact of cytotoxic T lymphocyte (CTL) escape mutations in HLA-B*57+ ES.

145 previously predicted high genetic barrier to escape mutations in host-targeted antivirals.

146 rus-specific CD8(+) T lymphocytes select for escape mutations in human immunodeficiency virus (HIV) a

147 he emergence of cytotoxic T-lymphocyte (CTL) escape mutations in human immunodeficiency virus type 1

148 Cytotoxic-T-lymphocyte (CTL) escape mutations in human immunodeficiency viruses encod

149 roach to define better the role of reverting escape mutations in immune control of HIV infection.

150 an studies, direct evidence for emergence of escape mutations in immunodominant major histocompatibil

151 of viral replication required for generating escape mutations in individual lineages can be directly

152 Escape mutations in Mamu-A*01 epitopes appeared first in

153 the significance of possible neutralization escape mutations in mosquito and mammalian cells, mice,

154 s underscored by the consistent emergence of escape mutations in multiple CD8(+) T cell epitopes duri

155 predicting the impact of ZMapp on potential escape mutations in ongoing or future Ebola outbreaks.

156 The high frequency of emergence of escape mutations in parallel viral lineages at the Tat-S

157 vel measures, such as the time to detectable escape mutations in plasma and the rate these mutations

158 ference by CRISPR consists of acquisition of escape mutations in regions targeted by CRISPR.

159 relative rate of escape and the location of escape mutations in response to T-cell-mediated immune p

160 The appearance of escape mutations in SIV Gag p11C was coincident with com

161 However, the presence of escape mutations in the acute stage of infection has rai

162 strain and those infected with a virus with escape mutations in the capsid were compared.

163 trate the long-term stability of stereotypic escape mutations in the immunodominant HLA-B27-restricte

164 xic T-lymphocytes (CTLs) select for multiple escape mutations in the infecting HIV population.

165 erved no dose-limiting adverse events and no escape mutations in the miR-122 binding sites of the HCV

166 of deleterious cytotoxic T lymphocyte (CTL) escape mutations in the NS5B KSKKTPMGF epitope might imp

167 detected long before the appearance of viral escape mutations in the plasma.

168 es that was observed for clinically relevant escape mutations in the Pol gene.

169 , and potential accumulation, of CD8+ T-cell escape mutations in the population may suggest a gradual

170 s reimposed after childbirth, at which point escape mutations in these epitopes again predominated in

171 Additionally, characterizing escape mutations in these epitopes aids in identifying N

172 development of cytotoxic T-lymphocyte (CTL) escape mutations in these regions may significantly impa

173 Common CTL escape mutations in this epitope were identified from a

174 to effectively target Gag and select for CTL escape mutations in this gene.

175 The selection of rare CTL escape mutations in this HLA-B27-restricted epitope dram

176 A-B*5703-restricted CTL responses select for escape mutations in three Gag p24 epitopes, in a predict

177 infected macaques with a cloned SIV bearing escape mutations in three immunodominant CTL epitopes, a

178 immunodeficiency virus (SIV) bearing common escape mutations in three immunodominant CTL epitopes.

179 r the question, the RRCs were quantified for escape mutations in three immunodominant HLA-B*57/B*5801

180 Escape mutations in viral epitopes can, however, abrogat

181 outstanding questions regarding the role of escape mutations in viral persistence and their fate in

182 Initial escape mutations, including the addition of a key glycan

183 Escape mutations, including those with reduced VRC, can

184 ltiple cohorts confirmed HLA-B*51-associated escape mutations inside the epitope in genotype 3a, but

185 se mutations on viral fitness, we introduced escape mutations into 30 epitopes (bound by five major h

186 Introduction of these escape mutations into the parental virus conferred resis

187 In one of these defined epitopes, escape mutations involving the substitution of amino aci

188 Escape mutation is a mechanism associated with OBI, whic

189 Critically, CR8020 escape mutation is seen in certain H7N9 viruses from rec

190 average sample size required to identify an escape mutation is smaller if the mutation escapes and r

191 benefit of transmitted HLA-B*5703-associated escape mutations is abrogated by the increase in viral l

192 individual-to-individual variation in viral escape mutations is not present among ferrets that have

193 of identifying cytotoxic-T-lymphocyte (CTL) escape mutations is to search for statistical associatio

194 the simian immunodeficiency virus (SIV) Gag escape mutation K165R in HAART-treated SIV-infected pigt

195 We show that "escape" mutations lower affinity of the NS3 protease for

196 Therefore, complete escape-mutation maps enable rational design of antibody

197 A new study now shows that one HIV-1 escape mutation may also result in impaired dendritic ce

198 Such viral escape mutations may (i) prevent peptide processing, (ii

199 However, escape mutations may give rise to new epitopes that coul

200 This possibly reflects an escape mutation mechanism to evade detection by the host

201 y, the SIVmac239 challenge virus accumulated escape mutations more rapidly in animals that received c

202 complex interplay of the immune response and escape mutation of the virus quasispecies inside a singl

203 e studied and by an analysis of all reported escape mutations of defined CTL epitopes in the HIV Immu

204 control, human immunodeficiency virus (HIV) escape mutations often arise in immunodominant epitopes

205 d studied the effect of these neutralization escape mutations on human and animal receptor usage as w

206 d studied the effect of these neutralization-escape mutations on in vitro and in vivo fitness.

207 Analysis of viral escape mutations on m157 that render it resistant to NK

208 ons capable of alleviating the impact of CD8 escape mutations on replication capacity may enable thei

209 Individually, the impact of the escape mutations on RRC was comparable to that of M184V,

210 The distribution of escape mutations on the DS-1 VP8* core indicates that ne

211 ng HIV-1 evolution and for the impact of CD8 escape mutations on viral fitness.

212 y observed, suggesting an impact of most CTL escape mutations on viral replication.

213 secretion defect caused by the G145R immune-escape mutation or mutation at N146, the site of N-linke

214 associated with transmitted or acquired CTL escape mutations or transmitted drug resistance mutation

215 g. transmitted cytotoxic T- lymphocyte (CTL) escape mutations) or infant factors (e.g. reduced CTL fu

216 CTL responses, an increased fitness cost of escape mutations, or an increased diversity of the CTL r

217 = 2 x 10(-10)) and functionally through CTL escape mutation (P = 2 x 10(-8)).

218 valent HBV contained antibody neutralization escape mutations (P = .01).

219 itude of the reductions in RRC caused by the escape mutations, particularly when coexpressed, suggest

220 ophylactic and therapeutic agents, but viral escape mutations pose a major challenge.

221 Antibody escape mutations pose a significant challenge to the eff

222 rt of HLA-B*27/57/58:01/81:01-associated Gag escape mutations previously shown to incur a fitness cos

223 cond, under the selective pressure of HC-11, escape mutations progressed from a single L438F substitu

224 Here, we illustrate that the CTL escape mutation R(264)K in the HLA-B27-restricted KK10 e

225 Additionally, the escape mutation R189S in V2, which conferred resistance

226 ia reveals an unexpectedly high level of CTL escape mutations reflecting selective pressure acting at

227 virus type 1 (HIV-1) cytotoxic T-lymphocyte escape mutations represent both a major reason for loss

228 The predominant escape mutations represented conservative substitutions

229 Moreover, this escape mutation represents a novel mechanism whereby HIV

230 CTL escape mutations restricted by protective HLA class I mo

231 wer than 10% of epitopes containing maternal escape mutations reverted to the consensus sequence foll

232 possible emergence of viruses carrying stalk escape mutation(s) under sufficient immune pressure.

233 ven by the HLA-B*57:03-KF11 response for the escape mutation S173T.

234 st, the occurrence of distinct, HLA-specific escape mutation; second, the recruitment of distinct TCR

235 that the Mem5 antibody binds at the sites of escape mutation selected by the other antibodies.

236 e regions of high mobility include the known escape mutation site for the neutralizing antibody A6.2

237 We show that the identified escape mutations stabilize the ground state of the envel

238 We further show that this escape mutation substantially diminished viral fitness i

239 Mapping viral escape mutations suggested that these antibodies bind at

240 ccurring HLA-B57- and HLA-B27-associated CTL escape mutations T242N and R264K resulted in delayed cap

241 The typical escape mutation (T242N) within this epitope diminishes v

242 ficant correlation between the number of Gag escape mutations targeted by specific HLA-B allele-restr

243 responses leaves predictable combinations of escape mutations, termed HLA "footprints." The most clea

244 tive subjects drove positive selection of an escape mutation that reverted to wild-type after transmi

245 tributes to persistent infection by evolving escape mutations that attenuate binding of inhibitory an

246 hment of hepatitis B surface antigen vaccine-escape mutations that could have played a crucial role i

247 response and identify novel VRC13-associated escape mutations that may be important to inducing VRC13

248 responses are those driving the selection of escape mutations that reduce viral fitness and therefore

249 ocyte (CTL) responses drive the selection of escape mutations that reduce viral replication capacity

250 majority (>98%) of latent viruses carry CTL escape mutations that render infected cells insensitive

251 However, the virus rapidly acquires "escape mutations" that reduce CD8(+) T cell recognition

252 tingly, transmission of an HLA-B8-associated escape mutation to an HLA-B8 negative subject resulted i

253 ver, have highlighted the propensity of some escape mutations to revert upon transmission to a new ho

254 CTL arise in acute infection, causing escape mutations to spread rapidly through the populatio

255 improvements, which could reduce the risk of escape mutations to this therapeutic modality.

256 ing of viral fitness loss resulting from CTL escape mutations together with strong CD8 T-cell immune

257 Whether this intrapatient accumulation of escape mutations translates into HIV evolution at the po

258 Cytotoxic-T-lymphocyte (CTL) escape mutations undermine the durability of effective h

259 smitted mutations and the impact of specific escape mutations upon viral replication suggest that com

260 ss cost of the 29 most common HIV-1B Gag CTL escape mutations using an in vitro RC assay.

261 A viral population with >/=1 immune-escape mutation was found in 53.2% of patients (intrapat

262 ion and the colocalization of neutralization escape mutations, we conclude that N-linked carbohydrate

263 d to hemagglutinins carrying combinations of escape mutations, we developed an exponential protein ba

264 ally assessing the effect of a subset of the escape mutations, we show that they resulted in a loss o

265 As predicted, these immune escape mutations were also observed in the field viruses

266 ion of viral replication, (ii) SIV K165R Gag escape mutations were archived in latent proviral DNA re

267 rhTRIM5alpha study, the mapped huTRIM5alpha escape mutations were distributed across the capsid exte

268 Escape mutations were identified at position 129, 165, o

269 to the results of the previous study, fewer escape mutations were identified, with particular mutant

270 Escape mutations were mapped upon a three-dimensional (3

271 Gag and RT escape mutations were monoclonal intra-epitope substitut

272 os HIV-1 database, we show that emerging CTL escape mutations were more often present at lower freque

273 Putative escape mutations were often rapidly replaced with mutual

274 Escape mutations were oligoclonal, suggesting fitness co

275 nd (iii) replication-competent SIV Gag K165R escape mutations were present in the resting CD4(+) T ce

276 Escape mutations were used to map the site of action for

277 observed in the ability of CTL to select for escape mutation when targeting the same epitope but rest

278 rise as a result of positive selection of an escape mutation, which is stable on transmission and the

279 indications of cytotoxic T lymphocyte (CTL) escape mutations while reversions appeared limited.

280 e alters VRC, and HIV-specific CTLs inducing escape mutations with fitness costs in this region may b

281 tect the emergence of viral variants bearing escape mutations with frequencies as low as 1% of the ci

282 pproach to efficiently identify enhancing or escaping mutations, with many then employing this inform

283 A second escape mutation within the epitope, by contrast, was mai

284 approach successfully identified 6 known CTL escape mutations within 3 Mane-A1*084-restricted epitope

285 n spite of the rapid development of multiple escape mutations within cytotoxic T lymphocyte epitopes.

286 tensive analysis of one subject for whom all escape mutations within defined CTL epitopes were studie

287 at the earliest time point tested, signature escape mutations within Gag that likewise impair viral r

288 ata show that the process of accumulation of escape mutations within HIV is not inevitable.

289 nstrate that dominant HLA-B27-associated CTL escape mutations within HIV-1 capsid lead to enhanced ca

290 investigate the generation and selection of escape mutations within individual viral lineages at the

291 ncy to drive multisite and/or anchor residue escape mutations within known CTL epitopes, and the abil

292 ther, these data demonstrate that CTL-driven escape mutations within p24 Gag restricted by protective

293 Escape mutations within the bNAb epitopes did not arise

294 CTL-mediated immune pressure selects escape mutations within the CTL epitope.

295 Furthermore, cytotoxic T lymphocyte (CTL) escape mutations within the immunodominant HLA-B57 (Bw4)

296 se data suggest that the selection of costly escape mutations within the immunodominant NS5B KSKKTPMG

297 utologous viral sequences did not reveal any escape mutations within the targeted epitope, and viral

298 ed epitopes, mother-to-child transmission of escape mutations within these epitopes could nullify its

299 We identified a unique pattern of escape mutations within this epitope in a large cohort o

300 equencing revealed the universal presence of escape mutations within TW10 among B57- and B5801-positi