ライフサイエンスコーパス: escape mutation

1 lymphocyte responses and frequency of viral escape mutation.

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

3 ventually be overwhelmed by viral growth and escape mutation.

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

5 licative defects imparted by the deleterious escape mutations.

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

7 region that does not tolerate neutralization escape mutations.

8 with the positions of the previously mapped escape mutations.

9 imarily as a result of neutralizing antibody escape mutations.

10 ical epitopes to determine the importance of escape mutations.

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

12 ell responses through the development of CD8 escape mutations.

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

14 ects should be considered when analyzing HIV escape mutations.

15 with the rapid development of neutralization escape mutations.

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

17 indicative of reversions of transmitted CD8 escape mutations.

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

19 o replicative fitness of viruses bearing the escape mutations.

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

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

22 ell epitopes that functionally act as immune escape mutations.

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

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

25 aints limit the available sites tolerable to escape mutations.

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

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

28 target epitopes and the development of viral escape mutations.

29 p mutational scanning, to catalogue antibody escape mutations.

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

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

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

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

34 eir ability to predict biologically relevant escape mutations.

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

36 , the virus typically evolves several immune escape mutations.

37 notype determination and detection of immune escape mutations.

38 To examine how escape mutations affect the presentation and recognition

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

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

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

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

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

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

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

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

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

48 Most escape mutations appeared during acute infection and rem

49 Escape mutations are believed to be important contributo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 Reversion of escape mutations following HAART initiation was extremel

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

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

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

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

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

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

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

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

95 Although escape mutations have also been characterized in major h

96 CTL escape mutations have been identified in several chronic

97 Thus, escape mutations identified as HLA associated systematic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 Escape mutations in viral epitopes can, however, abrogat

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

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

149 Escape mutations, including those with reduced VRC, can

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

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

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

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

154 Escape mutation is a mechanism associated with OBI, whic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 = 2 x 10(-10)) and functionally through CTL escape mutation (P = 2 x 10(-8)).

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

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

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

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

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

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

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

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

190 The predominant escape mutations represented conservative substitutions

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

192 CTL escape mutations restricted by protective HLA class I mo

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

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

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

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

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

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

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

200 Mapping viral escape mutations suggested that these antibodies bind at

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Putative escape mutations were often rapidly replaced with mutual

229 Escape mutations were oligoclonal, suggesting fitness co

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 Escape mutations within the bNAb epitopes did not arise

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

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

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

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

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

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

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