ライフサイエンスコーパス: escape mutant

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

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

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

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

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

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

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

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

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

10 ereby reducing the probability of generating escape mutants.

11 e emergence and competitive advantage of CTL escape mutants.

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

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

14 that such variants represent neutralization escape mutants.

15 evolution of antiviral resistance or vaccine-escape mutants.

16 immune pressure leading to the selection of escape mutants.

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

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

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

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

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

22 antiviral-resistant variants and host immune escape mutants.

23 ll immunity against commonly occurring virus escape mutants.

24 esistance and increasing the risk of vaccine escape mutants.

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

26 uppressed viral replication and generated no escape mutants.

27 ations of a neutralizing antibody to isolate escape mutants.

28 ll responses and limits recognition of viral escape mutants.

29 at these plasma Nef variants represent novel escape mutants.

30 topes and minimizes the likely generation of escape mutants.

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

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

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

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

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

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

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

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

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

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

41 Escape mutant assays identified five amino acid residues

42 1H3 selects an escape mutant at amino acid 273 on EBOV GP.

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

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

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

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

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

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

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

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

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

52 The escape mutants contain multiple nef mutations that impai

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Selecting escape mutants from parental versus sequential variants

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

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

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

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

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

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

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

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

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

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

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

79 Selection for escape mutant immunodeficiency viruses by cytotoxic T ly

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 Vaccine escape mutants selected by NA exposure were frequent and

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

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

125 The escape mutants selected in infected patients can be tran

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

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

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

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

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

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

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

133 An escape mutant that leads to a slightly longer infection

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 Selection of escape mutants with mutations within the target sequence

184 HIV escape mutants with reduced sensitivity to ALLINIs commo

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

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

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

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

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

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