ライフサイエンスコーパス: escape variant

1 against infection with the DBN3a sofosbuvir escape variant.

2 ss-reactive immune responses against the Gag escape variant.

3 vent the emergence of cytotoxic T-lymphocyte escape variants.

4 o immune editing and recognize newly arising escape variants.

5 mother-to-child transmission of CD8+ T cell escape variants.

6 , hence, a greater efficiency in controlling escape variants.

7 a-mIgG), can select different populations of escape variants.

8 is is not due to the evolution of new immune escape variants.

9 gh functional avidity can rapidly select for escape variants.

10 es of pulmonary immunity in selection of CTL escape variants.

11 tumor growth but not the later appearance of escape variants.

12 for years without inducing detectable viral escape variants.

13 cantly reduced the emergence of immunoedited escape variants.

14 bs by preventing the emergence of bNAb viral escape variants.

15 as well as those that do rapidly select for escape variants.

16 to prevent the emergence of fully functional escape variants.

17 ork that could provide protection from virus-escape variants.

18 ich was consistent with immune selection for escape variants.

19 which give rise to drug-resistant and immune escape variants.

20 ons of residues that are mutated in antibody escape variants.

21 rs and help protect against the emergence of escape variants.

22 termined targets and are prone to select for escape variants.

23 ion without the emergence of S1P-independent escape variants.

24 h PSC-RANTES were analyzed for possible drug escape variants.

25 key contributor for the selection of immune escape variants.

26 y, resulting in the continuous generation of escape variants.

27 e animal to mount secondary responses to the escaped variants.

28 over several weeks without the emergence of escape variants able to use other cellular proteases for

29 n at position 6 (L6M), which arises as a CTL escape variant after primary infection but is sufficient

30 ease and the emergence of antigen-loss tumor escape variants after treatment demonstrate the need to

31 sis of representative variants revealed that escape variants also induced NAbs within a few weeks of

32 oceeded by neutralizing Ab production to the escape variant and subsequent escape.

33 ral pathogenesis and the emergence of immune escape variants and for design of vaccine strategies.

34 However, antigen-loss tumor escape variants and the absence of currently targeted an

35 aid in the prediction of potential antigenic escape variants and the selection of future vaccine cand

36 ted in the rapid selection of neutralization escape variants and treatment failure in mice.

37 enotype 1-7 prototype isolates and resistant escape variants, and investigated the effects of pre-exi

38 c T helper cells, the emergence of antigenic escape variants, and the expression of an envelope compl

39 nvergent microevolution, appear to be immune-escape variants, and were evolutionarily constrained at

40 addition to the emergence of HVR-1 antibody escape variants are involved in maintaining viral persis

41 Tumor escape variants are likely to emerge after treatment wit

42 receptors and thus still be immunogenic when escape variants are passed to individuals expressing the

43 plex provide a strong basis for why some CTL escape variants are selected, our results also show that

44 Patterns of immune escape variants are similar in HIV type 1-infected human

45 ell responses that do not rapidly select for escape variants are unable to control viral replication

46 The results demonstrate that neutralization-escape variants arise periodically in HIV-1-infected lon

47 eradicate virus did not reflect selection of escape variants because the gag epitope remained unmutat

48 g to HLA-B57, suggesting that sensing of CTL escape variants by NK cells can contribute to the protec

49 his antigenic redundancy may prevent vaccine escape variants by recombinational loss, which is freque

50 preclinical models of glioblastoma, antigen escape variants can lead to tumor recurrence after treat

51 None of the escape variants caused breakthrough replication in LTNPs

52 ian reservoir host, during which time immune escape variants continually arise in part because of var

53 These findings indicate that sofosbuvir escape variants could compromise the effectiveness of nu

54 iation of therapy, and then finally to a new escape variant during continued therapy.

55 t(28-35) SL8, which reproducibly selects for escape variants during acute infection, and Gag(181-189)

56 rapy and for the selection of neutralization escape variants during hE16 treatment.

57 T-lymphocyte responses select for new viral escape variants during the acute phase of infection.

58 system cannot control tumor growth, but how escape variants emerge during immunotherapy remains poor

59 es exert selective pressure on the virus but escape variants emerge within a short period of time.

60 Escape variants emerged rapidly in the group 1 vaccinees

61 Our results suggest that some escape variant epitopes evolving in infected individuals

62 e parental West Nile virus, a neutralization escape variant failed to cause lethal encephalitis (at h

63 hree were on-drug relapses, with the CD19(-) escape variant first detected after only 2 treatment cou

64 We also selected antigenic escape variants from human viruses treated with convales

65 Engineered escape variants had high levels of fitness.

66 CTLs in viral clearance and selection of CTL escape variants have been evaluated.

67 ical peptide and KIR binding residues of the escape variants have selectively converged to resemble t

68 ls significantly faster (P = 0.004) and that escape variants have significantly higher fitness costs

69 HBV) genome able to explain an immunological escape variant.HBV genome has a very compact coding orga

70 inhibited NA activity but did not result in escape variants, highlighting its suitability for develo

71 us epitopes tested represented potential CTL escape variants; however, in most cases strong responses

72 immunodeficiency virus type 1 generate viral escape variants; however, the mechanisms of escape are n

73 Selection of immune escape variants impairs the ability of the immune system

74 g oligoclonality resulted in an LCMV epitope escape variant in vivo resembling the natural Lassa viru

75 uble mutant (E1-K61T E2-D59N) neutralization escape variant in WT mice.

76 t an example of shifting immune responses to escape variants in a patient with sequential metastases

77 Here, we describe the evolution of antigenic escape variants in a rhesus macaque that developed unusu

78 The occurrence of viral escape variants in an N6-LS-monotreated animal, however,

79 CD8(+) T lymphocytes (CD8-TL) select viral escape variants in both human immunodeficiency virus and

80 (Nef(165-173)IW9) typically select for viral escape variants in early SIV(mac)239 infection.

81 Maintenance of such escape variants in human populations could pose an obsta

82 r could function to prevent the emergence of escape variants in infected hosts.

83 hat have the potential to rapidly select for escape variants in the early phase of infection are need

84 ocument transmission of viruses encoding CTL escape variants in this dominant Gag epitope that no lon

85 tive inhibitor of NA activity selected pH1N1 escape variants in vivo.

86 ng disclosed highly aberrant CTCs as therapy-escaping variants in breast cancer.

87 ast to influenza viruses for which 4-GU-DANA escape variants include hemagglutinin mutants with decre

88 city CD8(+) T cells led to the appearance of escape variants, indicating that broader epitope specifi

89 contrast to the relatively high frequency of escape variants initially observed, the subsequent emerg

90 also suggested that the number of potential escape variants is limited by previous exposure to seaso

91 An escape variant, J178V, was generated in vitro, and the l

92 ation, preemptive immunization against these escape variants led to the generation of secondary CD8(+

93 bility of emergence of S1P-independent viral escape variants make S1P-mediated GPC processing by pept

94 Mother-to-child transmission of CD8+ T cell escape variants may particularly affect CD8+ T cell reco

95 ve described previously the generation of an escape variant of human immunodeficiency virus type 1 (H

96 ajority of the subjects targeted the G(357)S escape variant of the Gag(349-359) epitope, while the wi

97 a demonstrate that de novo responses against escape variants of CD8(+) T-cell epitopes can be generat

98 Neutralization-escape variants of human immunodeficiency virus type 1 (

99 y tract is a suitable site for generation of escape variants of influenza virus selected by CTL in vi

100 body was mapped by sequencing neutralization escape variants of the virus.

101 HIV-infected cells and recognized all common escape variants of this epitope.

102 mutation, which leads to the generation of 'escape' variants of HCV that persist as a quasi-species

103 f emergence and the biological impact of CTL escape variants on the clinical outcome of influenza pne

104 We investigated to what extent reactivity to escape variant peptides in standard enzyme-linked immuno

105 However, recognition of escape variant peptides was commonly observed in both EC

106 e (CTL) selection of hepatitis C virus (HCV) escape variants plays a role in HCV persistence.

107 Escape variant populations derived by propagating suscep

108 including two that do not rapidly select for escape variants, predominated during early m3KODeltanef

109 TL-targeted epitope changed from an apparent escape variant prior to the initiation of therapy, to th

110 An understanding of ZM1 and other escape variants provides insight into the effects of thi

111 If an escape variant reaches fixation in the population, the e

112 We conclude that selection of viral CTL escape variants reflects coordinate action between the t

113 These CTL escape variants remain stable without reversion in the a

114 Selection of an escape variant revealed that NS5A is directly or indirec

115 studied, although the spectrum of viral CTL escape variants selected varied profoundly.

116 All escape variants showed evidence of mild clinical attenua

117 Three out four huTRIM5alpha escape variants showed resistance to all primate TRIM5al

118 ame donor were able to neutralize some VRC01 escape variants, suggesting that CD4bs antibodies contin

119 A common acute escape variant, T170I, unexpectedly and uniquely degrade

120 Tumor escape variants (TEV) recovered from the lungs of CTL-tr

121 Interestingly, the one escape variant that was detected proved to be a CTL anta

122 he patients were infected with potential CTL escape variants that contained nonimmunogenic and noncro

123 This implies that many pathogen epitope escape variants that could manifest as single amino-acid

124 riving the development of more complex viral escape variants that disrupt antigen presentation.

125 ineered receptors, enabling the formation of escape variants that elude CAR T cell targeting.

126 es not appear to be a result of selection of escape variants that lack the MAb 2H1 epitope.

127 dy (aNAB) in selective transmission of HIV-1 escape variants to infants.

128 These data suggest that TW10 escape variants undergo a postentry block that is partia

129 to capture a wild-type and a neutralization escape variant virus equally well.

130 MAb resistance, we engineered neutralization escape variant viruses (E1-K61T, E2-D59N, and the double

131 ngly, we found evidence for the selection of escape variant viruses by CTL specific for Nef(159-167)

132 These so-called "CTL escape variant viruses" are commonly selected during per

133 gnition of cells infected with corresponding escape variant viruses.

134 developed clinical disease, and harbored CTL escape variant viruses.

135 otecting from the selective outgrowth of CTL escape variant viruses.

136 Transmission of escape variants was confirmed.

137 e to TL-3, a panel of chronological in vitro escape variants was generated.

138 Thus, a less-restricted repertoire of escape variants was observed in mice with an intact perf

139 served, the subsequent emergence rate of CTL escape variants was very low.

140 Based on selection of escape variants, we show that D1-8 targets a novel epito

141 alence of subtypes/genotypes and drug/immune-escape variants were characterized by comparing recently

142 with control of viremia, and neutralization escape variants were detected concurrently with the gene

143 Several CD8+ T cell escape variants were detected in maternal plasma.

144 Neutralization escape variants were discovered shortly thereafter, and,

145 Emerging escape variants were generally resistant to the related

146 Several HIV-1 CD8(+) T cell escape variants were identified within maternal plasma v

147 Escape variants were observed at different time points w

148 e expression efficiency, as well as antibody escape variants, were also identified.

149 iding broad neutralization and prevention of escape variants when combined with other nAbs that targe

150 rtoire that fails to recognize specific KF11 escape variants which frequently arise in clade C-infect

151 ressure from pathogen decoys selects for IgA escape variants which, in turn, selects for FcalphaRI va

152 dren exhibited a robust response to the TW10 escape variant while recognizing the wild-type epitope w

153 3a to sofosbuvir led to identification of an escape variant with substitutions in NS5B, including the

154 Escape variants with alterations in the lgtG repeat trac

155 of mouse hepatitis virus, which exhibit CTL escape variants with mutations in a single epitope from

156 This coincided with the emergence of an escape variant within the Tat epitope and an additional

157 ogous viruses revealed the absence of immune escape variants within five of the six epitopes.