ライフサイエンスコーパス: viral variant

1 appeared to have been derived from a single viral variant.

2 tive V3 loop form emerged from a preexisting viral variant.

3 n is typically established by a single donor viral variant.

4 mechanisms leading to infection by a single viral variant.

5 e diverse TCRBV genes and did not select for viral variants.

6 ing infection requires prolonged exposure to viral variants.

7 ure and/or selective outgrowth of aggressive viral variants.

8 ting the development of de novo responses to viral variants.

9 linical significance of minor drug-resistant viral variants.

10 terized by cloning and sequencing individual viral variants.

11 originates either from a single or multiple viral variants.

12 d by the successful transmission of multiple viral variants.

13 uding epitopes from clade and drug-resistant viral variants.

14 ponses that may be required to control HIV-1 viral variants.

15 t cellular immune responses to control HIV-1 viral variants.

16 t for genetic modifications and selection of viral variants.

17 o transmit single or multiple major maternal viral variants.

18 thus a determining force in the selection of viral variants.

19 oring the emergence of neutralization escape viral variants.

20 cluding the relative expression of different viral variants.

21 I reactivity against multiple antigenic H1N1 viral variants.

22 of immunodiagnostics for detecting emergent viral variants.

23 e host's immune system to neutralize certain viral variants.

24 , and urine most often did not contain minor viral variants.

25 smission is established by one or only a few viral variants.

26 es cells might function as an "incubator" of viral variants.

27 nfection is established by one or only a few viral variants.

28 omplete GHV genomes, comprising two distinct viral variants.

29 ces and estimating frequencies of individual viral variants.

30 y that quantifies the relative importance of viral variants.

31 etoamide resistance among naturally existing viral variants.

32 omatic hypermutation in response to emerging viral variants.

33 g a previously undetected complex pattern of viral variants.

34 nt-naive persons as harboring drug-resistant viral variants.

35 rved differences in specific mutations among viral variants, 13 of the 14 women showed highly concord

36 These avirulent viral variants acquire positively charged amino acids on

37 ion with soluble PVR, and (iii) selection of viral variants adapted to use mutant PVRs.

38 However, viral variants altered in inclusion morphology displayed

39 sion inhibitory activity against an M-tropic viral variant and found an inverse relationship between

40 is a powerful new tool that can detect minor viral variants and characterize complex quasispecies mix

41 ), together with the continuous emergence of viral variants and drug resistant mutants, highlights th

42 tment strategies, track the emergence of new viral variants and ensure that diagnostic assays are con

43 econstruction of the whole-genome intra-host viral variants and estimation of their frequencies were

44 e condition of a complex CR network (CRN) of viral variants and examine the contribution of CR to est

45 ising molecular clones bearing envs from six viral variants and its replicative capacity compared in

46 obtained HIV-1 RNA sequences from 280 unique viral variants and then determined the resistance genoty

47 des valuable information for those analyzing viral variants and, in some cases, offers a rapid and ac

48 n-swapping experiments, genetic selection of viral variants, and site-directed mutagenesis.

49 istance mutations may arise in a fraction of viral variants, and these variants may differ between co

50 seeking to elicit functional responses from viral variants, and to HIV cure strategies that require

51 Thus, Culicoides might be a source of new viral variants, and viral population diversity can be an

52 ent sequence is preserved in most cases, and viral variants are competent to establish infection afte

53 Two viral variants are known: HHV-6A and HHV-6B.

54 eficiency virus (SIV) Mne-infected macaques, viral variants are selected that encode sequences with s

55 ncing coverage is high enough that even rare viral variants are sequenced, the presence of sequencing

56 ver time, but often only a limited number of viral variants are transmitted from a chronic carrier to

57 Ultradeep pyrosequencing showed that viral variants arose with identical kinetics in SIVmac23

58 ay be important in the selection of specific viral variants as a result of an antiviral immune respon

59 greater capacity to suppress replication of viral variants as well as to survive in the absence of s

60 ults are consistent with immune selection of viral variants at the epitope and molecular levels that

61 ults are consistent with immune selection of viral variants at the epitope level, which may enable HC

62 ng us to confidently detect the emergence of viral variants bearing escape mutations with frequencies

63 No single viral variant can induce sufficiently broad immunity, an

64 cing is decreased so that even low-frequency viral variants can be accurately detected.

65 he selective forces driving the emergence of viral variants can provide critical insight into the int

66 lts from transmission or outgrowth of single viral variants carrying mutations in CTL epitopes that w

67 whole of the consensus population and minor viral variants) contained in different body compartments

68 We found that viral variants containing either a Phe or Leu at GP resi

69 nificance of hepatitis B virus genotypes and viral variants continues to be elucidated worldwide.

70 The viral variants described in this report should prove use

71 clone, SHIVSF33, into a pathogenic biologic viral variant, designated SHIVSF33A.

72 ervoir virus, corresponding instead to minor viral variants detected during the course of treatment i

73 Viral variants detected in blood plasma were compared to

74 Each viral variant differently impacted on the epitope's flex

75 ease, mice were infected with two attenuated viral variants differing in a hypervariable region of th

76 had a detectable CVL HCV RNA load, we found viral variants differing in the 5' untranslated region t

77 Half of the subjects had more than one V1/V2 viral variant during primary infection, indicating the f

78 CD8+ T cell responses rapidly select viral variants during acute human immunodeficiency virus

79 The appearance of antigenically distinct viral variants during recurrent viremic episodes is thou

80 mals generated cytotoxic T-lymphocyte escape viral variants during the course of their infections.

81 n tracked the relative decline of individual viral variants during the initial days of antiretroviral

82 Viral variants emerged after week 12 in 36 of the 49 eva

83 ine immunodeficiency virus (FIV), a range of viral variants emerged with distinct modes of interactio

84 aimed to characterize treatment outcomes and viral variants emerging in telaprevir-treated patients n

85 nded our previous finding that IDV-resistant viral variants exhibit various patterns of cross-resista

86 ncluding the selective tropism of individual viral variants for different CD4+ target cells and the m

87 t importance, provides criteria for choosing viral variants for further characterization, diagnostics

88 nd RAVV in mice resulted in the selection of viral variants from among the quasispecies with differen

89 utralizing antibodies (bNAbs) that recognize viral variants from different HIV-1 clades.

90 This is particularly true for viral variants from early stages of infection, which rep

91 rovirus was based on the outgrowth of single viral variants from minority populations already present

92 ogical factors and selection of 'preadapted' viral variants from the existing viral community.

93 Surprisingly, viral variants from the Main group replicate even in the

94 ovel computer algorithms able to reconstruct viral variant genomes present in mixtures with an accura

95 cing assay that detects minor populations of viral variants (>or=5%), mutations were identified that

96 It is unlikely that minority viral variants harboring DRM are transmitted and maintai

97 Minor viral variants have important implications for drug resi

98 fferences in virus-host interactions between viral variants have potential consequences for transmiss

99 structure determines specific roles for each viral variant in host adaptation, with variants elicitin

100 ) macaques suggest the evolution of a common viral variant in RP macaques.

101 However, a specific viral variant in the SIVmac251 stock was not consistentl

102 sure led to the outgrowth of more aggressive viral variants in all three species.

103 We have performed infections with both viral variants in human progenitor-derived astrocytes (H

104 n viral control is influenced by preexisting viral variants in important target epitopes and the deve

105 DNA polymerase, were developed for screening viral variants in lamivudine-treated patients' sera cont

106 ges that lead to the emergence of pathogenic viral variants in macaques initially infected with a mil

107 ntalized, suggesting segregation of specific viral variants in malignant hepatocytes.

108 these epitopes by comparing the frequency of viral variants in plasma to the frequency of the CD8+-T-

109 uable reagent to study the roles of specific viral variants in rapid progression in vivo.

110 iants, indicating clearance and evolution of viral variants in response to pressure from neutralizing

111 We did not find differences between viral variants in the absence versus presence of vaccina

112 hanges in viral replication and emergence of viral variants in the context of T cell homeostasis and

113 ng Vbeta13.2 TCRs tolerate naturally arising viral variants in the FL8 epitope that escape recognitio

114 gh more macaques were infected with multiple viral variants in the gingivitis group.

115 ithm to estimate abundances of the assembled viral variants in the population.

116 he replication and cellular tropisms of four viral variants in the tissues of infected rhesus macaque

117 ement in order to target a broad spectrum of viral variants, including those that resemble primary is

118 selecting and sequencing antibody-resistant viral variants indicated that the cross-neutralizing MAb

119 ons were independent of the phenotype of the viral variant, indicating that virus neutralization by C

120 J mice develop tumors when infected with all viral variants, irrespective of the gag gene sequences.

121 ping of cultures infected with two competing viral variants, kinetics of viral antigen production, an

122 Decreasing epitope numbers, using a viral variant lacking dominant epitopes or C57BL/6J mice

123 ster than host miRNAs, it is surprising that viral variants lacking these 'antiviral' miRNA target se

124 These viral variants may induce difficult-to-treat HBV forms;

125 ompartmentalized in tissues where individual viral variants may interact locally.

126 s well as the challenges of predicting which viral variants may pose the greatest threats for zoonoti

127 to-child transmission (IU MTCT), transmitted viral variants must pass through multiple unique environ

128 zation by maternal plasma than were maternal viral variants near the time of transmission.

129 text of shared and non-shared HLA alleles in viral variants obtained from five mother-to-child transm

130 he hypothesis that the selection of specific viral variants occurs in the genital tracts of individua

131 nt seems to have been recently infected by a viral variant of HIV-1 resistant to multiple classes of

132 lizing antibodies (ANAbs) against individual viral variants of the quasispecies in a cohort of drug-n

133 atches multinomial distributions of distinct viral variants overlapping across the genome division.

134 Surprisingly, one viral variant (P5-Glu to P5-Asp) effectively changed res

135 and breadth of the genetic complexity of the viral variant population in the earliest stages of syste

136 detected in the p17 Gag epitope; a dominant viral variant present in the patient was well recognized

137 Moreover, Ad-5/3-kappaBF512HRE, a viral variant pseudotyped with a chimeric 5/3 fiber, exe

138 gradual diversification of a common dominant viral variant rather than the preferential migration of

139 The presence of viral variants resistant to NS5A inhibitors at baseline

140 l properties and expressing activity against viral variants resistant to the currently available agen

141 The relatedness between viral variants sampled at different locations through ti

142 First, we identified minority viral variants, termed bNAb-initiating envelopes, that w

143 a population of distinct but closely related viral variants, termed the "viral quasispecies." These v

144 virus, or the selection and persistence of a viral variant that abrogates the presentation of a singl

145 ical characteristics of the patients and the viral variant that infected them.

146 r these conditions led to the emergence of a viral variant that was able to replicate efficiently in

147 e RNA virus because it identifies subsets of viral variants that are most important to overall viral

148 Viral variants that arise in the global influenza popula

149 We now describe resistant viral variants that arose after drug selection, using vi

150 often a complex mixture composed of multiple viral variants that contribute to the quasispecies.

151 ection was characterized by the selection of viral variants that displayed accelerated expansion kine

152 nses in the human host; forcing selection of viral variants that escape cellular and antibody (Ab)-me

153 However, CTLs select for viral variants that escape immune detection.

154 Given that mAb AP33 efficiently neutralizes viral variants that escaped the humoral immune response

155 s on virus in such animals and suggests that viral variants that evolve in these animals may play a r

156 notherapy; viral rebound was associated with viral variants that had been previously implicated in re

157 t integration sites, act effectively against viral variants that have acquired mutations in their pro

158 stochastic processes determine the specific viral variants that infect an animal after IVAG SIV expo

159 immunity, but we did find that the SIVsmE660 viral variants that infected the monkeys, regardless of

160 controls to determine whether the SIVsmE660 viral variants that infected these two groups were diffe

161 etroviruses, it is not the generation of new viral variants that limits the extent of diversity and t

162 ues for the detection of these low-abundance viral variants that predict an increased risk of treatme

163 strategies currently exist to select actual viral variants that should be included or excluded in po

164 sceptible to infection by syncytium-inducing viral variants that use this coreceptor for entry.

165 ns; and a system for providing nonselectable viral variants (the result of mutations, insertions, and

166 However, in spite of exposure to multiple viral variants, the T cell responses in these patients w

167 ing the potential emergence of more virulent viral variants through amino acid substitutions.

168 ) restored efficient replication of the C92R viral variant, thus demonstrating a genetic interaction

169 ked differences in the ability of individual viral variants to replicate were noted in Group 2; those

170 Furthermore, a unique viral variant was randomly ingested by C. sonorensis ins

171 ty of T cells with population and endogenous viral variants was determined following viral sequence a

172 ore, CD8(+) T-cell recognition of autologous viral variants was preserved in most cases.

173 ersification and the evolution of beneficial viral variants, we have examined the impact of A3G on th

174 R5-like viral variants were identified in both fluids of all sub

175 In two patients, responses to autologous viral variants were not demonstrable at one epitope.

176 ts were available, we found that only 1 to 4 viral variants were present, suggesting that productive

177 For HPV16, non-European viral variants were significantly more likely than Europ

178 e, including HIV-1-specific CTLs that select viral variants which escape T-cell recognition.

179 est that after immune failure newly produced viral variants, which would be rapidly cleared under nor

180 etroviral vectors by generating a library of viral variants with a DNA-binding domain inserted at ran

181 ein and suggests drug therapy may select for viral variants with altered susceptibility to establishe

182 Viral variants with different mutations are selected by

183 Here we (i) evaluated the ability of the viral variants with either a Phe or Leu at GP residue 26

184 The data suggest that viral variants with GL8-like characteristics have an ear

185 the use of tenofovir gel did not select for viral variants with higher replication capacity.

186 ome replaced over time by emerging wild-type viral variants with improved fitness.

187 Selection of viral variants with increasing concentrations of ABT-378

188 still be beneficial even in the presence of viral variants with reduced susceptibility to PMPA.

189 issues of adherence, and by the selection of viral variants with reduced susceptibility.

190 large-scale mutagenesis studies to identify viral variants with unique functional properties.

191 Additionally, the abundance of viral variants within a host, as well as the impact of v

192 Viral variants within each patient were screened for rec

193 thin the two targeted CTL epitopes; however, viral variants within the immunodominant Env epitope wer