ライフサイエンスコーパス: viral variant

1 mechanisms leading to infection by a single viral variant.

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

3 Effects were not modified by predominant viral variant.

4 by individual participant characteristics or viral variant.

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

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

7 manized mice without selecting for resistant viral variants.

8 g a previously undetected complex pattern of viral variants.

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

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

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

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

13 linical significance of minor drug-resistant viral variants.

14 terized by cloning and sequencing individual viral variants.

15 gainst multiple antigenically different H1N1 viral variants.

16 d by the successful transmission of multiple viral variants.

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

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

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

20 t for genetic modifications and selection of viral variants.

21 o transmit single or multiple major maternal viral variants.

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

23 oring the emergence of neutralization escape viral variants.

24 cluding the relative expression of different viral variants.

25 prolong inflammation, and be a source of new viral variants.

26 ntinued high disease burden and emergence of viral variants.

27 uggesting a mechanism for the development of viral variants.

28 but T-cell responses were preserved against viral variants.

29 onserved epitopes that are seldom mutated in viral variants.

30 nts in vitro better than earlier circulating viral variants.

31 hanging landscape of population immunity and viral variants.

32 ting illness caused by antigenically drifted viral variants.

33 s monovalent vaccine cross-protection to new viral variants.

34 p with continuously circulating and mutating viral variants.

35 of the virus, including the detection of new viral variants.

36 edding, burden of disease and infection, and viral variants.

37 azilian spike genes and isogenic recombinant viral variants.

38 n, nor is the effectiveness against emerging viral variants.

39 educes viral titers following challenge with viral variants.

40 difference between the wild-type and omicron viral variants.

41 and delayed viral clearance may lead to new viral variants.

42 I reactivity against multiple antigenic H1N1 viral variants.

43 the only-sites of replication for all three viral variants.

44 ith persistent infections can transmit these viral variants.

45 rals that could fight against drug-resistant viral variants.

46 ion, and providing potential sources for new viral variants.

47 omatic hypermutation in response to emerging viral variants.

48 ing infection requires prolonged exposure to viral variants.

49 originates either from a single or multiple viral variants.

50 of immunodiagnostics for detecting emergent viral variants.

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

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

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

54 S-CoV-2 with continuous turnover of dominant viral variants.

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

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

57 omplete GHV genomes, comprising two distinct viral variants.

58 ces and estimating frequencies of individual viral variants.

59 y that quantifies the relative importance of viral variants.

60 etoamide resistance among naturally existing viral variants.

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

62 requency of a potentially more transmissible viral variant (614G) over time can potentially be explai

63 antibodies (bnAbs) that can neutralize many viral variants, a key focus of HIV-1 vaccine design.

64 These avirulent viral variants acquire positively charged amino acids on

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

66 An understanding of how viral variants affect protein-protein binding is importa

67 an individual was infected with two distinct viral variants: Alpha (B.1.1.7) and Epsilon (B.1.429).

68 However, viral variants altered in inclusion morphology displayed

69 cular epidemiology, comparison of intra-host viral variants among infected persons is frequently used

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

71 ral load and Ag-RDT sensitivity according to viral variant and immunisation status (previous vaccinat

72 HCWs were stratified by viral variant and vaccination status at time of their fi

73 unding viral populations arose from a single viral variant and were CCR5 tropic, even though CXCR4 va

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

75 e infectivity and competitive ability of the viral variants and detect an interaction between host ge

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

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

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

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

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

81 to understand the impact of waning immunity, viral variants and other determinants of changing vaccin

82 s to the fight against future drug-resistant viral variants and the development of broad-spectrum ant

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

84 p a computational framework for inference of viral variants and validate it by successful early detec

85 ucts will be to address the emergence of new viral variants and viruses, there is an urgent need for

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

87 of demographic and clinical characteristics, viral variant, and trial with polymerase chain reaction-

88 because of changes in vaccination efficacy, viral variants, and mask mandates, and because universit

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

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

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

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

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

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

95 ulate the cell-intrinsic response to arising viral variants are needed.

96 ssive genetic variability, and many of these viral variants are now defined as variants of concern (V

97 their geographical range increases and more viral variants are produced that could have new biologic

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

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

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

101 with neutralizing antibody responses to one viral variant arising to the near exclusion of neutraliz

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

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

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

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

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

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

108 significant genetic compartmentalization of viral variants between saliva and nasal swab sample site

109 Patients with viral variants C1817T and A1838G had viral loads nearly

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

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

112 on rate, such that within one host different viral variants can emerge.

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

114 is and examination of virus samples and even viral variants can yield beneficial results.

115 ective pressures have the potential to yield viral variants capable of resisting these interventions.

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

117 s may provide substantial protection against viral variants carrying single E484K RBD mutations.

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

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

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

121 -like phage genotypic data revealed distinct viral variants correlated with different groups of cyano

122 The viral variants described in this report should prove use

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

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

125 Viral variants detected in blood plasma were compared to

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

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

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

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

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

131 e research on its role in the persistence of viral variants during long-term antiretroviral therapy (

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

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

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

135 arly stages of a viral pandemic, or as novel viral variants emerge.

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

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

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

139 hanged, leading to a majority of circulating viral variants encoding RT-184I.

140 to SARS-CoV-2 variants and to predict future viral variant evolutionary trends.

141 ithin single infected hosts with co-existing viral variants evolving differently in distinct cell typ

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

143 Participant characteristics and viral variant explained only 5.9% of the variability in

144 ody escape data, we show that fast-spreading viral variants exploit combinatorial mutations possessin

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

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

147 es revealed limited impact of vaccination on viral variant frequency, evolutionary rates, and nucleot

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

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

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

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

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

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

154 e, we report on a collection of more than 50 viral variants from wild-caught Caenorhabditis.

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

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

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

158 Minor viral variants have important implications for drug resi

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

160 n indicates the clinical importance of these viral variants.IMPORTANCE Genomic differences within HIV

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

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

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

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

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

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

167 Circulating viral variants in infant elite neutralizers are suscepti

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

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

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

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

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

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

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

175 al health insecurities from the evolution of viral variants in the bodies of the unvaccinated.

176 the CNS, and independent evolution of HIV-1 viral variants in the CNS and plasma can occur.

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

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

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

180 Viral variants in the HIV-1 reservoir may limit the capa

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

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

183 ight underestimate the presence of resistant viral variants in tissues.

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

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

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

187 arget CHI3L1 are effective inhibitors of SC2 viral variant infection.

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

189 If a viral variant is introduced into a prison that has resum

190 Antibody breadth against viral variants is lower after infection compared with al

191 Study of viral variants isolated from immunosuppressed patients w

192 oV-2) prevent COVID-19, the emergence of new viral variants jeopardizes their efficacy.

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

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

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

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

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

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

199 Regardless of viral variant, mRNA1273 is the most immunogenic, followe

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

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

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

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

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

205 ctions, with high affinity to all SARS-CoV-2 viral variants of concern, including the divergent Omicr

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

207 wave occurred after the introduction of new viral variants or lineages, or both, generally those alr

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

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

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

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

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

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

214 body testing with a panel of nine SARS-CoV-2 viral variant receptor binding domain (RBD) proteins rev

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

216 t HIV-2 and all major HIV-1 types, including viral variants resistant to the ARVs currently in clinic

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

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

219 We discovered novel viral variants strongly associated with viral load and H

220 ect cells, as demonstrated recently when new viral variants switched dominant infection pathways.

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

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

223 ing titers (ID(50) 1,504-22,978) against all viral variants tested.

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

225 e Republic of Korea in 2015, the spread of a viral variant that contained mutations in the viral spik

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

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

228 However, in the wake of the emergence of viral variants that are able to evade vaccine-induced ne

229 cidence of severe COVID-19, but emergence of viral variants that are antigenically distinct from the

230 However, the emergence of viral variants that are more transmissible and, in some

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

232 Viral variants that arise in the global influenza popula

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

234 by the World Health Organization or a set of viral variants that cocirculated during the same time pe

235 s new class of antiviral agents can overcome viral variants that confer resistance to traditional enz

236 ified that bat cells repeatedly selected for viral variants that contained mutations in the viral ope

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

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

239 Numerous studies have shown that viral variants that elude the host immune response may i

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

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

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

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

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

245 S outbreak in Korea, emergence and spread of viral variants that harbored mutations in the RBD, D510G

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

247 o virus evolution and rapid emergence of new viral variants that helps evade host's antiviral strateg

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

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

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

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

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

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

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

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

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

257 dherence and the emergence of drug-resistant viral variants, thereby limiting future treatment option

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

259 cost-effective, can be easily adapted to new viral variants through phage display, and can potentiall

260 marker to follow any further spread of these viral variants throughout the country.

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

262 However, the potential of rare resistant viral variants to abrogate bNAb-based protection remains

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

264 Clinical (comorbidities, predominant viral variant, treatment for malignant neoplasm, booster

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

266 Neutralization of viral variants was comparable between children and adult

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

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

269 ide phylogenetic analysis, emergence of both viral variants was specifically triggered by acquisition

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

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

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

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

274 In addition, a smaller proportion of H3N2 viral variants were shared between seeder pigs and vacci

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

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

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

278 erological findings, and the extent to which viral variants will escape from current immunity.

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

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

281 Viral variants with different mutations are selected by

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

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

284 for HTLV-1 replication and the selection of viral variants with greater fitness.IMPORTANCE Humanized

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

286 ficacy is weakened by the rapid emergence of viral variants with immunoevasive properties.

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

288 n of a second, thus initiating selection for viral variants with increased capacity for spread.

289 fections escalates, so does the evolution of viral variants with increased transmissibility and patho

290 Given the clinical importance of emergent viral variants with increased transmission, there is an

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

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

293 No treatment-experienced viral variants with reduced susceptibility to the drugs

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

295 t can be easily reprogrammed to discriminate viral variants with single-nucleotide resolution, as we

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

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

298 Viral variants within each patient were screened for rec

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

300 or understanding TCR cross-reactivity toward viral variants within the S(269-277) peptide.