ライフサイエンスコーパス: viral genome

1 5B is responsible for the replication of the viral genome.

2 immune system but sufficient to maintain the viral genome.

3 eplication when CpGs are introduced into the viral genome.

4 roducing this reporter gene into ORF7 of the viral genome.

5 rtners and replication in the context of the viral genome.

6 polymerase, NS5, inhibits translation of the viral genome.

7 sses on the three segments that comprise the viral genome.

8 defined by a single base substitution in the viral genome.

9 aining the highest structural density in the viral genome.

10 that contain tandemly repeated copies of the viral genome.

11 tions stabilize the particle and protect the viral genome.

12 rganization of miR-122/Ago2 complexes on the viral genome.

13 capable of transcribing and replicating the viral genome.

14 for vRNA synthesis during replication of the viral genome.

15 inhibit the interaction between LANA and the viral genome.

16 t random sequence inserted directly into the viral genome.

17 Rta stimulates RBP-Jkappa DNA binding to the viral genome.

18 l recruitment of the Pol II machinery to the viral genome.

19 ersifying selection at multiple sites in the viral genome.

20 embrane fusion and subsequent release of the viral genome.

21 for the replication and transcription of the viral genome.

22 are critical sites for the synthesis of the viral genome.

23 voir that maintains functional copies of the viral genome.

24 y targeting specific vital components of the viral genome.

25 compensatory mutations occurring across the viral genome.

26 fied, predominantly toward the 3' end of the viral genome.

27 ly(C)-binding protein (PCBP) 1 or 2 with the viral genome.

28 can restrict HIV-1 infection by mutating the viral genome.

29 vity and one of the most diverse loci in the viral genome.

30 ss which involves the transmission of entire viral genomes.

31 rming sequences (RLFS) across more than 6000 viral genomes.

32 re efficient endocytic transport of incoming viral genomes.

33 ient and scale to simulate large plasmids or viral genomes.

34 ne, hivmmer, for Illumina sequences from HIV viral genomes.

35 ool for annotation and GenBank deposition of viral genomes.

36 upports annotation of nearly all unsegmented viral genomes.

37 te in neurons that suppresses replication of viral genomes.

38 mapped to 380 bacterial, 56 archaeal, and 39 viral genomes.

39 protein that mediates episome persistence of viral genomes.

40 free chlorine access to viral RNA to damage viral genomes.

41 E KSHV LANA mediates episomal persistence of viral genomes.

42 cRNAs) are prevalent in eukaryotic cells and viral genomes.

43 defend against invading foreign DNA, such as viral genomes.

44 rboring integrated and replication-competent viral genomes.

45 us (FMDV), is responsible for replication of viral genomes.

46 g adaptive mutations in both the nuclear and viral genomes.

47 l of 14637 RLFS loci were identified in 1586 viral genomes.

48 located in the 5' untranslated region of the viral genome, acts as a promotor for viral replication a

49 known how the number and position of CpGs in viral genomes affect restriction by ZAP and whether CpGs

50 olytic adenoviruses and selection of optimal viral genome alterations to generate improved mutants.

51 As RNF168 knockdown impairs viral genome amplification in differentiated keratinocyt

52 s replicase, binds viral RNA, and suppresses viral genome amplification.

53 related (ATR) DNA damage repair pathways for viral genome amplification.

54 capsid formation that may fail to encase the viral genome and (2) rapid disassembly of the capsid, wh

55 d their abundance in multiple regions of the viral genome and analyzed the effect on RNA expression,

56 otein complex (vRNP) consisting of a dimeric viral genome and associated proteins, together constitut

57 ced the amount of Pol II associated with the viral genome and confined most of the remaining Pol II t

58 from database submissions, are mapped to the viral genome and grouped together into "annotation track

59 e, which led to premature degradation of the viral genome and IN in target cells.

60 ied by proteasomal-independent losses of the viral genome and integrase enzyme.

61 re virus-cell membrane fusion to release the viral genome and replicate.

62 viral DNA replication reduced Pol II on the viral genome and restricted much of the remaining Pol II

63 These interactions reveal that the viral genome and subgenomes adopt alternative topologies

64 d to promote the efficient nuclear import of viral genome and suggests that MAPK/ERK-2-mediated Vpx p

65 on KSHV reactivation by interacting with the viral genome and suppressing viral gene expression is im

66 on of CA from viral cores, which exposes the viral genome and the integrase enzyme for degradation in

67 olecular matchmaker that recognizes both the viral genome and the main motor component, the large ter

68 gap is how the capsid engages the replicated viral genome and the subsequent packaging of a unit-leng

69 (L) polymerase protein of RSV replicates the viral genome and transcribes viral mRNAs.

70 taset of 91,534 toehold switches spanning 23 viral genomes and 906 human transcription factors.

71 Nearly 60% of the viral genomes and genome fragments are clustered into 11

72 to appreciate the surprising versatility of viral genomes and how replication-competent and -defecti

73 d with 365 nm light to crosslink 4SU-labeled viral genomes and interacting proteins from host or viru

74 Many studies assemble new viral genomes and study viral diversity using marker gen

75 s), exert their effect by incorporation into viral genomes and subsequent disruption of viral replica

76 iral particles depending on their content of viral genomes and their intracellular localization.

77 nctional RNA polymerases to replicate entire viral genomes and transcribe viral mRNAs from individual

78 ty of SARS-CoV-2 genome is exceptional among viral genomes and we develop a method to directly compar

79 enza polymerases are unable to replicate the viral genome, and infectious virus cannot propagate.

80 -CoV-2 is among the largest and most complex viral genomes, and yet its RNA structural features remai

81 e uncoating and reverse transcription of the viral genome are coordinated processes rather than discr

82 Our results indicate that these viral genomes are maintained inside the nucleus, bound t

83 However, viral genomes are not known to encode the core component

84 Instead, multiple viral genomes are often required in a given cell.

85 atasets, we identify 14 different RPs across viral genomes arising from cultivated viral isolates and

86 w that KSHV-infected BECs progressively lose viral genome as they proliferate.

87 22:HCV RNA complex at the 5' terminus of the viral genome as well as hAgo2:miR-122 interactions with

88 to the ability to encode the gene within the viral genome, as well as the ability to limit off-target

89 ites and chromatin accessibility of host and viral genomes at the single-cell resolution in CAR-T cel

90 us positively charged groove compatible with viral genome binding.

91 liced transcripts encoding Gag, Pol, and the viral genome, but KoRV-A piRNAs are almost exclusively d

92 igen (LANA) is essential for maintaining the viral genome by regulating replication and segregation o

93 introduced at the Ca(2+) binding site in the viral genome by reverse genetics failed to allow recover

94 and thus is critical for recognition of the viral genome by the viral polymerase NS5.

95 unctioning of a nuclear episomal form of the viral genome called cccDNA, the most stable HBV replicat

96 secondary and tertiary structures within its viral genome (canonical PRF), as well as a noncanonical

97 aline exonucleases play an important role in viral genome cleavage and packaging.

98 Furthermore, we were not able to retrieve viral genomes closely related to Yaravirus in 8,535 publ

99 In cells enriched in full-length virus, viral genomes clustered in a perinuclear region and asso

100 ween the coding and noncoding regions of the viral genome combined to elicit an epidemiologic fitness

101 used in nature to consistently build stable viral genome containers through subtle adaptation of the

102 SOX18 enhanced the number of intracellular viral genome copies and bound to the viral origins of re

103 howed reduced replication and persistence of viral genome copies compared to levels with the wild-typ

104 Of note, we achieved titers of 10(10)-10(11) viral genome copies per ul with a typical production vol

105 us expression of oncogenic lytic genes, high viral genome copies, and release of infectious virus.

106 Ad-3Delta-A20T-treated animals showed higher viral genome copy numbers and E1A gene expression in tum

107 Importantly, manipulating the CpG content in viral genomes could help create new vaccines.

108 a DENV-specific cDNA primer did increase the viral genome coverage immediately 5' to the primer bindi

109 ing and DNMT3B was identified as an upstream viral genome CpG methylation initiator.

110 young, immunocompetent health care worker as viral genomes derived from the first and second episode

111 ation and sequence context of the CpG in the viral genome determines its antiviral activity.IMPORTANC

112 Chromatin modification of the viral genome determines the phase of the viral life cycl

113 irus core protein, a chaperone that promotes viral genome dimerization.

114 in this analysis mapped to the 5' end of the viral genome, distinct patterns of enhanced coverage wit

115 We determined ICP4 discriminately binds the viral genome due to the absence of cellular nucleosomes

116 is an ordered protein shell that houses the viral genome during early infection.

117 ing was performed to identify changes in the viral genome during passaging in the presence or absence

118 eaminate numerous sites across a 10,000 base viral genome during the reverse transcription process.

119 y virus (SIV) and are likely to carry latent viral genomes during antiretroviral therapy (ART), contr

120 the universality and diversity of defective viral genomes during infections and discuss their predic

121 ellular localization of DVGs and full-length viral genomes during infections with the paramyxovirus S

122 Defective viral genomes (DVGs) are generated during viral replicat

123 Defective viral genomes (DVGs) generated during RNA virus replicat

124 ctions during infection.IMPORTANCE Defective viral genomes (DVGs) generated during Sendai virus infec

125 Recent studies have identified defective viral genomes (DVGs) in human infections, including resp

126 Barr virus) in 293L/Q129H cells restored the viral genome encapsidation defects.

127 Viral genomes encode transcriptional regulators that alt

128 The discovered viral genomes encoded a wide range of proteins with puta

129 The medium (M) segment of the viral genome encodes two envelope glycoproteins, G(N) an

130 ust understanding of all of the proteins the viral genome encodes.

131 Bank submissions, new submission wizards for viral genomes, enhancements to BankIt and improved handl

132 viral transcriptional units activated after viral genome entry into the host cell nucleus are the E1

133 an automated pipeline for identifying closed viral genomes, estimating the completeness of genome fra

134 Since the viral genome exists as a covalently closed circle of dou

135 Major advances in our understanding of plant viral genome expression strategies and the interaction o

136 to the restricted capacity of the influenza viral genome for including foreign sequences.

137 our genome browser visualization tool to the viral genome for this purpose.

138 y for incorporating foreign sequences in the viral genome forced researchers to select a fluorescent

139 The viral genome forms the basis for chronic infection and h

140 ion, datasets covering the whole hepatitis B viral genome from large patient cohorts are lacking, gre

141 The timely release of the viral genome from the capsid-referred to as uncoating-is

142 s of double-stranded DNA viruses protect the viral genome from the harsh extracellular environment, w

143 utility of our method by amplifying partial viral genomes from 6 HeV-infected tissue samples from Sy

144 Sequencing of 1,314 SARS-CoV-2 viral genomes from available patient samples enabled us

145 within the United States, we sequenced nine viral genomes from early reported COVID-19 patients in C

146 Sequencing whole viral genomes from samples later in infection did not re

147 etagenomic data with new metagenomic-derived viral genomes from sea stars collected from Antarctica,

148 which highlights the challenge of assembling viral genomes from short-read metagenomes.

149 Phylogenetic analyses of viral genomes from two cases revealed these viruses were

150 current knowledge of the types of defective viral genomes generated during the replication of RNA vi

151 7syn (+) Strikingly, we show that the KOS(M) viral genomes have a higher burden of heterochromatin ma

152 re consistent with selection pressure on the viral genome imposed by local and systemic movement.

153 nown to be involved in the nuclear import of viral genome in nondividing cells, but the mechanism rem

154 We report the near-complete viral genome in one HIV-1 positive specimen from Kinshas

155 , packaging, and stable incorporation of the viral genome in the HSV-1 capsid.

156 se recovered cell populations maintained the viral genomes in a quiescent state for at least 5 wk pos

157 r virus (CAEBV) presents with high levels of viral genomes in blood and tissue infiltration with Epst

158 videnced by the bilateral presence of latent viral genomes in both trigeminal ganglia, while for any

159 Active viral replication and viral genomes in bronchoalveolar-lavage (BAL) fluid and

160 We focus on applying CATCH to capture viral genomes in complex metagenomic samples.

161 genes and the replication and maintenance of viral genomes in host cells.

162 cribe a MetaviralSPAdes tool for identifying viral genomes in metagenomic assembly graphs that is bas

163 ound a significant decrease in the number of viral genomes in mouse trigeminal ganglia (TG) infected

164 Yet, viral genomes in only some cells in a population of late

165 ation and fibrosis as well as persistence of viral genomes in the heart tissue and by cardiac dysfunc

166 sequences with a large database of complete viral genomes, including 76,262 identified from a system

167 e roles of epigenetic modifications of these viral genomes, including DNA methylation, histone modifi

168 unctions, as a translation template and as a viral genome, individual RNA molecules carry out only on

169 he severity of viral infections, and how the viral genome influences host immune responses to viral i

170 bacteriophages, a molecular motor drives the viral genome inside a protein capsid.

171 Prophages (viral genomes integrated within a host bacterial genome)

172 xonuclease-based proofreader to maintain the viral genome integrity.

173 g questions about where and when coinfecting viral genomes interact.

174 a herpesvirus capsid powers ejection of the viral genome into a host cell nucleus.

175 xibility necessary to uncoat and deliver the viral genome into a host cell.

176 lopes with cellular membranes to release the viral genome into cells.

177 ediates the integration of a DNA copy of the viral genome into host chromatin.

178 ase (IN), which catalyzes integration of the viral genome into the host cell DNA.

179 ng, (v) cleavage and stable packaging of the viral genome involve an ordered interaction of the termi

180 ata suggest that the epigenetic state of the viral genome is an important determinant of reactivation

181 In this situation the viral genome is not recapitulated in a single virus part

182 In these cancers the viral genome is predominantly latent; i.e., most viral g

183 formation of a fusion pore through which the viral genome is transferred into a target cell.

184 associated with long-range insulators in the viral genome, it is still unknown whether host transcrip

185 stein-Barr virus (EBV) switches between four viral genome latency and lytic programmes to navigate th

186 f EAV and identified critical regions of the viral genome likely associated with the establishment an

187 The potyvirus-derived viral genome-linked protein (VPg) is covalently bound to

188 portal is the entrance and exit pore for the viral genome, making it an attractive pharmacological ta

189 entry into a target cell, replication of the viral genome, maturation of viral proteins and genome pa

190 mechanism for deleting this region from the viral genome may exist, given that the deletion variant

191 n between virus-derived small RNAs (vsRNAs), viral genome methylation and gene expression, we obtaine

192 RNA polymerase II transcribing the circular viral genome more than once.

193 We performed phylogenetic analysis of viral genomes obtained from infected study volunteers to

194 ck of experimental systems to manipulate the viral genome of interest, raising questions about in viv

195 Here, we analyze the viral genomes of 5,328 HPV16-positive case-control sampl

196 ed mapping approaches yielded eight complete viral genomes of BRRV (genus Soymovirus, family Caulimov

197 The viral genomes of the precancer/cancer cases are less lik

198 6A modification sites were identified in the viral genome, of which mutations resulted in decreased v

199 enge, and limited inflammation or detectable viral genome or antigen was noted in lungs of animals in

200 Among the open reading frames within the viral genome, ORF3, ORF5, and the nsp2-coding region of

201 The viral genome, packaged by the nucleoprotein (N), serves

202 These studies suggest that viral genome packaging is insensitive to DNA sequence an

203 amino acid substitutions greatly impairs the viral genome packaging process.

204 al mechanism for the role of N in SARS-CoV-2 viral genome packing and in host-protein co-opting neces

205 AAV9-hNIS (2x10(11) viral genome particles) was injected into nonischemic or

206 Next-generation deep sequencing of viral genomes, particularly on the Illumina platform, is

207 tration of a pressure-dependent mechanism of viral genome penetration into a host nucleus, leading to

208 Here, we describe viral genomes persisting in ART-treated, simian immunode

209 The viral genome persists in infected hepatocytes even after

210 RNA secondary structure in the viral genome plays an important role in the lifecycle of

211 ch protein, NS1, encoded as a monomer by the viral genome, plays a major role via symmetric oligomeri

212 a4 in exerting selective pressure across the viral genome, possibly by a novel mechanism.

213 7's proposed DNase activity is essential for viral genome processing and encapsidation and, hence, ca

214 ion of the KSHV SOX protein is essential for viral genome processing and packaging and capsid maturat

215 protein forms a liquid-like compartment for viral genome processing.

216 Viral genomes recovered from 9 of 12 (75%) cases co-clus

217 Surprisingly, despite viral genome reduction, RNase L activity did not reduce

218 We find that the viral genome remains largely nucleosome-free, and this i

219 All of the compounds tested inhibited viral genome replication and gene transcription, and non

220 project examines the mechanisms that control viral genome replication and may allow the development o

221 ion of E2 with the Brd4 CTM is necessary for viral genome replication and suggest that this interacti

222 During viral genome replication and transcription, the tetramer

223 ules that are responsible, respectively, for viral genome replication and virion morphogenesis.

224 generate replication organelles that promote viral genome replication and virus production.

225 g cellular factors for viral translation and viral genome replication at the endoplasmic reticulum is

226 hospholipid reconfiguration was required for viral genome replication but not for the other steps of

227 defects in re-expression of viral genes and viral genome replication in the THP-1 latency model.

228 modifications of viral proteins coordinates viral genome replication is less explored.

229 of loss or inactivation of DNase activity on viral genome replication, cleavage, and packaging.

230 d recombinant protein systems to investigate viral genome replication, RNA-binding affinity, ATP hydr

231 RNA virus survival depends on efficient viral genome replication, which is performed by the vira

232 that rely upon host replication proteins for viral genome replication.

233 e, which creates a protected environment for viral genome replication.

234 s critical for VP1-VP2 interaction(s) during viral genome replication.IMPORTANCE Group A rotaviruses

235 egulator of HCV replication involved in both viral-genome replication and infectious-virus assembly.

236 es generated from four different 'levels' of viral genome representation: nucleotide, amino acid, ami

237 s RNase L antiviral activity by generating a viral genome reservoir protected from RNase L cleavage d

238 to establish a chronic infection whereby the viral genome resides within the cell in either an exclus

239 the portal vertex, and (vi) packaging of the viral genome results in a dramatic displacement of the p

240 dated epitopes sequences on 3985 full-length viral genomes revealed 19 highly conserved epitopes acro

241 alysis along the unintegrated and integrated viral genomes revealed major differences in nucleosome d

242 ally, in BHK-21 cells, many mutations in the viral genome reverted to the wild type (WT) and compensa

243 an be visualized along the linear map of the viral genome sequence and programmatically downloaded in

244 Annotation and submission of viral genome sequence is a non-trivial task, especially

245 nt, the EBOV genome exists around a dominant viral genome sequence.

246 (and thus most informative) positions in the viral genomes sequenced from different individuals.

247 Furthermore, rapidly deployable viral genome sequencing can be an integral part of outbr

248 Viral genome sequencing confirmed four reinfections out

249 Viral genome sequencing has emerged as a powerful approa

250 Viral genome sequencing of the paired first-positive and

251 Viral genome sequencing showed that the majority of HCWs

252 Viral genome sequencing was performed on donor and recip

253 Quantification of incomplete viral genomes showed that their complementation accounts

254 inds nearly exclusively to different sets of viral genome sites during latency and reactivation.

255 dent manner.IMPORTANCE Constraints placed on viral genome size require that these pathogens must empl

256 flavodoxin reductase) were not found in any viral genome so far described, implying that host redox

257 a first step in assessing the feasibility of viral genome studies, the structure of encapsidated MS2

258 Metagenomic sequencing of 39 viral genomes suggested that the outbreak originated lar

259 ish different epigenetic scenarios along the viral genome, suggesting that in addition to its functio

260 established latency with a higher number of viral genomes than strain 17syn (+) Strikingly, we show

261 Mutations in the viral genome that reduced or restored translation preven

262 s the computational challenge of identifying viral genomes that are often difficult to detect in meta

263 thin this diversity is a subset of defective viral genomes that retain replication competency, termed

264 This revealed 44,652 high-quality viral genomes (that is, >90% complete), although the vas

265 efficiently targets a specific region of the viral genome, that the number of CpGs does not predict t

266 ookshelf, My Bibliography, Assembly, RefSeq, viral genomes, the prokaryotic genome annotation pipelin

267 proteins (MPs) that ensure the transport of viral genomes through plasmodesmata (PD) and use cell en

268 One mode of adaptation is modifying the viral genome to contain noncanonical nucleotides.

269 ome in the nuclei of cells; partitioning the viral genome to daughter cells in dividing cells; avoidi

270 r, the ability to genetically manipulate the viral genome to express two foreign genes offers the pos

271 (Q129H) mutation into the ORF37 gene of the viral genome to generate ORF37-Q129H recombinant virus (

272 cations that are regularly spaced across the viral genome to maximize coverage (collectively referred

273 ells; modulating the epigenetic state of the viral genome to regulate viral gene expression; and reac

274 replication and efficient segregation of the viral genome to the daughter cells following cell divisi

275 resulting in less efficient delivery of the viral genome to the host cell nucleus.

276 hich enabled the cloning and manipulation of viral genomes to express genes of interest (vectors 1.0)

277 host mitotic chromosomes, thus enabling the viral genomes to hitchhike or piggyback into daughter ce

278 endoplasmic reticulum (ER), for delivery of viral genomes to PD and formation of PD-anchored virus r

279 This polymerase transcribes viral genomes to produce RNAs that lead to induction of

280 rects the successful trafficking of incoming viral genomes to the nucleus.

281 cts of infection, including the transport of viral genomes to the site of replication.

282 w that the mode B site is important for both viral genome transcription and replication in influenza

283 Our data offer insight into the mechanism of viral genome transcription by the influenza virus polyme

284 Visualization of viral genomes using RNA fluorescent in situ hybridizatio

285 ing (NGS) is a potent method to sequence the viral genome, using molecular enrichment methods, from c

286 h HBV to investigate the association between viral genome variation and patients' clinical characteri

287 The viral genome was not homogenously methylated showing two

288 Further, the viral genome was sequenced and subjected to phylogenetic

289 translation-competent copies of the incoming viral genome, we reasoned that (+)ssRNA viruses will be

290 between transcription and replication of the viral genome were observed.

291 Whole viral genomes were analyzed for the presence of RASs to

292 The viral genomes were converted into the four different lev

293 Viral genomes were de novo assembled, yielding 10 comple

294 es the immediate translation of the incoming viral genome, whereas negative-sense single-stranded RNA

295 uld be unequivocally assigned to the seventh viral genome, which apparently represents a new virus ty

296 tly closed circular DNA (cccDNA) form of the viral genome, which is formed by the repair of lesion-be

297 ing a small, genetically unique tag into the viral genome, which is retained in progeny virus.

298 iminately drives high nucleosomal density of viral genomes, which is restrictive to viral gene expres

299 We performed viral genome-wide association studies using human and vi

300 proximately 30% of total Pol II relocated to viral genomes within 3 h postinfection (hpi), when it oc