ライフサイエンスコーパス: viral gene

1 ing RNA-mediated knockdown of the respective viral gene.

2 n combat this response through the gamma34.5 viral gene.

3 pisome and expressing only a small subset of viral genes.

4 s dependent on the expression of a subset of viral genes.

5 transcripts for the expression of individual viral genes.

6 pressor protein that blocks the silencing of viral genes.

7 equired for virus entry or the expression of viral genes.

8 through the decay factor Xrn1 and evaded by viral genes.

9 ring transactivation of diverse cellular and viral genes.

10 reased Ser5P modified forms of RNA Pol II on viral genes.

11 that ORF18 and ORF30 control the same set of viral genes.

12 replication and the mechanisms of action of viral genes.

13 erpesviruses that likely relies on conserved viral genes.

14 increased E2F1 and DP1 factors to transcribe viral genes.

15 xonomic classification according to hallmark viral genes.

16 aHVs exist as viral episomes and express few viral genes.

17 was associated with silencing of particular viral genes.

18 , and a reduction of RNA pol II occupancy on viral genes.

19 fenses consisting of RNAi-based silencing of viral genes.

20 but they are quite distinct from other known viral genes.

21 replication by regulating the expression of viral genes.

22 n of the viral genome and expression of late viral genes.

23 cle of HCV and the roles played by different viral genes.

24 anscription termination of cellular, but not viral, genes.

25 ected by mutational burden and expression of viral genes, (2) the composition and activity of a preex

26 -1 clade C antigens but lacks three specific viral genes (A52R, K7R, and B15R).

27 in Tregs is involved in their suppression of viral gene activation and expression.

28 has the potential to modulate the pattern of viral gene activation.

29 omplementarity to the mRNA for the important viral gene activator ICP0, inhibition of ICP0 expression

30 in nonneuronal cells in the absence of toxic viral-gene activity has been elusive.

31 50 RTA is a known transactivator of multiple viral genes, allowing it to control the switch between l

32 Viral gene and protein expression were evaluated by usin

33 io and is utilized in the expression of many viral genes and a number of cellular genes.

34 OGT is required for efficient expression of viral genes and for assembly of new virions.

35 and processes in IAV, including the flow of viral genes and genomes within and between host lineages

36 action is important for the virus to express viral genes and produce infectious virions.

37 s harboring ciHHV-6A/B spontaneously express viral genes and proteins.

38 virus requires the coordinated expression of viral genes and replication of the genome by the viral p

39 rovirus (AcMNPV) leads to expression of ~156 viral genes and results in dramatic cell remodeling.

40 A (72%) genomes contain a full set of intact viral genes and therefore appear to have the capacity fo

41 Viral genes and transcripts can be visualized on both li

42 mes appear to retain the capacity to express viral genes, and most are predicted to be capable of ful

43 fication genes; a region containing probable viral genes; and putative urea utilization genes.

44 neration approaches and the rapid cloning of viral genes are critical for basic research, diagnostics

45 During lytic replication of herpesviruses, viral genes are expressed in an ordered cascade.

46 host, during which only a limited number of viral genes are expressed.

47 oplasmic viral cores are activated and early viral genes are expressed.

48 The majority of archaeal viral genes are of unknown function hindering our unders

49 in-assembled episomes in which all but a few viral genes are transcriptionally silent.

50 AC-C-KC vector was generated by deleting the viral gene B19R, an inhibitor of the type I interferon r

51 we generated chimeric viruses by exchanging viral genes between the thermostable TS09-C strain and t

52 me replication, or the expression of typical viral genes but clearly impacted cytoplasmic envelopment

53 ranscriptional regulation of host as well as viral genes, but their precise role in HPV-infected cerv

54 from the prevailing view that Zta activates viral genes by binding exclusively at promoter elements.

55 infection on transcription of host cell and viral genes by RNA polymerase II (Pol II).

56 rom a host genome and that expression of the viral gene can alter the nutrient uptake behavior of hos

57 The viral genes can be classified into three distinct kineti

58 he relative abundance of a few bacterial and viral genes can predict a significant fraction of the va

59 -modified polyethylenimine (PEI-DA) as a non-viral gene carrier.

60 ithelium; however, even the most widely used viral gene carriers are unable to efficiently do so.

61 atency-associated transcript (LAT), the only viral gene consistently expressed during neuronal latenc

62 Our findings suggest that viral gene constellations circulating among diving ducks

63 Our results suggest that viral gene constellations circulating among diving ducks

64 HTLV-1, HTLV-1 bZIP factor (HBZ) is the only viral gene constitutively expressed in infected cells.

65 etagenomic studies provide information about viral gene content but rarely provide knowledge about vi

66 electroporation as a safe and effective non-viral gene delivery approach needed in many biological r

67 Electroporation serves as a promising non-viral gene delivery approach, while its current configur

68 vancements in optimizing the efficacy of non-viral gene delivery for ocular diseases.

69 PB) transposon system is a highly active non-viral gene delivery system capable of integrating define

70 Non-viral gene delivery systems are one of the most potentia

71 861 as a new transfection multiplier for non-viral gene delivery systems.

72 Viral and non-viral gene delivery vectors are in development for human

73 ntirety for the development of optimized non-viral gene delivery vectors.

74 The design of a non-viral gene delivery vehicle capable of delivering and re

75 ocular clinical trials, which currently use viral gene delivery, but focus primarily on new advancem

76 ave been incorporated into materials for non-viral gene delivery, cancer therapy or treatment of micr

77 By viral gene delivery, we downregulated mTORC2 solely in t

78 ds that have led to exciting advances in non-viral gene delivery.

79 mesolimbic brain regions that we targeted by viral gene delivery.

80 not in the PFC (postsynaptic site), using a viral gene-delivery approach, rescued the otherwise abse

81 the family Fuselloviridae, where >90% of the viral genes do not have detectable homologs in public da

82 hich identified transcription of a number of viral genes during primary infection.

83 nto the human genome is challenging with non-viral gene-editing reagents, since most of the edited se

84 The viral genes either are separated by intergenic regions (

85 ense transcription from the 3' LTR, allowing viral genes encoded on opposite DNA strands to be simult

86 This viral gene encodes a cell surface G protein-coupled rece

87 ic adaptive immunity and expression of early viral genes exclusively in the bone marrow.

88 e an important site of HCMV latency, and one viral gene expressed by latently infected myeloid cells

89 s and patient T cells, hbz is often the only viral gene expressed.

90 trand genes hbz and aph-2 are often the only viral genes expressed in HTLV-infected T cells.

91 The core set of viral genes expressed in natural infection and different

92 subjects (clinical) to define the breadth of viral genes expressed.

93 A second block, which appears to suppress viral gene expression after the viral genome has integra

94 trolled balance of differentiation-dependent viral gene expression allows the virus to stimulate cell

95 Through viral gene expression analysis, we detected expression o

96 pression of EMT genes was dependent on early viral gene expression and correlated with induction E-ca

97 ce the viral reservoir by activating dormant viral gene expression and directing T lymphocytes to lys

98 ction resulted in a significant reduction in viral gene expression and DNA replication.

99 nt provirus, but exhibit little or no active viral gene expression and effectively resist combination

100 the cellular function of Ssu72 to stimulate viral gene expression and facilitate the early S5P-S2P t

101 role of EBV in ARL pathogenesis, we analyzed viral gene expression and found highly heterogeneous pat

102 nd therefore appear to have the capacity for viral gene expression and full reactivation.IMPORTANCE I

103 itive cells resulted in diminished levels of viral gene expression and genome amplification.

104 cycle demonstrate that bisbenzimides inhibit viral gene expression and genome replication.

105 This mechanism regulates CRM1-dependent viral gene expression and is a determinant of HIV-1's ca

106 er gene (MV-NIS) facilitates localization of viral gene expression and offers a tool for tumor radiov

107 ression of Cdc25a in U-251MG cells increased viral gene expression and production of infectious proge

108 ors form a feed-forward loop that stimulates viral gene expression and productive infection following

109 he GR and KLF15 to synergistically stimulate viral gene expression and productive infection may be cr

110 Similar patterns of reduced viral gene expression and progeny virus production were

111 processes but subsequently acted to shut off viral gene expression and replication after they reached

112 HN-L intergenic region, resulting in reduced viral gene expression and replication in avian cells but

113 ed, the role, if any, of m(6)A in regulating viral gene expression and replication was previously unk

114 When viral gene expression and replication were low, the inna

115 ers these changes, in the absence of de novo viral gene expression and replication, through engagemen

116 te immune response that was able to modulate viral gene expression and replication.

117 that the SRT plays an important role in VZV viral gene expression and replication.

118 ate immune response that, in turn, modulates viral gene expression and replication.

119 ction in both cccDNA and other parameters of viral gene expression and replication.

120 V genome, resulting in robust suppression of viral gene expression and replication.

121 These viruses share common strategies for viral gene expression and replication.

122 ogenous miRNAs have the potential to inhibit viral gene expression and replication.

123 rehalose had a profound inhibitory effect on viral gene expression and strongly impaired viral spread

124 establish chromatin structure permissive for viral gene expression and the establishment of latent in

125 an essential role in the regulation of early viral gene expression and transcript processing.

126 We show that viral gene expression and virion production are signific

127 al role in KSHV lytic infection by promoting viral gene expression at the posttranscriptional level.

128 : the mutations caused no apparent effect on viral gene expression but reduced the yield of progeny v

129 Thus, we propose that NS1 facilitates late viral gene expression by acting as an adaptor between vi

130 This study demonstrates that viral gene expression can also be radically altered by m

131 This study determined the kinetics of the viral gene expression during de novo KSHV infections and

132 atin immunoprecipitation assays and enhances viral gene expression during early infection.

133 ing strand-specific RNA-seq, we have studied viral gene expression during EBV reactivation and have d

134 o viral ORFs, ORF18 and ORF30, in regulating viral gene expression during KSHV lytic replication.

135 required for the establishment of selective viral gene expression during latency.

136 was accompanied by a noticeable decreased in viral gene expression during lytic reactivation.

137 To determine the role of pIE611 for viral gene expression during MCMV infection in an unbias

138 rinsic resistance involves the repression of viral gene expression during the very early stages of in

139 integrates in regions that are favorable for viral gene expression in a variety of cell types.

140 HIV-1 latency have focused on regulation of viral gene expression in cells in which latent infection

141 recruitment to this conserved site regulates viral gene expression in differentiating epithelia.

142 there is considerable information regarding viral gene expression in infected cells, little is known

143 latency-reversing agents that induce active viral gene expression in latently infected cells, follow

144 noninvasive method to identify intracellular viral gene expression in real time.

145 Dexamethasone stimulates lytic cycle viral gene expression in sensory neurons of calves laten

146 Three-dimensional imaging of viral gene expression in the nucleus allows us to study

147 vities in order to achieve optimal levels of viral gene expression is incompletely understood.

148 mes are retained in a low number of neurons, viral gene expression is minimal, and infectious virus i

149 cancer, where replication-competent (RC) Ad viral gene expression is needed, E1A has been either mut

150 pt for viral polymerase (L) gene expression, viral gene expression is not negatively impacted or incr

151 lls, MLV integration occurs normally, but no viral gene expression is observed.

152 icted form of latency (type I) in which most viral gene expression is silenced by promoter DNA methyl

153 c cycle or to a quiescent infection in which viral gene expression is suppressed while the viral geno

154 The relative permissiveness of TG neurons to viral gene expression near the joint region is likely si

155 he effectors induced were unable to suppress viral gene expression or replication.

156 ratinocytes exhibited a predominantly latent viral gene expression program with some lytic or abortiv

157 ection entails a choreographic regulation of viral gene expression program.

158 ion (NCCR) sequences permitted greater early viral gene expression than kidney-associated NCCR sequen

159 and early-late genes during a second wave of viral gene expression that commenced at between 24 and 4

160 ating host cellular processes and activating viral gene expression through recruitment of cellular pr

161 l-intrinsic antiviral defenses that restrict viral gene expression upon virus infection.

162 applied for recessive null conditions via a viral gene expression vector transferring a cDNA encodin

163 In these AVG-positive cells, viral gene expression was inhibited.

164 exacerbated defects in viral DNA synthesis, viral gene expression, and production of infectious prog

165 significant defects in viral DNA synthesis, viral gene expression, and viral replication, which were

166 en together, UL92 is a key regulator of late viral gene expression, apparently functioning with four

167 ation and the screening of drugs influencing viral gene expression, as well as the release of infecti

168 They are involved in viral gene expression, counter host defenses by suppress

169 hoid tissue may facilitate the repression of viral gene expression, enabling establishment of true la

170 f miR-21 in NPCs and U-251MG cells inhibited viral gene expression, genome replication, and productio

171 ndependent of viral DNA synthesis or de novo viral gene expression, implicating cellular factors and/

172 1 with DDX21 leads to temporal regulation of viral gene expression, influenza A virus likely uses the

173 In most cells, it slowed and reduced viral gene expression, manifested as a shift in mean lat

174 ), marking latent, immediate early, and late viral gene expression, respectively.

175 ring infection, including transactivation of viral gene expression, suppression of innate immune resp

176 133/8 revealed a role for UL135 in promoting viral gene expression, viral DNA synthesis, and viral re

177 IRA is, however, required for suppression of viral gene expression, virus replication and lytic infec

178 they escape immune detection by restricting viral gene expression.

179 and the stability of the virions and affect viral gene expression.

180 post-translational modification, may impact viral gene expression.

181 al subversion of nuclear speckles to promote viral gene expression.

182 al mRNAs further increases the complexity of viral gene expression.

183 ockdown of miR-21 in U-251MG cells increased viral gene expression.

184 th a stable reorganization of the control of viral gene expression.

185 mpetition for proteins/ribosomes and promote viral gene expression.

186 the inhibition of early and immediate early viral gene expression.

187 es use this feedback mechanism to facilitate viral gene expression.

188 in parallel with a prior study of changes in viral gene expression.

189 nt of novel antiviral strategies that target viral gene expression.

190 ail repression of productive cycle ("lytic") viral gene expression.

191 are important for regulation of cellular and viral gene expression.

192 lar proteins that have repressive effects on viral gene expression.

193 This inhibition did not require late viral gene expression.

194 al cycle in iLC is restricted at the step of viral gene expression.

195 w factors in VSV entry and 20 new factors in viral gene expression.

196 d to reduced VSV replication at the level of viral gene expression.

197 ription antiterminator that is essential for viral gene expression.

198 Host miRNAs can also regulate viral gene expression.

199 tructural elements govern crucial aspects of viral gene expression.

200 (IE) genes, resulting in virtual absence of viral gene expression.

201 nuclear components to regulate cellular and viral gene expression.

202 s, m(6)A residues in IAV transcripts enhance viral gene expression.

203 latent state, during which there is limited viral gene expression.

204 capacity to activate optimal levels of late viral gene expression.

205 al subversion of nuclear speckles to promote viral gene expression.

206 d T cells and were enriched for functions in viral gene expression.

207 d in significant decreases in KSHV entry and viral gene expression.

208 as made, leading to more profound effects on viral gene expression.

209 converges at the incoming DNA and represses viral gene expression.

210 he absence of this protein does not restrict viral gene expression; however, cleavage of viral DNA in

211 duce viral transcription, as demonstrated by viral-gene expression analysis in U2OS cells carrying ep

212 I16 inhibits HPV18 replication by repressing viral-gene expression and replication.

213 in primary human cells in the absence of any viral-gene expression.

214 tterns of DNA methylation and both human and viral gene expressions.

215 inally, we evaluated potential correlates of viral gene flow across anatomical compartments.

216 hout Southeast Asia, documenting patterns of viral gene flow.

217 irus-targeting RNAi libraries to investigate viral gene function and suggest therapeutic avenues.

218 nt universally applicable tools for studying viral gene functions and for applications as a safety sw

219 europathogenesis and the roles of individual viral genes have not yet been fully determined.

220 s enhanced expression of eukaryotic human or viral genes in chloroplasts and offered unique insights

221 Information is needed on how viral genes in general influence phenotypic variance for

222 l mRNAs whose major role may be in silencing viral genes in latently infected neurons, suggests that

223 the 5' LTR controls expression of all other viral genes, including tax.

224 inhibitors triggered the expression of many viral genes, including U39, U90, and U100, without the p

225 Surprisingly, JNK-mediated viral gene induction occurs independently of histone dem

226 he non-invasive and targeted delivery of non-viral genes into the CNS for therapeutic purpose.

227 evolutionary histories of both the host and viral genes involved in this so-called arms race.

228 tically modified live attenuated ASFVs where viral genes involved in virus virulence were removed fro

229 Specifically, the translation of these viral genes is independent of PKR activation, but their

230 -mediated disease, in relation to individual viral genes, is a promising approach to host-oriented dr

231 creased 5-hydroxymethylation of cellular and viral genes may contribute to NPC formation.

232 ich resembles miRNAs, specifically targets a viral gene, opening an avenue for possible utilization o

233 The viral gene pe38 is not only essential for the infectivit

234 An early, IE1-regulated viral gene product acts on a necroptosis step that follo

235 levated expression of DNMT1, Notch1, and the viral gene product E1insertion markE4 in CD66(high) cell

236 RTA is an essential viral gene product involved in the initiation of gammahe

237 derstanding how expression of this essential viral gene product is regulated may identify new strateg

238 y in individual baboons, the identity of the viral gene product that is the major target of cellular

239 Although Nef is the viral gene product used by most simian immunodeficiency

240 study, we examined the relative roles of two viral gene products for the ability to promote loss of t

241 We further found that viral gene products of IE1, pp71, and UL26 play roles in

242 In this work, we identify two viral gene products required for postentry tropism in en

243 ominent feature of HCMV is the wide range of viral gene products that it encodes which function to mo

244 Among the influenza viral gene products, the hemagglutinin (HA) glycoprotein

245 Three viral gene products-IE1, pp71, and UL26-were shown to in

246 vealed that c-Fos directly binds to multiple viral gene promoters and enhances viral transcription.

247 associated with herpesvirus latency and the viral genes regulating entry into and exit from latency

248 Such a system would enable viral gene regulation and control of the viral life cycl

249 of KSHV with potentially important roles in viral gene regulation and pathogenesis.

250 l likely expand further our understanding of viral gene regulation and the proteome.

251 ese findings illustrate unique mechanisms of viral gene regulation and to the importance of virus-med

252 ase into the cytoplasm and the expression of viral genes remain elusive.

253 Viral gene sequences from an enlarged set of about 200 E

254 alysis of the transcription profiles of each viral gene showed specific expression patterns in differ

255 P34.5-targeting miRNAs and to activate lytic viral genes suggests that ICP4 could play a key role in

256 helia requires the activation of a subset of viral genes, termed early genes.

257 atency-associated transcript (LAT), the only viral gene that is abundantly transcribed during latency

258 viruses, and the identification of conserved viral genes that mediate this process will aid in the de

259 es the ordered induction of approximately 90 viral genes that participate in the generation of infect

260 Due to the absence of viral genes, the virus-like particles are unable to spre

261 hese results pave the way toward a novel non-viral gene therapy approach for DMD using PB transposons

262 romise for the successful application of non-viral gene therapy in skin disease.

263 With the leukemogenic concerns of viral gene therapy there is a need to explore alternativ

264 ippocampal neurons in BAI1-deficient mice by viral gene therapy was sufficient to compensate for Bai1

265 n rhodopsin in the inner retina, mediated by viral gene therapy, can restore light sensitivity and so

266 ction of MMP-9 function using gene ablation, viral gene therapy, or pharmacological inhibition signif

267 Primates have co-opted a viral gene to produce an envelope protein that prevents

268 study, we evaluated the contribution of each viral gene to virulence individually and in different co

269 Virus activation is not mediated by viral gene transactivation, given that these mutations d

270 ion packaged transcripts and the profiles of viral genes transcribed after de novo infections of vari

271 multicopy episomes with complex patterns of viral gene transcription and chromatin structure.

272 These cells exhibit limited viral gene transcription and no evidence of de novo viri

273 iate early gene E1A initiates the program of viral gene transcription and reprograms multiple aspects

274 nderstanding of the mechanisms that regulate viral gene transcription during latency.

275 Viral gene transcription in host cell assemblages reveal

276 ed state of the virus and the maintenance of viral gene transcription throughout.

277 ENS infection led to robust viral gene transcription, pathological inflammatory resp

278 the HSV-1 genome, reflecting a high level of viral gene transcription.

279 host cell genes, suggesting a unique mode of viral gene transcription.

280 ent KSHV-infected B cells leads to increased viral gene transcription.

281 es via protein-protein interaction to enable viral gene transcription.

282 (HCMV) homologue pUL79 are required for late viral gene transcription.

283 and it blocks repressor complexes to enable viral gene transcription.

284 us (AAV) has become the vector of choice for viral gene transfer and has shown great promise in clini

285 Magnetofection, a non-viral gene transfer approach deploying magnetic nanopart

286 This review is supplemented with in vivo viral gene transfer experiments and comparisons of avail

287 Viral gene transfer expressed vglut1-pHluorin in IHCs an

288 e and ultrasound-mediated enhancement of non-viral gene transfer in vivo.

289 proposed therapy for cocaine abuse based on viral gene transfer of butyrylcholinesterase (BChE) muta

290 Viral gene transfer of full-length dystrophin could rest

291 Here we applied viral gene transfer of the acyl-ghrelin hydrolyzing enzy

292 Using viral gene transfer of transcription factor EB (TFEB), a

293 and may overcome limitations associated with viral gene transfer vectors and transient nonviral gene

294 We used novel targeted viral gene transfer vectors expressing redox-sensitive G

295 physiological recording, calcium imaging and viral gene transfer.

296 zation/preimplantation development, vertical viral gene transmission, gene function and regulation, a

297 The expression of viral genes (UL122, UL44, UL54, UL55, and UL84) affected

298 Here we show that one of the conserved viral genes, UL51, has an important role in cell-to-cell

299 phylogenetic trees were constructed for each viral gene using the nucleotide sequences, thereby defin

300 e therapy with various viral vectors and non-viral gene vectors is well tolerated by patients, and co