ライフサイエンスコーパス: viral gene

1 ndem to enable transcriptional regulation of viral gene.

2 sRNA cassette targeting a shrimp yellow head viral gene.

3 -type-specific requirements for a particular viral gene.

4 erminus of E1A to regulate the expression of viral genes.

5 generate cell lines expressing exogenous non-viral genes.

6 te the expression of antioxidative genes and viral genes.

7 ram, including an orchestrated expression of viral genes.

8 oviding insights into functions for multiple viral genes.

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

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

11 r altering the expression or function of the viral genes.

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

13 xonomic classification according to hallmark viral genes.

14 was associated with silencing of particular viral genes.

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

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

17 replication by regulating the expression of viral genes.

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

19 and points of interaction between human and viral genes.

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

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

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

23 transcripts for the expression of individual viral genes.

24 ruses and we show uORFs are enriched in late viral genes.

25 -stranded (dsRNA) designed to knock down key viral genes.

26 cell and activate transcription of all other viral genes.

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

28 ing a system that assigns a genotype to each viral gene according to its nucleotide sequence.

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

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

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

32 50 RTA is a known transactivator of multiple viral genes, allowing it to control the switch between l

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

34 Expression of viral genes and activation of innate antiviral responses

35 siRNAs corresponding to integrated viral genes and LTR retrotransposons, but not to DNA tra

36 ted cells vary widely in their expression of viral genes and only occasionally activate innate immuni

37 We additionally discovered pro-viral genes and pathways, including HMGB1 and the SWI/SN

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

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

40 oteins are integral for the transcription of viral genes and the replication and maintenance of viral

41 differentially expressed genes: 63 DEGs were viral genes and their expression in WSSV group either pe

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

43 Viral genes and transcripts can be visualized on both li

44 ults in striking defects in re-expression of viral genes and viral genome replication in the THP-1 la

45 ase protein PB1, large internal deletions in viral genes, and failure to express the virus's interfer

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

47 genome, represses transcription of numerous viral genes, and suppresses productive in vitro infectio

48 ome, silencing the transcription of numerous viral genes, and ultimately limiting overall infection.I

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

50 l genome is predominantly latent; i.e., most viral genes are not expressed, most viral proteins are n

51 Whether viral genes are transcriptionally active in these indivi

52 s and transcribe viral mRNAs from individual viral genes as well as synthesize 5' methylated cap and

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

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

55 genes but also by control of elongation into viral gene bodies.

56 regulated not only by Pol II recruitment to viral genes but also by control of elongation into viral

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

58 erpes simplex virus 1 (HSV-1), can derepress viral genes by degrading ND10 organizers to disrupt ND10

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

60 The viral genes can be classified into three distinct kineti

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

62 pounds widely investigated to be used as non-viral gene carriers including lipids, polymers, carbon m

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

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

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

66 Previous attempts to identify the viral genes containing trout virulence determinants of v

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

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

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

70 These studies demonstrate that non-viral gene delivery is impacted by proteoglycan interact

71 We also show that viral gene delivery of Yap5SA in the postnatal inner ear

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

73 The design of a non-viral gene delivery system that can release a functional

74 e will discuss the recent discoveries on non-viral gene delivery systems.

75 as to examine the effectiveness of novel non-viral gene delivery systems.

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

77 eveal that silica cloaking of Ad can enhance viral gene delivery while reducing immunogenicity.

78 cells in the brain, autophagy in the retina, viral gene delivery, and chemical diffusion through the

79 skin more efficiently than adeno-associated viral gene delivery.

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

81 ur results uncover a novel role for co-opted viral genes, demonstrating that they are used to modulat

82 c) viral antigen detection, among which the viral gene detection by RT-PCR has been found as the mos

83 tools available so far have been based on a) viral gene detection, b) human antibody detection, and c

84 nduced cytokines/chemokines and cellular and viral genes differed among the infected type 1, 2, and 3

85 Comparing EBV types, viral genes displayed differential variation rates as ty

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

87 ral replication, our results indicate that a viral gene drive can be used as a strategy to suppress a

88 n signaling, and it upregulates putative pro-viral genes (e.g., DYNLL1 and HSPA5), nominating pathway

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

90 The viral genes either are separated by intergenic regions (

91 Specifically, activation of ancient viral genes embedded in the human genome is theorized to

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

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

94 Whether inactivation of multiple viral genes enhances replication in the host cells or ha

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

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

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

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

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

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

101 y, ARS2 knockdown has only modest effects on viral gene expression 24 h after lytic reactivation of w

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

103 We find extreme variability in the level of viral gene expression among individually infected cells

104 al role during infection, because it enables viral gene expression and blocks antiviral responses.

105 HSV, by promoting open chromatin needed for viral gene expression and by inhibiting the DNA damage r

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

107 vation from latency requires reinitiation of viral gene expression and culminates in the production o

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

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

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

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

112 not completely explain-the heterogeneity in viral gene expression and immune activation in single in

113 down of RUNX1 in neuroblastoma cells induced viral gene expression and increased HSV-1 infection in v

114 n during RSV entry, leading to inhibition of viral gene expression and infection.

115 t not all of the cell-to-cell variability in viral gene expression and innate immune induction.

116 be binding HSV-1 genome directly to suppress viral gene expression and lytic infection.

117 ropinocytosis and endocytosis reduced latent viral gene expression and precluded reactivation.

118 the glucocorticoid receptor (GR), stimulates viral gene expression and productive infection during re

119 e GR form a feed-forward loop that activates viral gene expression and productive infection following

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

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

122 ation compartments, and is required for late viral gene expression and progeny production.

123 find that elimination of Nrp-1 impairs early viral gene expression and reduces infection rates in end

124 otein facilitates the multiple regulation of viral gene expression and replication and reveals a nove

125 XBP1u inhibits viral gene expression and replication by blocking the ac

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

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

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

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

130 lenges, we sought to merge the robustness of viral gene expression and the versatility of nanoparticl

131 ty of viral genomes, which is restrictive to viral gene expression and which E1A overcomes via a dire

132 tic and epitranscriptomic processes regulate viral gene expression at the levels of chromatin and RNA

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

134 nfection, suggesting potential regulation of viral gene expression by EBNA-antisense transcription du

135 ovel mechanism by which the virus can adjust viral gene expression by modifying its genome's nucleoso

136 mation of stress granules (SGs) and modulate viral gene expression by subverting different proteins i

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

138 LF4) correlates with stimulating lytic cycle viral gene expression following stressful stimuli.IMPORT

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

140 explanation for the selective activation of viral gene expression in DCs by IL-6, dependent on conco

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

142 dent RNA polymerase (vRNAP) that carries out viral gene expression in the host cytoplasm.

143 for the hypothesis that there is persistent viral gene expression in the HSV-1 latently infected TG.

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

145 ranscription, which was confirmed by reduced viral gene expression in TZM-bl or P4R5 cells.

146 acting with the viral genome and suppressing viral gene expression is important because it might lead

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

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

151 It has been presumed that viral gene expression is reinitiated via de-repression o

152 ve and UV-inactivated KSHV demonstrated that viral gene expression is responsible for the upregulatio

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

154 Consequently, viral gene expression is stimulated by the activated GR.

155 The initial activation of viral gene expression may be mediated by oxidative stres

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

157 performed at high MOIs resulted in increased viral gene expression per cell and stronger antagonist e

158 We demonstrate a novel viral gene expression strategy to target cells with spec

159 Traditional promotor-based viral gene expression techniques, however, cannot captur

160 K activation and included an initial wave of viral gene expression that was independent of histone de

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

162 programming to ensure the proper control of viral gene expression, DNA replication, and genome copy

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

164 llular gene expression, upregulation of late viral gene expression, inhibition of apoptosis, preventi

165 se epigenetic modifications can also repress viral gene expression, potentially functioning as a pote

166 nt KSHV restriction factor by impeding early viral gene expression, suggesting that its ability to es

167 in the latently infected TG is influenced by viral gene expression, suggests that Tim-3 is an indicat

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

169 he host transcription factor Sp1 that drives viral gene expression.

170 o reprogram the host cell, and the levels of viral gene expression.

171 directly stimulate productive infection and viral gene expression.

172 educes the effects of FAM111A restriction on viral gene expression.

173 bortive, which occurred at the stage of late viral gene expression.

174 ng these cancers involve activation of lytic viral gene expression.

175 on of HIV-1 mRNA, thereby affecting directly viral gene expression.

176 he GR can stimulate productive infection and viral gene expression.

177 genome and allows the temporal regulation of viral gene expression.

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

179 immunodeficiency virus 1 (HIV-1) to increase viral gene expression.

180 tructural elements govern crucial aspects of viral gene expression.

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

182 nuclear components to regulate cellular and viral gene expression.

183 iptomic modifications as a means to maximize viral gene expression.

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

185 antiviral necroptotic cell death upon early viral gene expression.

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

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

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

189 signals could induce upregulation of latent viral gene expression.

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

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

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

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

194 they escape immune detection by restricting viral gene expression.

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

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

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

198 ead repurposed by influenza virus to promote viral gene expression.

199 utilize these processes in order to regulate viral gene expression.

200 A conformation regulates splice-site use and viral gene expression.

201 rinsic immune response that is important for viral gene expression.

202 minished the effects of FAM111A depletion on viral gene expression.

203 h and reduced nuclear Nrf2, antioxidant, and viral gene expression.

204 by interacting with KSHV DNA and inhibiting viral gene expression.IMPORTANCE Kaposi's sarcoma-associ

205 /Meq heterodimer, which targets cellular and viral gene expression.IMPORTANCE MDV is a potent oncogen

206 d highlight a novel mechanism that regulates viral gene expression.IMPORTANCE To successfully replica

207 enetic state of the viral genome to regulate viral gene expression; and reactivating to infect other

208 Geospatial diffusion (ie, viral gene flow) was evaluated using a Slatkin-Maddison

209 actor is required for the induction of lytic viral genes for KSHV lytic reactivation, it is still unk

210 nology should be useful for knocking out any viral genes from a genome to dissect functions of indivi

211 ifferentiation, cell signaling pathways, and viral gene functions.

212 genome in great detail to better understand viral gene functions.

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

214 ne system processes, in addition to reported viral genes.IMPORTANCE Lymphoid leukosis (LL)-like lymph

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

216 system that allows for deletion of specific viral genes in discrete populations of cells.

217 substantially increasing the scale of known viral genes in eukaryotic genomes.

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

219 anscriptome and full-length sequences of all viral genes in single cells infected with a nominally "p

220 a genome to dissect functions of individual viral genes in the context of the virus genome and to un

221 and, as described here, numerous integrated viral genes including viral envelope genes that are part

222 inae, ICP27 regulates the expression of many viral genes, including expression of pUL44 (gC), pUL47 (

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 ithelial cells with subsequent expression of viral genes, including vpr.

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

227 transcription factor regulating hundreds of viral genes- is only partially correlated with viral pro

228 rf2) is essential for both the expression of viral genes (latency) and modulation of the host antioxi

229 a combination of host cell type and specific viral gene-level differences.

230 In addition to viral genes missing from the Wolbachia reference genome,

231 ether host transcription factors can repress viral genes more proximately to promote latency in dorsa

232 e observed, indicating de novo expression of viral genes postvaccination.

233 Our findings reveal that a viral gene product can function in distinct cellular sub

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

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

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

237 irus is produced, is mainly regulated by the viral gene product, Zta.

238 tend the current nomenclature to include all viral gene products and provide a genome browser that vi

239 to HCMV UL148.IMPORTANCE In myriad examples, viral gene products cause striking effects on cells, suc

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

241 tency establishment, an understanding of how viral gene products function in specific B cell subsets

242 Whether and how these viral gene products function in specific cells of the im

243 ath by necroptosis requires the detection of viral gene products late in infection; mu1 limits cell d

244 properties and interactions between host and viral gene products that can be exploited for the develo

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

246 ent betaherpesvirus that encodes a number of viral gene products that modulate cellular antiviral sig

247 ecause it prevents excessive accumulation of viral gene products that trigger cell death.

248 riptional template for the production of all viral gene products, and thus, it is the molecular basis

249 zed cores and the consequent accumulation of viral gene products.

250 s diversity on the structure and function of viral gene products.

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

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

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

254 hanism, DNA methylation could have a role in viral gene regulation.

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

256 This study provides a proof of principle for viral gene replacement therapy targeted to Schwann cells

257 d versions of TR3 were generated by deleting viral genes required to counteract intrinsic and innate

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

259 lass II-restricted CD8+ T cells with an anti-viral gene signature expressed both CD4+ and CD8+ T cell

260 sites in the HSV-1 genome, repress numerous viral genes spanning all three kinetic classes, and supp

261 In summary, the miRNA-based viral gene targeting strategy described here allows us t

262 nterneurons, labeled via a novel miRNA-based viral gene targeting strategy, combinatorial to traditio

263 gnificant differences between swabs for both viral gene targets in the Roche cobas assay (p=0.05 and

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

265 ional machinery and direct it to a subset of viral genes that are required for completion of the vira

266 nt of the expression of previously described viral genes that regulate the MHC class II complex or th

267 this process requires the products of seven viral genes: the terminase proteins pUL15, pUL28, and pU

268 s, such as nucleotide-based therapeutics and viral gene therapies, are rapidly maturing towards wides

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

270 A4 based nanoparticles are promising for non-viral gene therapy for Stargardt disease and can be expe

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

272 Viral gene therapy is a means of delivering genes to rep

273 eviously, we have developed an effective non-viral gene therapy using self-assembled nanoparticles of

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

275 vidual polymerase II (Pol II) transcripts of viral genes to each one of the mapped pA sites at single

276 Essential contributions of viral genes to viral replication are known, but the pote

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

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

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

280 Viral gene transcription in host cell assemblages reveal

281 re more enriched and more closely located to viral gene transcription start sites than would be expec

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

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

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

285 e RNA genome in the virion and regulation of viral gene transcription.

286 f poxviruses through the inhibition of early viral gene transcription.

287 bining VLT and ORF63 proteins, induces broad viral gene transcription.

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

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

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

291 Viral gene transfer of full-length dystrophin could rest

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

293 livery, these bioinks supported enhanced non-viral gene transfer to stem cells in vitro.

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

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

296 loped and used to image tumor cells, cardiac viral gene transfer, and oncolytic virotherapy.

297 physiological recording, calcium imaging and viral gene transfer.

298 s the splicing and the expression of another viral gene, UL44, which is essential for viral transmiss

299 plasma samples were tested for mutations in viral genes UL97, UL54 and/or UL27.

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