ライフサイエンスコーパス: RNA replication

1 nificantly reduced HCV infection but not HCV RNA replication.

2 ession inhibited HCV protein translation and RNA replication.

3 iral nonstructural (NS) proteins involved in RNA replication.

4 ll of which are important for 5'-capping and RNA replication.

5 y be partly involved in the process of viral RNA replication.

6 l step involving protein synthesis and viral RNA replication.

7 ellular virus assembly without affecting HCV RNA replication.

8 rect the DI RNA to a critical site, enabling RNA replication.

9 ediate cap-independent translation and viral RNA replication.

10 wever, cleaved PCBP2 remains active in viral RNA replication.

11 emplate for both viral protein synthesis and RNA replication.

12 al WAPEFPWM domain is required in cis for DI RNA replication.

13 de novo formation of the membranous web and RNA replication.

14 tivity is central to viroplasm formation and RNA replication.

15 switch in template usage from translation to RNA replication.

16 ponses in these cells modestly increased HCV RNA replication.

17 particle production but not in HCV entry or RNA replication.

18 icated in cyclophilin A (CypA)-dependent HCV RNA replication.

19 t act as a template for both translation and RNA replication.

20 switch in template usage from translation to RNA replication.

21 inal portion of ORF B, is required for viral RNA replication.

22 infectious cycle at the step of steady-state RNA replication.

23 5B that may facilitate de novo initiation of RNA replication.

24 stead occurs inside the cell at the level of RNA replication.

25 d genetically separable functions of NS5A in RNA replication.

26 the CRE, the 5BSL3.2 stem-loop, impairs HCV RNA replication.

27 lipid rafts to autophagosomes to mediate its RNA replication.

28 ere shown to be required for efficient viral RNA replication.

29 ntal demonstration of effective nonenzymatic RNA replication.

30 te that functions as a negative regulator of RNA replication.

31 lymerase-polymerase interactions facilitates RNA replication.

32 alpha (IFNalpha), but have no effect on HCV-RNA replication.

33 ed to generate the membrane platform for HCV RNA replication.

34 es autophagosomal membranes as sites for its RNA replication.

35 1 is an essential gene linked to early viral RNA replication.

36 o their well-documented inhibitory effect on RNA replication.

37 conveys signals to the cytoplasm to regulate RNA replication.

38 he alpha- and beta-segments are required for RNA replication.

39 nal RNA elements required for translation or RNA replication.

40 erdomain interaction within NS5 required for RNA replication.

41 in human hepatoma cells with persistent HCV RNA replication.

42 2C(ATPase) polypeptide that are required for RNA replication.

43 the idea that Pkc1p is an inhibitor of TBSV RNA replication.

44 ymerase, 3D(pol), that is required for viral RNA replication.

45 turase gene OLE1, which is essential for BMV RNA replication.

46 pid rafts, from autophagosomes abolished HCV RNA replication.

47 n RNA secondary structure required for viral RNA replication.

48 ifunctional HCV protein that is required for RNA replication.

49 raction between NS4A and NS4B contributes to RNA replication.

50 the 5' end of negative-strand RNA during PV RNA replication.

51 membranes to generate specialized sites for RNA replication.

52 NAs were used as reciprocal templates during RNA replication.

53 between the 5' and 3' ends of the genome for RNA replication.

54 translation start site selection as well as RNA replication.

55 the HCV life cycle that is important for HCV RNA replication.

56 inositol 4-kinase IIIbeta (PI4KB) for genome RNA replication.

57 n RNA secondary structure required for viral RNA replication.

58 erules play an important role in stimulating RNA replication.

59 etails of how the viral helicase facilitates RNA replication.

60 egion present in the 3' NCR to enhance viral RNA replication.

61 of redundancy in the use of host factors in RNA replication.

62 nstructural (NS) proteins and inhibits viral RNA replication.

63 RNA stem-loops that are essential for viral RNA replication.

64 d a lethal growth phenotype due to defective RNA replication.

65 ce, and function during positive-sense viral RNA replication.

66 triple alanine mutants exhibited defects in RNA replication.

67 gion increases viral titer without affecting RNA replication.

68 ge one viral RNA template for another during RNA replication.

69 n diameter and known to be the site of viral RNA replication.

70 c RNA synthesis and may have aided prebiotic RNA replication.

71 factors responsible for the lack of genomic RNA replication.

72 he N- and C-terminal regions inhibited viral RNA replication.

73 articles with no effect on HCV attachment or RNA replication.

74 ced JAK1 and IRF9 expression and reduced HCV RNA replication.

75 prior to the evolution of ribozyme-catalyzed RNA replication.

76 cells, leading to the establishment of viral RNA replication.

77 the HCV replication factory, independent of RNA replication.

78 the following two distinct functions in HCV RNA replication: a cis-acting function that likely occur

79 Inhibition of DENV RNA replication abrogated these responses.

80 Intracellular RNA replication activates a strong innate immune respons

81 sion activity and slightly reduces the viral RNA replication activity.

82 The compounds prevent viral RNA replication after the synthesis of the uridylylated

83 of charged residues for NS4B function in HCV RNA replication, alanine substitutions were engineered i

84 s effect on HCV entry, FQ also inhibited HCV RNA replication, albeit at a higher concentration.

85 characterized kinetics and thermodynamics of RNA replication allow us to determine the physicochemica

86 pism for human PDA cells, resulting in viral RNA replication and a potent induction of apoptosis in v

87 stimate based on models of intracellular HCV RNA replication and accumulation that cells in clusters

88 process the viral polyprotein to facilitate RNA replication and antagonize the host innate immune re

89 Intracellular RNA replication and assembly and release of new particle

90 nd the functional mechanism of NS2B in viral RNA replication and assembly.

91 Semliki Forest virus (SFV) requires RNA replication and Bax/Bak for efficient apoptosis indu

92 nd dasatinib inhibit DV at the step of viral RNA replication and demonstrate a critical role for Fyn

93 repression of alphavirus replicon and helper RNA replication and demonstrate the feasibility of miRNA

94 coating, host cell membrane alterations, and RNA replication and encapsidation have previously been i

95 virus 2C(ATPase) has important roles both in RNA replication and encapsidation.

96 cting proteins, L and NP, required for virus RNA replication and gene expression were exchangeable in

97 acting viral factors required for both virus RNA replication and gene transcription, requires the pre

98 ribonucleoprotein (vRNP) that directs viral RNA replication and gene transcription.

99 In contrast, RNA replication and infection of genotype 2a were minima

100 roRNA in HepG2 cells permitted efficient HCV RNA replication and infectious virion production.

101 NS5A is required for HCV RNA replication and is involved in viral particle format

102 th AZD0530 and dasatinib, is involved in DV2 RNA replication and is probably a major mediator of the

103 uctures that are crucial for translation and RNA replication and may play additional, uncharacterized

104 he function of its nonstructural proteins in RNA replication and modification of the intracellular en

105 s had a significant decrease in both genomic RNA replication and mRNA transcription.

106 are assembled in the cytoplasm during genome RNA replication and must migrate to the plasma membrane

107 tombusviruses could adjust the efficiency of RNA replication and new VRC assembly to the limiting res

108 cycle infection experiments showed that ZIKV RNA replication and nonstructural protein 5 translation

109 rhesus macaques are also permissive for HCV-RNA replication and particle production, which is enhanc

110 2-E158G had a much stronger influence on the RNA replication and pathogenesis of H1N1pdm viruses than

111 deletion of ACBD3 drastically impairs viral RNA replication and plaque formation.

112 Elucidating the molecular mechanisms of RNA replication and recombination may help mankind achie

113 apted mutations had 10-fold-higher levels of RNA replication and RNA release into the supernatant but

114 tinguish among the two enantiomers, enabling RNA replication and RNA-based evolution to occur.

115 lpful for both the emergence of nonenzymatic RNA replication and the early evolution of functional RN

116 the arterivirus PRRSV participates in viral RNA replication and transcription through interacting wi

117 t due to its ability to interfere with viral RNA replication and transcription.

118 he biological impact of these factors on HCV RNA replication and treatment response.

119 RNA replication and viral titre were unaltered in viruse

120 as three structural domains, is required for RNA replication and virion assembly, and exists in hypo-

121 role that HCV polyprotein precursors play in RNA replication and virion assembly.

122 atitis C virus NS5A protein is essential for RNA replication and virion assembly.

123 e TMDs of JEV NS2B participate in both viral RNA replication and virion assembly.

124 xible N-terminal arm of the CP increased BMV RNA replication and virion production.

125 le of the NS4A TM domain in coordinating HCV RNA replication and virus particle assembly.

126 d NV RNA into mammalian cells leads to viral RNA replication and virus production.

127 olyprotein expression independent from viral RNA replication and which recapitulate the major alterat

128 nase is a necessary step for efficient viral RNA replication and, as such, may be important for media

129 ional autophagy components facilitates viral RNA replication and, more importantly, is required for i

130 tabilized NS4A dimers also caused defects in RNA replication and/or virus assembly.

131 roteases and precursors, monitoring of viral RNA replication, and evaluation of antiviral agents.

132 Helicase activity is required for RNA replication, and genetic evidence implicates the hel

133 Pro(314)-Trp(316) turn, is essential for HCV RNA replication, and its disruption alters the subcellul

134 ed cleavage efficiency did not support viral RNA replication, and only revertant viruses with a resto

135 play of these 5' RNA elements in relation to RNA replication, and our data indicate that two separate

136 host innate immunity, and possibly in viral RNA replication, and that it can serve as a novel target

137 t steps of the viral cycle, including entry, RNA replication, and virion biogenesis.

138 er only minor or no negative effects on SINV RNA replication; and (vii) in mosquito cells, at any tim

139 rase (RdRp) initiates mRNA transcription and RNA replication are poorly understood.

140 However, Mga2p processing and BMV RNA replication are restored by supplementing free ubiqu

141 at disrupts VP1 expression was defective for RNA replication, as quantified by luciferase reporter as

142 ase, flavivirus NS2B also functions in viral RNA replication, as well as virion assembly.

143 hepatitis C virus (HCV) life cycle including RNA replication, assembly, and translation.

144 ive replication phenotype with no detectable RNA replication at 39 degrees C, demonstrating that cond

145 Additionally, FAK inhibition impeded viral RNA replication at later times of infection and ultimate

146 VS(-/-) miR-122 cells sustained vigorous HCV RNA replication, attaining levels comparable to the high

147 quired for efficient hepatitis C virus (HCV) RNA replication both in cell culture and in vivo.

148 two DB structures are required not only for RNA replication but also for optimal translation.

149 ition in the JFH1 genome did not alter viral RNA replication but reduced infectivity by approximately

150 expressing the NS5-specific TCR reduced HCV RNA replication by a noncytotoxic mechanism, the NS3-spe

151 S4B protein that overcomes the inhibition of RNA replication by AZD0530, dasatinib, and Fyn RNAi.

152 The process of RNA replication by dengue virus is still not completely

153 Here we study the details of HCV RNA replication by determining crystal structures of sta

154 ndings show the potential for blocking viral RNA replication by modulating lipid synthesis at multipl

155 evelopment of a comprehensive description of RNA replication by NS5B and is relevant to understanding

156 Inhibition of protease activity can block RNA replication by preventing expression of mature repli

157 5HC, restricts HCV primarily at the level of RNA replication by preventing formation of the viral rep

158 phenotypic effects on ketoamide resistance, RNA replication capacity, and infectious virus yields in

159 BMV RNA replication compartments are not released from their

160 al ER tubules to the interior of BMV-induced RNA replication compartments on perinuclear ER.

161 BMV RNA replication compartments show parallels with membran

162 RHPs interact with 1a, are incorporated into RNA replication compartments, and are required for multi

163 ized features of Flock house nodavirus (FHV) RNA replication compartments.

164 d lymphoid tissue, CD4 T-cell-associated HIV RNA, replication competent viral size of 2.1 copies per

165 erent factors in the hepatitis C virus (HCV) RNA replication complex are not well understood.

166 g proteins that play multiple roles in viral RNA replication complex formation and function.

167 herefore provides the first link between NoV RNA replication complex formation and the pathogenesis o

168 us HA, we demonstrated the role of the viral RNA replication complex in efficient replication of viru

169 The association of the HCV RNA replication complex with the autophagosomal membrane

170 hich are two important components of the HCV RNA replication complex, and nascent HCV RNA to autophag

171 disparate localization of NS1 and the viral RNA replication complex, as the latter is present on the

172 Here we show that NoV establishes RNA replication complexes (RCs) in association with mito

173 rosophila cells, Flock House nodavirus (FHV) RNA replication complexes form on outer mitochondrial me

174 protein (G3BP) and sequesters it into viral RNA replication complexes in a manner that inhibits the

175 possibly facilitating the assembly of viral RNA replication complexes on the cytoplasmic face of int

176 e hypothesis that Nodamura virus establishes RNA replication complexes that associate with mitochondr

177 Prior studies established that initiation of RNA replication could be facilitated by starting with a

178 an or avian cell lines, and viral as well as RNA replication could not be detected at 37 degrees C or

179 tact forms of PCBP2 have a role in the viral RNA replication cycle.

180 e-containing reporter virus, we demonstrated RNA replication defects in all lethal and quasi-infectio

181 Thus, BMV replication vesicle formation and RNA replication depend on the direct linkage and concert

182 Our results also show that BMV RNA replication depends on additional Mga2p-regulated ge

183 pendent sets of protein complexes supporting RNA replication, distinguishable by the minimum polyprot

184 has been studied as a model for nonenzymatic RNA replication during the origin of life.

185 However, the reason for inefficient HCV RNA replication efficiency in mouse liver cells remains

186 The truncated RdRp required a cis-acting RNA replication element and soluble host factors, while

187 ed in initiation and elongation during viral RNA replication, establish the allosteric mechanisms by

188 es was specific and productive, resulting in RNA replication, expression of Gag and Env, and generati

189 ence that VLVs arise from membrane-enveloped RNA replication factories (spherules) containing VSV G p

190 ltrastructure and function of organelle-like RNA replication factories.

191 Peretinoin inhibited RNA replication for all genotypes and showed the stronge

192 es in vitro and found a strong inhibition of RNA replication for genotype 1a and genotype 1b.

193 ition was due not to interference with virus RNA replication, gene expression, or budding but rather

194 ving an RNA secondary structure required for RNA replication have been recently reported as a possibl

195 mplex formed with proteins involved in viral RNA replication.IMPORTANCE Dilated cardiomyopathy is the

196 n of lipid rafts with autophagosomes for its RNA replication.IMPORTANCE HCV can cause severe liver di

197 te copying, which renders multiple rounds of RNA replication impossible.

198 ed from HCV replicon cells could mediate HCV RNA replication in a lipid raft-dependent manner, as the

199 human microRNA 122 (miR-122) further boosted RNA replication in all knockout cell lines.

200 usly reported that B2 is dispensable for FHV RNA replication in BHK21 cells; therefore, we chose this

201 acids in the NS3 helix alpha(0) impaired HCV RNA replication in cells with a functional RIG-I pathway

202 Using a system to study Sindbis virus RNA replication in Drosophila melanogaster, we found tha

203 ic, protect double-stranded RNA, and enhance RNA replication in general.

204 HCV growth and RNA replication in hepatoma cell lines stably expressing

205 d analyzed the effects of deletions on viral RNA replication in Huh7 cells.

206 Together, these results indicate that HuNoV RNA replication in mammalian cells does not induce an IF

207 e, we investigated the IFN response to HuNoV RNA replication in mammalian cells using Norwalk virus s

208 Our results show that HuNoV RNA replication in mammalian epithelial cells does not i

209 fected the timing of CP expression and viral RNA replication in plants.

210 ss loss in the form of reduced efficiency of RNA replication in the absence of the drug.

211 -7977 being the more active inhibitor of HCV RNA replication in the HCV replicon assay.

212 (ii) The VEEV HVD is not required for viral RNA replication in the highly permissive BHK-21 cell lin

213 in combination with reduced levels of viral RNA replication in yeast or in vitro based on cell extra

214 residues for multiple NS4B functions in HCV RNA replication, including the formation of a functional

215 y, we also found that FAK can regulate viral RNA replication independently of its role in entry.

216 None of these mutations affected RNA replication, indicating that the N-terminal region o

217 promoter located in the alphavirus-specific RNA replication intermediate and is not further amplifie

218 machinery to recognize viral double-stranded RNA replication intermediates and transposon transcripts

219 eplication enzymes are produced in excess to RNA replication intermediates, and a large fraction of t

220 Consistent with a lack of IFN induction, NV RNA replication is enhanced neither by neutralization of

221 We show that BMV RNA replication is inhibited 80-90% by deleting the reti

222 cellular co-factor cyclophilin A (CypA), HCV RNA replication is markedly diminished, providing geneti

223 ere that involvement of DOA4 and BRO1 in BMV RNA replication is not dependent on the MVB pathway's me

224 ntation experiments with SINV suggested that RNA replication is restricted by the inability of the EI

225 Using this system, we show here that NV RNA replication is sensitive to type I (alpha/beta) and

226 Prior results show that BMV RNA replication is severely inhibited by deletion of the

227 One unsolved difficulty with non-enzymatic RNA replication is that template-directed copying of RNA

228 However, the plausibility of nonenzymatic RNA replication is undercut by the lack of a protocell-c

229 ; while TRIM56 curbs intracellular YFV/DENV2 RNA replication, it acts at a later step in HCoV-OC43 li

230 EILV is restricted both at entry and genomic RNA replication levels in vertebrate cells.

231 ), the minimum components required for viral RNA replication lie in the NS3-5B region, while virion a

232 s-induced spherular invaginations similar to RNA replication-linked spherules induced by many (+)RNA

233 elusive but essential component of the viral RNA replication machine.

234 monstrated a strong positive impact on viral RNA replication, mediated the development of a more cyto

235 l entry, primary translation, or ongoing HCV RNA replication, nor do they suppress persistent HCV inf

236 a possible explanation for the low level of RNA replication observed for the 5'-deleted viral genome

237 strand RNA viruses, brome mosaic virus (BMV) RNA replication occurs in membrane-invaginated vesicular

238 prebiotically plausible protocell, in which RNA replication occurs within a fatty acid vesicle, have

239 ture model allowing a thorough comparison of RNA replication of both viruses.

240 tion of a single cDNA, SEC14L2, that enabled RNA replication of diverse HCV genotypes in several hepa

241 ulture model enabling comparative studies on RNA replication of HAV and HCV in a homogenous cellular

242 troduction of NS4B F86C specifically rescued RNA replication of mutant WNV but did not affect the wil

243 bound viral replicase, we performed complete RNA replication of Tomato bushy stunt virus (TBSV) in ye

244 Ice furthermore relieves the dependence of RNA replication on prebiotically implausible substrate c

245 perature-sensitive mutants were defective in RNA replication only at the restricted temperatures.

246 ibited a post-attachment entry step, but not RNA replication or assembly; its inhibitory concentratio

247 PF-429242 did not affect virus RNA replication or budding but had a modest effect on vi

248 7 cells but had only minimal impact on viral RNA replication or cell proliferation and viability.

249 f NS5A in RNA-transfected cells but not with RNA replication or core protein expression levels.

250 of E-cadherin, however, had no effect on HCV RNA replication or internal ribosomal entry site (IRES)-

251 The introduced mutations did not affect RNA replication or structural protein synthesis but had

252 tations did not affect GPC processing, virus RNA replication, or gene expression.

253 uridine residues to the virus genome-encoded RNA replication primer VPg prior to positive-strand synt

254 andidates for playing important roles in the RNA replication process.

255 ts may occur in a concerted mode to regulate RNA replication, processivity, and fidelity.

256 o genomic RNAs; RNA1 encodes multifunctional RNA replication protein A and RNA interference suppresso

257 ing structure containing multifunctional FHV RNA replication protein A.

258 ate step in the viral life cycle after viral RNA replication, protein synthesis, and polyprotein proc

259 helial IFN response in host control of HuNoV RNA replication, providing important insights into our u

260 cing antiviral defense response and in viral RNA replication, respectively.

261 Furthermore, the EILV RNA replication restriction is independent of the 3' unt

262 nd double-stranded RNA, a presumed marker of RNA replication, revealed that the subcellular localizat

263 packaging signal, which overlapped with the RNA replication signal.

264 is required for the recruitment of PI4KB to RNA replication sites.

265 ACBD3, and 3A are all localized to the viral-RNA replication sites.

266 ive strategy for recruitment of PI4KB to the RNA replication sites.IMPORTANCE Enterovirus 71, like ot

267 copying RNA into DNA had similar fidelity to RNA replication, so information could be maintained duri

268 the complex possess multiple roles in viral RNA replication, some of which can be provided in trans

269 Among patients with HCV coinfection, HCV RNA replication status at retransplantation was the only

270 t linkage generated during the viral genomic RNA replication steps of a picornavirus infection.

271 translated cannot function as a template for RNA replication, suggesting that there is a switch in te

272 uctures and an important site at which viral RNA replication takes place.

273 orally bioavailable inhibitor of hepatitis C RNA replication targeting NS4B, compound 4t (PTC725), ha

274 nd their volumes are closely correlated with RNA replication template length.

275 syntheses in time and regulate asymmetrical RNA replication that leads to abundant (+)RNA progeny.

276 d CTLs were polyfunctional and inhibited HCV RNA replication through antigen-specific cytotoxicity.

277 d with kinetic/thermodynamic descriptions of RNA replication to analyze the collective behavior of RN

278 gene Tm-1 encodes a direct inhibitor of ToMV RNA replication to protect tomato from infection.

279 tombusviruses could adjust the efficiency of RNA replication to the limiting resources of the host ce

280 avirus RNA structures which likely influence RNA replication, translation and genome packaging.

281 Here, we show that BeAn virus RNA replication, translation, polyprotein processing int

282 RNAs were capable of downregulating replicon RNA replication upon delivery of VRP into animals, demon

283 RNA replication was dependent on mouse cyclophilin and p

284 istent with published results, we found that RNA replication was indeed vigorous but the yield of pro

285 Both analyses found that RNA replication was intrinsically error-prone compared t

286 Furthermore, a decrease in HCV RNA replication was observed by blocking the LDLR with a

287 s with a functional RIG-I pathway, but viral RNA replication was rescued in cells lacking RIG-I signa

288 iral protein 3A and to be required for viral RNA replication, was readily recovered along with immuno

289 ellular and viral proteins involved in viral RNA replication, we investigated the binding of the host

290 e found that the genetic regions involved in RNA replication were mostly intolerant of mutations.

291 S4B mutations dispensable for efficient Con1 RNA replication were tested in the context of the chimer

292 isolate, and uniquely allowed for ZIKV viral RNA replication when compared to dengue virus (DENV).

293 The data support a model of PV RNA replication wherein reiterative transcription of hom

294 ry effect by 25HC on HCV was at the level of RNA replication, which was observed using subgenomic rep

295 itochondrial preparations for complete viral RNA replication, while CIRV preferentially replicated in

296 that Huh7-Lunet cells supported HAV- and HCV-RNA replication with similar efficiency and limited inte

297 cribe inter alia nonlinear kinetic models of RNA replication within a primordial Darwinian soup, the

298 d to destabilize the helix, diminished viral RNA replication without significantly affecting ATP-depe

299 A plausible process for non-enzymatic RNA replication would greatly simplify models of the tra

300 A fast and accurate pathway for nonenzymatic RNA replication would simplify models for the emergence