ライフサイエンスコーパス: RNA replication

1 RNA strand as it exits the polymerase during RNA replication.

2 n RNA secondary structure required for viral RNA replication.

3 erules play an important role in stimulating RNA replication.

4 etails of how the viral helicase facilitates RNA replication.

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

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

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

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

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

10 triple alanine mutants exhibited defects in RNA replication.

11 l inclusion bodies (IBs), the site for viral RNA replication.

12 gion increases viral titer without affecting RNA replication.

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

14 nd nonhomologous RNA templates during sexual RNA replication.

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

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

17 factors responsible for the lack of genomic RNA replication.

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

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

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

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

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

23 mRNA synthesis but is required for efficient RNA replication.

24 the HCV replication factory, independent of RNA replication.

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

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

27 l step involving protein synthesis and viral RNA replication.

28 ellular virus assembly without affecting HCV RNA replication.

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

30 ediate cap-independent translation and viral RNA replication.

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

32 emplate for both viral protein synthesis and RNA replication.

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

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

35 tivity is central to viroplasm formation and RNA replication.

36 switch in template usage from translation to RNA replication.

37 ponses in these cells modestly increased HCV RNA replication.

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

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

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

41 switch in template usage from translation to RNA replication.

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

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

44 5B that may facilitate de novo initiation of RNA replication.

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

46 d genetically separable functions of NS5A in RNA replication.

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

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

49 ntal demonstration of effective nonenzymatic RNA replication.

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

51 lymerase-polymerase interactions facilitates RNA replication.

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

53 es autophagosomal membranes as sites for its RNA replication.

54 1 is an essential gene linked to early viral RNA replication.

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

56 conveys signals to the cytoplasm to regulate RNA replication.

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

58 nal RNA elements required for translation or RNA replication.

59 G, revealing it to be required for a step in RNA replication.

60 ral replicase complexes, which perform viral RNA replication.

61 that include viral proteins responsible for RNA replication.

62 cyclophilin A (CypA) is essential for viral RNA replication.

63 eract with SETD3 are severely compromised in RNA replication.

64 uced NS2-NS3 autoprocessing and impaired HCV RNA replication.

65 ring infection at the initial steps of viral RNA replication.

66 sphodiester backbone is not an end point for RNA replication.

67 RNA synthesis complicates analysis of viral RNA replication.

68 NS2-NS3 precursor, an essential step in HCV RNA replication.

69 nificantly reduced HCV infection but not HCV RNA replication.

70 ession inhibited HCV protein translation and RNA replication.

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

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

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

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

75 lipid rafts to autophagosomes to mediate its RNA replication.

76 erdomain interaction within NS5 required for RNA replication.

77 pid rafts, from autophagosomes abolished HCV RNA replication.

78 n RNA secondary structure required for viral RNA replication.

79 ifunctional HCV protein that is required for RNA replication.

80 ous and nonhomologous partners during sexual RNA replication?

81 Inhibition of DENV RNA replication abrogated these responses.

82 Intracellular RNA replication activates a strong innate immune respons

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

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

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

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

87 gulation of viral polyprotein processing and RNA replication and a host factor for alphaviruses.

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

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

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

91 Intracellular RNA replication and assembly and release of new particle

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

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

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

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

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

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

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

99 us assembly sites, which in turn promote HCV RNA replication and infectious-particle assembly, respec

100 tion likely allows NS2 to fine tune both HCV RNA replication and infectious-particle assembly.IMPORTA

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 tion to examine the putative linkage between RNA replication and packaging in the Picornavirales We h

110 in of SARS-CoV, which is essential for viral RNA replication and packaging into new virions.

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

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

113 Oleic acid supplementation rescues viral RNA replication and production of infectious particles i

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

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

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

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

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

119 ticle that contains the enzymes required for RNA replication and transcription(10-12).

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

121 icase activities that are required for viral RNA replication and transcription.

122 RNA replication and viral titre were unaltered in viruse

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

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

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

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

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

128 t two major functions of NS2 involved in HCV RNA replication and virus assembly, i.e., NS2-NS3 autopr

129 ve as a promising target to inhibit both HCV RNA replication and virus assembly, representing a new a

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

131 ltifunctional protein implicated in both HCV RNA replication and virus particle assembly.

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

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

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

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

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

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

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

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

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

141 ost functions used during viral translation, RNA replication, and other steps of infection by picorna

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

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

144 es a valuable tool to study CHIKV replicase, RNA replication, and virus-host interactions.IMPORTANCE

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

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

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

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

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

150 ta suggest a role of the viral 2A protein in RNA replication beyond facilitating proteolytic cleavage

151 somal neutralization not only prevents viral RNA replication but also affects the maturation of DENV

152 P2 not only has enzymatic functions in viral RNA replication but also is a critical inhibitor of the

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

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

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

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

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

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

159 5HC, restricts HCV primarily at the level of RNA replication by preventing formation of the viral rep

160 that NS2 palmitoylation is critical for HCV RNA replication by promoting NS2-NS3 autoprocessing.

161 Using in vitro RNA replication by the transcription polymerase of T7 ba

162 ted by a template-switching mechanism during RNA replication by the viral replicase.

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

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

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

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

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

171 yoelectron microscopy (cryo-EM) of nodavirus RNA replication complexes revealed that the viral double

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

173 pose that TMEM41B is recruited to flavivirus RNA replication complexes to facilitate membrane curvatu

174 rs at poorly understood membrane-bound viral RNA replication complexes.

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

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

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

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

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

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

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

182 disordered NS5A-D2, thereby regulating viral RNA replication efficiency.

183 his fraction is directly correlated with HCV RNA replication efficiency.

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

185 -genomic replicon systems, we identified six RNA replication elements essential to efficient CHIKV ge

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

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

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

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

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

191 Viral RNA replication from an endogenous transgene replicon sy

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

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

194 oplasmic sites of nucleocapsid formation and RNA replication, housing key steps in the virus life cyc

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

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

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

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

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

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

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

209 es significantly higher levels of N to drive RNA replication in the presence of P(DeltaOD) We conclud

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

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

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

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

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

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

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

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

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

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

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

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

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

223 controls both regulation of IB formation and RNA replication itself and that is mediated by a newly i

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

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

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

227 und, and they serve to concentrate the viral RNA replication machinery.

228 Because sexual RNA replication mechanisms counteract ribavirin-induced

229 Asexual RNA replication mechanisms involve one parental template

230 nvolve one parental template, whereas sexual RNA replication mechanisms involve two or more parental

231 Template-dependent RNA replication mechanisms render picornaviruses suscept

232 e consequences of asexual template-dependent RNA replication mechanisms, namely, error catastrophe.

233 y polymerase residues that facilitate sexual RNA replication mechanisms.

234 catastrophe coincides with defects in sexual RNA replication mechanisms.

235 Picornaviruses have both asexual and sexual RNA replication mechanisms.

236 Picornaviruses have both asexual and sexual RNA replication mechanisms.

237 short periods of time via template-dependent RNA replication mechanisms.

238 rimer grip of the viral polymerase in sexual RNA replication mechanisms.

239 ity of RNA synthesis and to efficient sexual RNA replication mechanisms.IMPORTANCE Picornaviruses hav

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

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

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

243 increased fluidity of the membrane where HCV RNA replication occurs.

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

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

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

247 and the P4 residue of the 1/2 site for viral RNA replication of Old World alphaviruses.

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

249 7 cells but had only minimal impact on viral RNA replication or cell proliferation and viability.

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 virus only use autophagy components for post-RNA replication processes.

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

256 complex that contains multifunctional viral RNA replication protein A.

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 cle of VSV (DI-T) that is only competent for RNA replication requires significantly higher levels of

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

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

263 Sexual RNA replication shapes picornavirus species groups, cont

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

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

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

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

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 ts methylation activity, is required for the RNA replication step in the viral life cycle.

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

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

273 e confirm that both bRSV and human RSV viral RNA replication takes place in these inclusion bodies, l

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

275 exes revealed that the viral double-stranded RNA replication template is coiled inside a 30- to 90-nm

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

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

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

279 directly regulates the lipid environment for RNA replication through direct effects on the host lipid

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

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

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

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

284 RNA replication was dependent on mouse cyclophilin and p

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

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

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

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

291 or target for antiviral therapies is genomic RNA replication, which occurs at poorly understood membr

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

293 Template-dependent RNA replication, while efficient, can be disadvantageous

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

295 cation cycle, such as mRNA transcription and RNA replication, with other roles being likely.

296 Achieving multiple cycles of RNA replication within a model protocell would be a crit

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