ライフサイエンスコーパス: viral replication

1 the cells, we observed severe impairment of viral replication.

2 e for the circadian components in regulating viral replication.

3 rf6 plays a previously unappreciated role in viral replication.

4 ovirus 3CL protease, an enzyme essential for viral replication.

5 proteins and their multiple functions during viral replication.

6 ral response, thereby allowing for efficient viral replication.

7 tion that mitochondrial inhibitors attenuate viral replication.

8 ts cellular factors to complete each step of viral replication.

9 eding or spreading, despite reduced systemic viral replication.

10 for viral and cellular mRNAs and ultimately viral replication.

11 own to be important for a very early step in viral replication.

12 enhanced ER turnover and the suppression of viral replication.

13 ll intrinsic antiviral program that inhibits viral replication.

14 iation of antiretroviral therapy to suppress viral replication.

15 d with HIV-1 in vitro and were monitored for viral replication.

16 oteins to determine the biological impact on viral replication.

17 and apoptosis inhibition in later stages of viral replication.

18 f two cysteine viral proteases essential for viral replication.

19 innate immunity is essential for successful viral replication.

20 rus and reveal a functional role of m(5)C in viral replication.

21 mune responses, thereby potently restricting viral replication.

22 action was found to not be a prerequisite of viral replication.

23 in revealing molecular mechanisms underlying viral replication.

24 olysis of infected cells, and suppression of viral replication.

25 Here, we report its activity against viral replication.

26 ion modulates cellular metabolism to support viral replication.

27 family is a likely candidate for control of viral replication.

28 gy and macromolecules required for efficient viral replication.

29 sses cellular antiviral immunity to suppress viral replication.

30 e evolved as first-line defenses to suppress viral replication.

31 to IAV in the environment but had no active viral replication.

32 evolutionary history and certain aspects of viral replication.

33 trate, PI(4)P phosphoinositide, in promoting viral replication.

34 ell-death pathways in an attempt to suppress viral replication.

35 subverted host membranes to promote optimal viral replication.

36 tes both to T cell activation and to reduced viral replication.

37 ected fibroblasts, where the RNA facilitates viral replication.

38 he deletion of QTQTN may restrict late-phase viral replication.

39 ll host molecules that play diverse roles in viral replication.

40 uitination of the 3D polymerase that boosted viral replication.

41 eparable from its contribution to high-titer viral replication.

42 ferentiation with PMA, supported an enhanced viral replication.

43 blished to regulate HIV-1 nuclear import and viral replication.

44 AP from its role as a replicative SSB during viral replication.

45 Gag-Pol is strictly maintained for efficient viral replication.

46 ownstream phosphoprotein functions vital for viral replication.

47 a few hours after transplantation, to block viral replication.

48 scriptional program that executes and drives viral replication.

49 tein (Rep) of geminiviruses is essential for viral replication.

50 gatively affects ZIKV protein expression and viral replication.

51 ficantly restricts both early and persistent viral replication.

52 EMCV-mediated beta-cell lysis by inhibiting viral replication.

53 y effects beyond autophagy that might affect viral replication.

54 hypothesized to promote the early stages of viral replication.

55 release non-structural proteins required for viral replication.

56 gent of COVID-19, is an essential enzyme for viral replication.

57 f the nonstructural proteins involved in its viral replication.

58 1-infected people that spontaneously control viral replication.

59 , synthesizes viral RNA and is essential for viral replication.

60 and elongation activities and essential for viral replication.

61 hin an infected cell to facilitate efficient viral replication.

62 iPARP, which we show is required for maximal viral replication.

63 st's anti-viral defenses by interfering with viral replication.

64 ll is partitioned into numerous vesicles for viral replication.

65 Host cell factors are integral to viral replication.

66 ith at least transient control of persistent viral replication.

67 ting a recent bottleneck followed by limited viral replication.

68 elerating RT maturation and interfering with viral replication.

69 induce metabolic activation and drive robust viral replication.

70 current treatments results in resumption of viral replication.

71 only a small percentage of cells undergoing viral replication.

72 ce of Zika virus infection, the mechanism of viral replication, a process commonly targeted by antivi

73 of innate immune signaling and inhibition of viral replication across ZIKV strains.

74 mmune system triggers pathways that restrict viral replication, activate innate immune cells, and reg

75 ng of the 5' UTR underlies the efficiency of viral replication and also determines viral virulence.

76 ng multifunctional proteins that function in viral replication and also modify the host environment t

77 th the holo-RdRp and nsp13 are essential for viral replication and are targets for treating the disea

78 etroviral pathogenesis, resulting in reduced viral replication and burden of disease outcomes.

79 nfected primary T cells results in increased viral replication and cell-to-cell spread.

80 VRC01 could promote HIV remission by halting viral replication and clearing infected cells.

81 identified HIV-infected individuals reduces viral replication and decreases the risk of transmission

82 ling, tuning protein expression, controlling viral replication and detecting cancer states.

83 These findings de-link viral replication and disease symptoms, illuminate the v

84 interferon (IFN) signaling so as to enhance viral replication and dissemination.

85 (HIV) RNA, HIV controllers have evidence of viral replication and elevated inflammation.

86 e (TK), which increases the pool of dTTP for viral replication and enhances lytic replication.

87 nvironment, allowing a higher level of early viral replication and enhancing ZIKV pathogenesis.IMPORT

88 These mice support viral replication and exhibit pathological findings foun

89 o viral genomes and subsequent disruption of viral replication and fidelity.

90 the effect of the 3' terminal nucleotide on viral replication and found that the EBOV polymerase ini

91 on to GP is associated with rapid decline in viral replication and illness severity.

92 ence for a bidirectional association between viral replication and immunity, and underscore the impor

93 T407A and S411A substitutions in NS3 reduce viral replication and increase the helicase-unwinding tu

94 Knockdown of TiPARP reduced viral replication and increased interferon expression, s

95 and in host-protein co-opting necessary for viral replication and infectivity.

96 ce with inputs being drug effects on ongoing viral replication and initial number of infected cells.

97 mentally infected animals showed that robust viral replication and intensive proinflammatory response

98 -1 DNA into the host genome is essential for viral replication and is catalyzed by the retroviral int

99 effect of cellular antioxidant responses on viral replication and latency is unknown.

100 es enables probabilistic bet hedging between viral replication and latency.

101 m enabling probabilistic bet hedging between viral replication and latency.

102 Persistent viral replication and latent HIV reactivation in the CNS

103 Based on inhibition of viral replication and limited reports on clinical effica

104 or IFI16 associates with CHIKV RNA, reducing viral replication and maturation.

105 have functionally important consequences for viral replication and may provide a novel insight into v

106 -viral inflammatory responses or restricting viral replication and neutrophils do not contribute to d

107 hlight an important role of VP3 in promoting viral replication and pathogenesis in vivo in addition t

108 al dynamics in neurons, thereby facilitating viral replication and pathogenesis.

109 ng H1N1 HA stalk mutation greatly diminishes viral replication and pathogenicity in vivo by modulatin

110 les on airway organoid cultures, and reduces viral replication and pathology in RSV-infected mice.

111 reduced immunogenicity might reflect reduced viral replication and possibly also the decrease in CpG

112 Nef enhances viral replication and promotes immune escape of HIV-infe

113 ovides mechanistic insight for the prolonged viral replication and protracted illness observed in H5N

114 d an in vitro HIV T-cell culture system with viral replication and raltegravir (RAL; an integrase inh

115 at can prevent or significantly downregulate viral replication and reduce morbidity by preventing dev

116 lability of novel assays to measure residual viral replication and reservoirs in NHP models may incre

117 her these lymphoid tissues could be sites of viral replication and sources of viable virus particles.

118 e proteins will enhance our understanding of viral replication and species restriction as well as sug

119 a rod-shaped structure was not required for viral replication and spread in cell culture but rather

120 ism of interferon (IFN) signaling to enhance viral replication and spread.

121 Panama and Puerto Rico significantly reduces viral replication and spread.

122 e signaling in beta-cells functions to limit viral replication and subsequent beta-cell lysis by atte

123 ulates the pathogenicity of WNV by affecting viral replication and T-cell infiltration in the brain.

124 aradoxical effects of CPO of an RNA virus on viral replication and the adaptive humoral immune respon

125 le, all CoV enzymes and proteins involved in viral replication and the control of host cellular machi

126 ell transcriptome profiling, we reveal rapid viral replication and the increased expression of interf

127 the lung immune environment, the control of viral replication and the peak severity of disease after

128 of the viral genome, acts as a promotor for viral replication and thus is critical for recognition o

129 major driver of this phenotype and that both viral replication and transcription are affected.

130 aviruses and has a pivotal role in mediating viral replication and transcription, making it an attrac

131 Active viral replication and viral genomes in bronchoalveolar-l

132 ctural protein 5A (NS5A) plays a key role in viral replication and virion assembly, and the regulatio

133 ing they may be infected and contributing to viral replication and VTx.

134 ctivation of the EBV lytic cycle, leading to viral replication and, in some patients, cancer developm

135 optimal drug inhibition which allows ongoing viral replication, and hence does not require latency fo

136 HIV-1 capsid plays multiple key roles in viral replication, and inhibition of capsid assembly is

137 Essential contributions of viral genes to viral replication are known, but the potential contribut

138 fection rather than the direct inhibition of viral replication as seen with nucleoside/tide analogs i

139 cellular pathways contributing to control of viral replication as well as to neurologic disease.

140 he virus polymerase gene that contributes to viral replication as well as to virus accessory function

141 H and C residues and W503 are essential for viral replication, as evidenced by the fact that their m

142 se proteins, pp71, is critical for efficient viral replication, as it undermines host antiviral respo

143 hology of the BBB, its ability to potentiate viral replication, as well as current therapies and insu

144 anscriptase (RT) inhibit RT in enzymatic and viral replication assays.

145 n-stimulated genes (ISGs), which can inhibit viral replication at different stages.

146 and function can be used as an indicator of viral replication before detectable plasma viremia.

147 so define the roles of these interactions in viral replication both in vitro and in vivo A mechanisti

148 helicase DDX3X is an essential cofactor for viral replication but dispensable for cell viability.

149 he HCV NS3-NS4A protease complex facilitates viral replication by cleaving and inactivating the antiv

150 hway and IL-1 receptor signaling, control of viral replication by interferon-stimulated genes, and cl

151 would limit its own expression, thus aiding viral replication by preventing the known toxic effects

152 rane (TM) protein that plays a vital role in viral replication by proton flux into the virus.

153 striction in which a TRIM E3 ligase controls viral replication by regulating the structure of host ce

154 Viral replication can be blocked by antiretroviral thera

155 smacytic differentiation of these cells, and viral replication can be observed in some infected cells

156 ect of HR mutant viruses in the formation of viral replication centers that can be rescued by depleti

157 nrichment of phosphatidylethanolamine in the viral replication compartment.

158 ic reticulum-derived COPII vesicles into the viral replication compartment.

159 eins and co-opted host proteins within large viral replication compartments in the cytosol of infecte

160 pends on recruitment of host components into viral replication compartments or organelles.

161 eling of nascent viral DNA to image aberrant viral replication compartments that form in the presence

162 -fold more rapidly than the wild type within viral replication compartments.

163 omain (HVD) in EEEV nsP3 for the assembly of viral replication complexes (vRCs).

164 We show that viral replication complexes traffic to and accumulate wi

165 required to stabilize the association of the viral replication complexes with nuclear speckles.

166 development of specialized domains harboring viral replication complexes, replication organelles.

167 rus nsP3 proteins recruit host proteins into viral replication complexes.

168 f host proteins into formation of functional viral replication complexes.

169 ular proteins, which mediate the assembly of viral replication complexes.

170 enes that are required for completion of the viral replication cycle and capsid assembly.

171 s Review, we reassess the major steps of the viral replication cycle by highlighting recent advances

172 Traditionally, the viral replication cycle is envisioned as a single, well-

173 e roles of HVT vNr-13 in early stages of the viral replication cycle, mitochondrial morphology disrup

174 and unique features that give nuance to the viral replication cycle.

175 hat are essential for multiple phases of the viral replication cycle.

176 us infection by posing several blocks to the viral replication cycle.

177 m-free conditions in the later stages of the viral replication cycle.

178 ed 32 times (which accounts for more than 60 viral replication cycles) on either the SUIT-2 (moderate

179 ytes efficiently become infected and support viral replication despite the presence of protective imm

180 Viral replication does not, however, correlate with FeLV

181 cells infected before ART and not by ongoing viral replication during ART.

182 ration (e.g., HDGF), or factors that promote viral replication (e.g., NBS1 and NFIC).

183 Because of the possibility of increased viral replication, each CPO virus was attenuated by the

184 Such a phenotypic trait of the viral replication efficiency appears to emerge randomly

185 udy demonstrates that phenotypic variants of viral replication efficiency exist among avian IAVs but

186 Through phenotypic analyses of viral replication efficiency, only a small set of avian

187 s both type I interferon (IFN)-signaling and viral replication events that lead to production of prog

188 ocyte derived DCs (moDCs) support productive viral replication following infection with a pathogenic

189 that G-N-7 MTase activity of PEDV modulates viral replication, gene expression, and innate immune re

190 However, the role of IIGP1 in restricting viral replication has not been reported.

191 ro and in vivo This model for restriction of viral replication has potential for broad applications i

192 oduction of HIV-1 proteins in the absence of viral replication helps explain persistent immune activa

193 V-1 virulence factor Nef promotes high-titer viral replication, immune escape, and pathogenicity.

194 ellular proliferation but further by limited viral replication.IMPORTANCE HIV-1 infection is a sexual

195 its antiviral effects and promote efficient viral replication.IMPORTANCE Host cells mount a response

196 ind to CHIKV HVD and thus may be involved in viral replication.IMPORTANCE Replication of chikungunya

197 ervoir during ART, we looked for evidence of viral replication in 5 donors after up to 13 years of vi

198 that while musculoskeletal disease requires viral replication in affected muscle, muscular pathology

199 ype 1 (HIV-1) accessory protein Vpr enhances viral replication in both macrophages and, to a lesser e

200 drome coronavirus 2 (SARS-CoV-2) vaccines on viral replication in both upper and lower airways is imp

201 under strong constraint during selection for viral replication in cell culture.IMPORTANCE The M1 matr

202 Carmofur inhibits viral replication in cells (EC(50) = 24.30 muM) and is a

203 primary-infection and a prolonged course of viral replication in CMV high-risk patients.

204 lls that may contribute to the resilience of viral replication in different cellular environments.IMP

205 Deletion of CTRL2 resulted in restricted viral replication in epithelial cells but not neuronal c

206 ct activation of ORF21 by XBP-1s can enhance viral replication in germinal center B cells and contrib

207 persistent viral isolate leads to long-term viral replication in hematopoietic and mesenchymal cells

208 iral diversity and provides new insight into viral replication in high-temperature environments.

209 ARS-CoV-2 strain, and found that it enhances viral replication in human lung epithelial cells and pri

210 O 5334 and apilimod were found to antagonize viral replication in human pneumocyte-like cells derived

211 ble to associate these proteins with altered viral replication in macrophages or to explain why Vpr i

212 A duplication in the 3'UTR that enhances viral replication in mosquito cells led to an overall in

213 ter activity long after the period of active viral replication in peripheral blood.

214 rsion against NiV glycoprotein and a lack of viral replication in primary and immortalized EFB-derive

215 iated with decreasing virion infectivity and viral replication in primary lymphocytes.

216 duced cellular immunity can prevent systemic viral replication in RMs that do not express MHC-I allel

217 RT-qPCR demonstrated viral replication in salmon brains up to 15 days postinj

218 PCR was used to confirm viral replication in SOT-recipients presenting with clin

219 duced persistent hypernociception, transient viral replication in target organs, systemic production

220 They can promote viral replication in the absence of FXR-HVD interactions

221 7K mutation attenuates TMUV through reducing viral replication in the blood, brain, heart (ducklings)

222 ne and human microglia and exhibited reduced viral replication in the brain.

223 sequelae and some with persistent, low-level viral replication in the CNS.

224 acity glucose transporter, partially rescues viral replication in the face of AMPK inhibition.

225 uid of RSV-infected mice, without increasing viral replication in the lung.

226 We found that neither drug inhibited viral replication in the lungs, but both protected again

227 the HIV-1 LTR promoter and facilitate HIV-1 viral replication in the nucleus.

228 oms and histopathological changes, increased viral replication in the respiratory system, and prolong

229 ccine studies have demonstrated reduction of viral replication in the upper and lower respiratory tra

230 Bictegravir may contribute to inhibit viral replication in this compartment.

231 PIA, ATP1A1, and the ARP2/3 complex, reduced viral replication in two human cell lines.

232 icant defects in viral protein synthesis and viral replication in Vero CCL-81 cells and intestinal po

233 G treatment resulted in robust inhibition of viral replication in vitro and ex vivo in cultured porci

234 ications of VEEV HVD have a strong impact on viral replication in vitro and pathogenesis.

235 rotein have an additional negative effect on viral replication in vivo Despite the inability to cause

236 that lead to severe defects in splicing and viral replication indicate the presence of unknown cis-r

237 of virus transport across the BBB as well as viral replication inside the brain, and we compute the b

238 show that the beta-cell response to dsRNA, a viral replication intermediate known to activate antivir

239 a cells via the recognition of intracellular viral replication intermediates and that beta cells lack

240 Targeting a cellular pathway to inhibit viral replication is a potential treatment strategy that

241 important to prevent cells from dying before viral replication is complete and the mature virus is re

242 ollowed by a phase with elevated function as viral replication is controlled to a set-point level, an

243 the cellular immune responses that regulate viral replication is important in diversifying the resou

244 evalent worldwide, but an in vitro model for viral replication is lacking.

245 Viral replication is suppressed by the adaptive immune r

246 sting ongoing pathological process even when viral replication is suppressed.

247 Negative-sense viral RNA, a marker of active viral replication, is found predominantly in intestinal

248 al therapy (ART) is effective in suppressing viral replication, it is incapable of restoring the "lea

249 NA nicking by Can1 is predicted to slow down viral replication kinetics by leading to the collapse of

250 fection, assessments of disease severity and viral replication kinetics in vivo provide crucial infor

251 of ZIKV and DENV replication suggesting that viral replication likely differentially modulated the re

252 is study, we show that normoxic HC increases viral replication, lung injury, and mortality in mice in

253 ription complex that plays a crucial role in viral replication, making nsp10 an important target for

254 nvironment enriched with IAVs but wherein no viral replication occurs.

255 role of octameric M(pro) in the early-stage viral replication of both viruses.

256 identification of 100 molecules that inhibit viral replication of SARS-CoV-2, including 21 drugs that

257 ctor that regulates HIV-1 nuclear import and viral; replication of TNPO3 is well established to regul

258 ing various metabolic pathways important for viral replication or by directly targeting viral protein

259 suggesting that it may play a direct role in viral replication or coupled processes.

260 ence of loxP sites flanking M2 did not alter viral replication or latency in mice that do not express

261 suggesting a possible defect at the level of viral replication or later in the lytic cascade.

262 ulum membranes that are transformed into the viral replication organelle (RO).

263 mediated silencing inhibits the formation of viral replication organelles.

264 reover, by targeting sequences necessary for viral replication, our results indicate that a viral gen

265 ased virus yields in MDCK cells and enhanced viral replication, pathogenicity, and transmission in do

266 senchymal stromal cell (hMSCs) was used as a viral replication-permissive carrier for oAd with an aim

267 upT1 CD4+ T cells at five time points of the viral replication process.

268 main prevalent potentially due to persistent viral replication, production of viral proteins, associa

269 a pattern recognition receptor that detects viral replication products to activate the IPR stress/im

270 1A and E4orf3 work together to fine-tune the viral replication program during the course of infection

271 replicase complexes (VRCs) with the help of viral replication proteins and co-opted host proteins wi

272 hysically and/or functionally with the other viral replication proteins.

273 e replicative, template viral RNA; essential viral replication proteins; and cellular proteins.

274 tomical sources responsible for reinitiating viral replication remain a subject of ardent debate, des

275 Importantly, the level of viral replication required for generating escape mutatio

276 tic interventions that impede these steps in viral replication requires a detailed understanding of m

277 though ART was indispensable for controlling viral replication, restoring CD4+ T cells, and preventin

278 ngth RNA (HIV-1 RNA) plays a central role in viral replication, serving as a template for Gag/Gag-Pol

279 We show that ATL3 is recruited to the viral replication site and colocalize with the viral pro

280 Germinal center (GC) B cells at viral replication sites acquire specificity to poorly im

281 us is poor, thus limiting investigation into viral replication steps.

282 eated with low-dose IFNs show a reduction in viral replication, suggesting the prophylactic effective

283 s to inhibit HIV-1 LTR promoter activity and viral replication, supporting a role for circadian clock

284 From the perspective of viral replication, the transgene is not only dispensable

285 en linked to drug resistance, apoptosis, and viral replication, their molecular functions remain uncl

286 Sac1 and PI(4)P are recruited to the site of viral replication to facilitate the assembly of the vira

287 cate that while SARS-CoV-2 maintains similar viral replication to SARS-CoV, the novel CoV is much mor

288 ected cells; ART is usually required to keep viral replication under control and disease progression

289 Here, we investigated the role of motif V in viral replication using West Nile virus (Kunjin subtype)

290 No viral replication was detectable in the nose of any of t

291 Viral replication was evaluated in activated and quiesce

292 myeloid-specific microRNA target sequences, viral replication was inhibited in myeloid cells by harn

293 Viral replication was not detectable in BAL fluid by day

294 Viral replication was observed mainly in the upper respi

295 egative-strand DWV RNA, which could indicate viral replication, was detected only in mites collected

296 (AGO2) and miR-17 binding were essential for viral replication, whereas let-7 binding was mainly requ

297 ponse to tumors, which are the only sites of viral replication, whereas tumored and nontumored Florid

298 ic cellularity reconstituted despite ongoing viral replication, with a rapid secondary thymic depleti

299 at receive antibiotics are unable to control viral replication within the brain leading to increased

300 Dysfunction of the BBB further potentiates viral replication within the CNS, which can lead to HIV-