ライフサイエンスコーパス: virus replication

1 by inducing type I interferons, which limits virus replication.

2 ivation of both mTORC1 and mTORC2 to promote virus replication.

3 ic protein-protein interactions required for virus replication.

4 a cellular environment that is favorable for virus replication.

5 fy antiviral genes that restrict influenza A virus replication.

6 ata that these organelles were conserved for virus replication.

7 nterferon response in cells undergoing lytic virus replication.

8 ormal cell-cycle progression, did not affect virus replication.

9 sicles formation, that are indispensable for virus replication.

10 e, IFI44L is a candidate target for reducing virus replication.

11 se L (RNase L), which cleaves RNA to inhibit virus replication.

12 B cells called B-1 cells that permit robust virus replication.

13 by provide a more permissive environment for virus replication.

14 of DNA sensing pathway in limiting influenza virus replication.

15 pping networks of genes and had no effect on virus replication.

16 Genome packaging is a critical stage during virus replication.

17 IX binding, CCL2-responsiveness and enhanced virus replication.

18 reporter, providing a sensitive readout for virus replication.

19 plays a critical role in efficient vaccinia virus replication.

20 utophagosome formation, all of which enhance virus replication.

21 The stimulation of CD63 exocytosis requires virus replication.

22 el the tricarboxylic acid cycle for vaccinia virus replication.

23 interact with the host cell machinery during virus replication.

24 ng means to target host polyamines to reduce virus replication.

25 mechanisms, and advance our understanding of virus replication.

26 amage whose repair may lead to inhibition of virus replication.

27 re specifically loaded onto Piwi4 to inhibit virus replication.

28 d MDV titers, suggesting that COX-2 promotes virus replication.

29 DDR signaling and improves the efficiency of virus replication.

30 ding cell motility, signal transduction, and virus replication.

31 the RNA-binding region that is essential for virus replication.

32 clearance by activating mitophagy to support virus replication.

33 1 RNA genome is central to the regulation of virus replication.

34 tagonist (CORT-108297) significantly reduced virus replication.

35 owing cytomegalovirus infection that control virus replication.

36 richment cultures under conditions favouring virus replication.

37 I interferon (IFN) induction and inhibit RNA virus replication.

38 m inactive histones and host DNA, maximizing virus replication.

39 tein kinase R (PKR), which potently inhibits virus replication.

40 autophagy and cell cycle arrest and benefits virus replication.

41 biquitination and is important for efficient virus replication.

42 ion also abolished HSP70-dependent influenza virus replication.

43 ial for SPL-mediated inhibition of influenza virus replication.

44 re evolutionarily conserved but also enhance virus replication.

45 act through different mechanisms to increase virus replication.

46 (+) T-cell immunity able to durably suppress virus replication.

47 ts subsequent effects on gK localization and virus replication.

48 access to plentiful ATP, facilitating robust virus replication.

49 ce of its function is important for vaccinia virus replication.

50 ted pathogenesis without directly preventing virus replication.

51 med by its activity in suppressing influenza virus replication.

52 n function significantly suppressed vaccinia virus replication.

53 of hydrolysing deoxynucleotides required for virus replication.

54 at least partially by the magnitude of early virus replication.

55 in persistently infected bat cells increased virus replication.

56 luenza virus polymerases and avian influenza virus replication.

57 erate energy and macromolecules required for virus replication.

58 RBD interaction with ACE2, and inhibit live virus replication.

59 nate immune response process that attenuates virus replication.

60 essing P50 in this cell line enhanced mutant virus replication.

61 performed on day four to confirm absence of virus replication.

62 a general strategy to interfere with NNS RNA virus replication.

63 rfering with cellular processes critical for virus replication.

64 factors required for restricting influenza A virus replication.

65 ifferentiated AP-7 cells but did not inhibit virus replication.

66 tagonists that modulate the host response to virus replication.

67 ary structures that are essential for proper virus replication.

68 acting type 1 interferon (IFN) production or virus replication.

69 ing the importance of this amino acid during virus replication.

70 ors and also may impact virion stability and virus replication.

71 itutions, exhibit pleiotropic effects during virus replication.

72 rrets exhibit elevated body temperatures and virus replication.

73 amental gaps in our understanding of NNS RNA virus replication.

74 rantees lifelong infection and resumption of virus replication after antiretroviral treatment interru

75 tations in noncoding regions that accelerate virus replication, all of which result in the outgrowth

76 n cell culture, and activin A inhibited Zika virus replication alone and in combination with IFN.

77 lieved to perform noncoding functions during virus replication, although an open reading frame (ORF)

78 a sustained viral infection characterized by virus replication and accumulation has yet to be demonst

79 s-specific factors contributing to efficient virus replication and acute inflammation in the lungs of

80 for VIB assembly, which in turn facilitates virus replication and assembly.IMPORTANCE After entering

81 severe respiratory disease due to effective virus replication and associated inflammation processes

82 pair of essential host factors for influenza virus replication and can be harnessed to inform future

83 e receptor 4 (TLR4), and thereby impact both virus replication and cellular inflammatory responses.

84 NA-dependent RNA polymerases responsible for virus replication and cellular RNA-dependent RNA polymer

85 JAK2 overexpression enhanced H5N1 virus replication and compromised the antiviral activity

86 viruses subvert intracellular membranes for virus replication and coopt numerous host proteins, whos

87 EVD is characterized by high levels of virus replication and dissemination, dysregulated immune

88 rrogate the functions of NoV proteins during virus replication and highlight the conserved properties

89 ght the existing gaps in our knowledge about virus replication and host immune responses to hCoV infe

90 nding protein that negatively regulates both virus replication and host inflammatory responses.

91 otease (3CL(pro)) plays an important role in virus replication and immune evasion, making it an attra

92 rogram that is broadly effective in limiting virus replication and in suppressing the pro-inflammator

93 increase in ROS levels, along with increased virus replication and inflammatory or apoptotic gene exp

94 cantly delayed in viroplasm formation and in virus replication and interferes with wild-type RV repli

95 The LYPX motif improves virus replication and its absence renders the virus less

96 ed for suppression of viral gene expression, virus replication and lytic infection and restricts muri

97 R signaling contributes to the efficiency of virus replication and may provide one explanation for th

98 ential role for IFITM3 in limiting influenza virus replication and pathogenesis in heart tissue and e

99 to full occupancy and have modest effects on virus replication and pathogenesis.

100 ation, Y17H (activation pH, 6.0), attenuates virus replication and pathogenicity in DBA/2 mice compar

101 mall intestine, a site of intense early AIDS virus replication and pathology in rhesus macaques.

102 ed IFN production, which resulted in reduced virus replication and pathology.

103 s human B cells and reprograms them to allow virus replication and persistence.

104 uring the first days of infection suppressed virus replication and prolonged survival, allowing the m

105 We evaluated the impact on control of virus replication and protection from pathogenic SIVmac2

106 ived from the emerging A(H7N9) with improved virus replication and protein yield in both MDCK cells a

107 similarly remove those cells through active virus replication and resulting cytopathicity.

108 rum of cytokines and growth factors to allow virus replication and spread in host animals.

109 rlying mechanisms that facilitate Bluetongue virus replication and spread through the usurpation of h

110 eroxisomes to support cellular processes for virus replication and spread.

111 both glutamine and glucose were required for virus replication and spread.

112 These particles interfere with virus replication and stimulate innate immune responses.

113 EVD is characterized by robust virus replication and strong host inflammatory response.

114 , these proteins were required for efficient virus replication and the ability of NS5A to spread thro

115 a mammalian host has paradoxical effects on virus replication and the adaptive humoral immune respon

116 c target, owing to its multifunctionality in virus replication and the high fitness cost of amino aci

117 s control the function of our immune system, virus replication and the severity of infections.

118 hat are observed, implicating a race between virus replication and the spread of the anti-viral state

119 throat and salivary glands as major sites of virus replication and transmission during early coronavi

120 Increased virus replication and type I IFN specifically inhibited

121 the E2-DCTN6 protein-protein interaction for virus replication and virulence in swine.

122 Interruption in cap snatching will inhibit virus replication and will likely improve the prognosis

123 viral population by interfering with normal virus replication and/or by stimulating the innate immun

124 loitation of specific sub-systems needed for virus replication and/or involved in the host response t

125 smission, a restricted time and location for virus replication, and a positive effect of virus activi

126 tensin-converting enzyme 2, serine protease, virus replication, and PAD-4.

127 t for viral protein synthesis and infectious virus replication, and the regulatory mechanism involved

128 ferent compounds, leads to reduced influenza virus replication, and we map the requirement of PLK act

129 how a host factor responsible for regulating virus replication, ANP32A, is different between swine an

130 merous host proteins, whose functions during virus replication are not yet completely defined.

131 Host factors of influenza virus replication are often found in key topological pos

132 ective viral genomes (DVGs) generated during virus replication are the primary triggers of antiviral

133 for their ability to interfere with standard virus replication as well as for their association with

134 ts) with a reduced response to sofosbuvir in virus replication assays.

135 s B1 protein kinase, an enzyme that promotes virus replication at multiple phases of the viral lifecy

136 Some of these mediate inhibitions of virus replication at the postentry stage or use Fc-depen

137 ht to exert an antiviral effect, suppressing virus replication before patients have mounted their own

138 ell frequency and resulted in suppression of virus replication but failed to fully restore T-cell fun

139 uster with 3 patients and showed evidence of virus replication but not of neutralizing antibodies in

140 Licensed antivirals inhibit virus replication, but do not affect latency.

141 have been implicated in supporting influenza virus replication, but most of the work to date has focu

142 R), is critical for the initiation of dengue virus replication, but quantitative analysis of the inte

143 a picornavirus-like cassette of enzymes for virus replication, but the capsid structure was at the t

144 pathways are required for the attenuation of virus replication, but their relative contributions in a

145 overlap with those necessary for control of virus replication, but there are also important differen

146 dies showed that lead agents 1 and 4 reduced virus replication by directly targeting IAV nucleoprotei

147 ation, while Hsp90 activity is important for virus replication by stabilizing BTV proteins and preven

148 2, and specifically the enzyme that mediates virus replication, can be inhibited by a panel of drugs

149 ough both E4orf4 and DNA-PK are recruited to virus replication centers (RCs), DNA-PK is later distanc

150 es the accumulation of membranes adjacent to virus replication centers called viroplasms.

151 or recruitment of either E4orf4 or PARP-1 to virus replication centers, suggesting that their associa

152 th CPSF6 in vitro and colocalizes within the virus replication centers.

153 l genomes to PD and formation of PD-anchored virus replication compartments.

154 dies in uninfected cells and with the dengue virus replication complex after infection.

155 ells and profound ART-induced suppression of virus replication, confirming a critical role for these

156 viral mRNA translation, tubule formation and virus replication, confirming a functional role for the

157 Although DTG initially reduced virus replication, continued treatment led to the emerge

158 investigate the possible role of ASP in the virus replication cycle and suggest that ASP may represe

159 tic basis for how eVP30 functions during the virus replication cycle is currently unclear.

160 n UL16 is involved in multiple events of the virus replication cycle, ranging from virus assembly to

161 the roles that TMEM41B and VMP1 play in the virus replication cycle.

162 rategies targeting pH-dependent steps in the virus replication cycle.

163 innate immune response throughout the whole virus replication cycle.

164 ve viral genomes (DVGs) generated during RNA virus replication determine infection outcome by trigger

165 immune response to vDeltaK1L infection, not virus replication, dictated lesion size.

166 Compensatory mutations that rescue virus replication do so by restoring Env incorporation a

167 Paradoxically, however, increased virus replication dramatically decreased the size of the

168 in primary macrophages and one that inhibits virus replication during reverse transcription.

169 ing site (RBS) resulted in viable virus, but virus replication, entry, and stability were often imped

170 eficiency virus (HIV) and a rapid rebound of virus replication follows analytical treatment interrupt

171 eins for degradation, as well as increase in virus replication for JCV, MCV, TSV and HPyV7.

172 d with reduced infection risk, or control of virus replication, for HIV-1 and related viruses.

173 However, for many viruses, replication generates dsRNA in the nucleus.

174 rtant roles of co-opted host proteins in RNA virus replication have been appreciated for a decade, th

175 Historically, EBV genes that contribute to virus replication have been excluded from consideration

176 ly important functions of cellular lipids in virus replication have been gaining full attention only

177 The cellular factors that are crucial for virus replication have been sought as novel molecular ta

178 hogens to achieve an optimal balance between virus replication, host disease, and survival.

179 CrmD does not affect virus replication; however, it provides the host advanta

180 target because (i) ICP0 is expressed before virus replication, (ii) it is essential for infection in

181 There is an urgent need for information on virus replication, immunity and infectivity in specific

182 in conserved residues that are essential for virus replication, implicating it as a potentially good

183 was independent of antiviral type 1 IFN and virus replication, implying that IRF5 could be specifica

184 r the accumulation of membranes required for virus replication.IMPORTANCE In a morphogenic step that

185 derstanding of FluPol function and influenza virus replication.IMPORTANCE Influenza viruses are respo

186 pathogenesis independently of type 1 IFN and virus replication.IMPORTANCE The inflammatory response t

187 Env that confer broad escape from defects in virus replication imposed by either mutations in the HIV

188 ns that prevented their expression inhibited virus replication in a host cell-dependent manner.

189 potential therapeutic benefit in controlling virus replication in acutely or chronically SHIV-infecte

190 lso demonstrate that VC CD8+ T cells inhibit virus replication in both a class I- and class II-depend

191 ission of the virus within wasps, as well as virus replication in both female wasps and fruit fly hos

192 In vitro evaluation of H5Nx virus replication in Calu-3 cells and the identification

193 e binding, dramatically inhibited the hazara virus replication in cell culture, illustrating the role

194 bited polymerase complex activity, inhibited virus replication in cells, prevented death in a lethal

195 that kinesin knockdown inhibits hepatitis-C virus replication in hepatocytes, likely because transla

196 ug combinations are effective in suppressing virus replication in HIV-infected persons.

197 ic promoter to synthesize the leader RNA and virus replication in host cells, but not for internal de

198 first to assess the role of MT in influenza virus replication in human bronchial airway epithelial c

199 ost pathways restricting positive-strand RNA virus replication in immortalized hepatocytes and identi

200 PORTANCE Host cells mount a response to curb virus replication in infected cells and prevent spread o

201 ynthesis of vRNA and, consequently, inhibits virus replication in infected cells.

202 ching is an early event in the initiation of virus replication in infected hosts.

203 pathogenicity was correlated with diminished virus replication in intranasally infected mice.

204 , severe pulmonary pathology, and high-titer virus replication in lungs.

205 ene expression is not required for influenza virus replication in mammals but might be important in t

206 R variants of CHIKV that are known to affect virus replication in mosquito cells.

207 In contrast, the HA-Y17H mutation reduced virus replication in murine airway murine nasal epitheli

208 We propose that H1N1 virus replication in neuronal cells can induce seeds of

209 tion, mutations that are selected to improve virus replication in one species may, by chance, alter t

210 s reports, CD4-depleted mice lost control of virus replication in persistently infected mice.

211 th type I and III IFNs significantly reduced virus replication in pHAE cultures that correlated with

212 ased in 2017-2018, indicating more efficient virus replication in shedding-positive children than the

213 dentify amino acids key to the regulation of virus replication in specific host environments.

214 ropod serves as a host as well by supporting virus replication in specific tissues and organs of the

215 nding properties of these viruses, affecting virus replication in the culture systems commonly used t

216 ce and shown that the absence of SPP affects virus replication in the eye of ocularly infected mice a

217 the development of M1 macrophages, increased virus replication in the eye; increased latency; and als

218 three strains of deficient mice in terms of virus replication in the eyes, levels of corneal scarrin

219 may be the critical IFN for limiting enteric virus replication in the human intestine.

220 tion, while respiratory infection results in virus replication in the lung.

221 Leflunomide inhibited virus replication in the lungs of IAV-infected mice, all

222 with a reduction in clinical signs, reduced virus replication in the lungs, and decreased presence a

223 ularization and suppressing peripheral nerve virus replication in the near absence of neutralizing an

224 at residue 145 showed no major impairment in virus replication in the presence of lower receptor bind

225 new antiviral CD8 T cells, despite sustained virus replication in the thymus, indicating an impairmen

226 The confirmation of active virus replication in the upper respiratory tract has imp

227 taORF2 vaccination prevented EHV-1 challenge virus replication in the upper respiratory tract in full

228 These results indicate that virus replication in the upper respiratory tract, the na

229 ith bat influenza A virus resulted in robust virus replication in the upper respiratory tract, wherea

230 es of COVID-19 that provides proof of active virus replication in tissues of the upper respiratory tr

231 e clinical disease, including high levels of virus replication in tissues, extensive pneumonia, weigh

232 e deletion of NSPRRAR likely does not affect virus replication in Vero and Vero-E6 cells; however, th

233 c cleavage site in SARS-CoV-2 did not affect virus replication in Vero or Vero-E6 cells.

234 hesis, and it alone had reduced single-cycle virus replication in vitro All CPO RSVs exhibited margin

235 l tolerated without having a major impact on virus replication in vitro All substitution mutants reta

236 is unique to SARS-CoV-2, is not fixed during virus replication in vitro These findings provide inform

237 CPO had no effect on multicycle virus replication in vitro, temperature sensitivity, or

238 s sufficient for noncytolytic suppression of virus replication in vivo and in vitro.

239 ced CD4 T cells exerted a negative effect on virus replication in vivo We conclude that GPI-scFv X5-m

240 of influenza virus is essential for limiting virus replication in vivo.

241 of the poxin gene (B2R) attenuates vaccinia virus replication in vivo.

242 t interactions that impact the efficiency of virus replication is essential for the further developme

243 ent infection of B lymphocytes, during which virus replication is not supported.

244 y is activated early in infection to counter virus replication, it is subsequently suppressed by mTOR

245 While viral HA acylation is crucial in virus replication, its physico-chemical role is unknown.

246 emia in all animals by 2 days post-exposure; virus replication kinetics are similar to those observed

247 A26L or G6R or both deleted, which increased virus replication levels and decreased particle/PFU rati

248 within the replication compartment allow the virus replication machinery an access to plentiful ATP,

249 significance of the components of the rabies virus replication machinery is incomplete.

250 w that, in addition to this direct effect on virus replication, manipulating cellular SAMHD1 activity

251 Baloxavir blocks virus replication more rapidly and completely than oselt

252 cGAS was necessary for the reduced DNA virus replication observed in OASL-deficient cells.

253 Measles virus replication occurs in the cytoplasm in association

254 ent way to identify host proteins supporting virus replication or enhancing resistance to virus infec

255 roves pulmonary function but does not reduce virus replication or severe lung pathology.

256 an be transmitted, generated de novo through virus replication, or technical errors.

257 er tests provide information on the level of virus replication, presence of specific variants, and pr

258 ing execution point analysis, we reveal that virus replication proceeds normally through early protei

259 cellular host factors to ensure a successful virus replication process.

260 us mutations, resulting in varied effects to virus replication, propagation and packaging.

261 itively correlated with increased virulence, virus replication rate and lytic infection dynamics in l

262 with both protein families strongly affects virus replication rates.

263 he formation of viroplasms and its impact on virus replication remain obscure.

264 rminal domain of NP (NP-Ct), but its role in virus replication remained unclear.

265 Virus replication requires critical interactions between

266 restored translation prevented and restored virus replication, respectively, in maize protoplasts an

267 dominantly target three enzymes required for virus replication: reverse transcriptase, protease, and

268 RSV coat protein transgene in the absence of virus replication showed the contribution of cellular RN

269 nd confocal laser scanning microscopy showed virus replication significantly decreased when aptamer I

270 Unexpectedly, NK accumulation in virus replication sites correlated with enhanced EBOV di

271 ically in a diverse set of assays, including virus replication, stability, and receptor specificity.

272 The visualization of dsRNA virus replication steps in living cells received much at

273 d ANP32B are essential for influenza A and B virus replication, such that in their absence cells beco

274 me, of which mutations resulted in decreased virus replication, suggesting that m6A modification play

275 Altering -1 PRF activity impairs virus replication, suggesting that this activity may be

276 n mutations showed substantial deficiency in virus replication, suggesting these RNA-capsid sites are

277 ssential yet quite poorly understood step of virus replication that enhances the coding potential of

278 of fatality or is a consequence of extensive virus replication that itself drives disease remains con

279 Recapitulating this in an assay for virus replication, these substitutions result in aberran

280 nded DNA cytosine deaminases, which inhibits virus replication through deamination-dependent and -ind

281 T cells resulted in loss of early control of virus replication, viremia and fatal Ebola virus disease

282 heal epithelial cell cultures and attenuated virus replication, virus spread, the severity of infecti

283 mutant DENV2-infected BHK-21 or Vero cells, virus replication was delayed.

284 Virus replication was determined by viral RNA quantifica

285 ast, the positive effect of G(2)/M arrest on virus replication was not observed in cells defective in

286 glycolylneuraminic acid (Neu5Gc) by NA in H9 virus replication was observed by reverse genetics, and

287 equirements based on optimal cell viability, virus replication was partially rescued by the addition

288 Inhibition of virus replication was robust in resistant RNase L(-/-) m

289 The virus replication was significantly reduced by 6 orders

290 Using deep mutational scans decoupled from virus replication, we report mutational landscapes for E

291 change, mutational landscapes decoupled from virus replication were determined for Env from BaL (clad

292 inding, pH of fusion, thermal stability, and virus replication were investigated.

293 Whereas increased survival and reduction in virus replication were observed in vaccinated mice chall

294 sphorylated viral transcripts and attenuated virus replication, which is rescued by reducing RIG-I ex

295 this to an inhibitory effect of estradiol on virus replication, which we were able to observe with re

296 surped by viral proteins, does not influence virus replication, while Hsp90 activity is important for

297 More generally, inhibiting virus replication with agents that can enter cells and d

298 cellular cholesterol, which would facilitate virus replication within membrane-associated replication

299 Our model provides useful insight into virus replication within the brain and suggests that the

300 gy provides a platform for the regulation of virus replication without targeting viral proteins direc