ライフサイエンスコーパス: virus replication

1 he function of many tegument proteins during virus replication.

2 tivated proton channel that is essential for virus replication.

3 pathways that are targeted by HPV to support virus replication.

4 N antagonist and that NSs is dispensable for virus replication.

5 it to control the switch between latency and virus replication.

6 pathway in chicken cells and can potentiate virus replication.

7 IM25 in specifically restricting influenza A virus replication.

8 ion also abolished HSP70-dependent influenza virus replication.

9 le SDF-1beta, CCL21, and CCL14 suppressed X4 virus replication.

10 omolar range, are not cytotoxic, and inhibit virus replication.

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

12 from 12S and 13S to 9S RNA at late stages of virus replication.

13 on-stimulated gene IRAV (FLJ11286) on dengue virus replication.

14 drug targets due to their critical roles in virus replication.

15 In some cases, cell death curbs virus replication.

16 re evolutionarily conserved but also enhance virus replication.

17 th the panhandle domain and HSPA8 motif 1 in virus replication.

18 the blinding eye disease and in controlling virus replication.

19 anti-dengue virus antibody may enhance Zika virus replication.

20 act through different mechanisms to increase virus replication.

21 al immune responses in the anatomic sites of virus replication.

22 ausing decreased viral protein synthesis and virus replication.

23 d interplay between host cell metabolism and virus replication.

24 l responses were narrow and poorly inhibited virus replication.

25 er with CK2, it regulates VIB morphology and virus replication.

26 f viral IE1 transcription and suppression of virus replication.

27 proteins, and membrane-deforming proteins in virus replication.

28 rations are insufficient to completely block virus replication.

29 ocessing is an important mechanism to ensure virus replication.

30 ctivity at both the early and late stages of virus replication.

31 on of viral response genes leading to higher virus replication.

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

33 g at the NS3/4A site as a mechanism ensuring virus replication.

34 up-regulate antiviral responses and suppress virus replication.

35 gy to identify cellular factors required for virus replication.

36 y m(6)A methylated, which promotes efficient virus replication.

37 ts subsequent effects on gK localization and virus replication.

38 nia virus late protein synthesis and inhibit virus replication.

39 past as a model to study negative-strand RNA virus replication.

40 argeted as potential therapeutics to disrupt virus replication.

41 glycosylation is responsible for effects on virus replication.

42 sis of viral proteins required for efficient virus replication.

43 ount for maturation-dependent restriction of virus replication.

44 hy ZAPL only moderately inhibits influenza A virus replication.

45 y cytokines, that act in concert to restrict virus replication.

46 GFP and thus allows convenient monitoring of virus replication.

47 ntiviral drugs that target key components of virus replication.

48 ression and usage is necessary for efficient virus replication.

49 regulated by an RNA-editing mechanism during virus replication.

50 overlapping cellular pathways to facilitate virus replication.

51 rminus and render LT incapable of supporting virus replication.

52 ased on a phenotypic assay measuring measles virus replication.

53 predicted to have distinct functions during virus replication.

54 access to plentiful ATP, facilitating robust virus replication.

55 d by these genes inhibit different stages of virus replication.

56 mes within incoming virus particles prior to virus replication.

57 ns are host factors required for hepatitis C virus replication.

58 microscopy and the impact of temperature on virus replication.

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

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

61 ted pathogenesis without directly preventing virus replication.

62 med by its activity in suppressing influenza virus replication.

63 n function significantly suppressed vaccinia virus replication.

64 of hydrolysing deoxynucleotides required for virus replication.

65 factors in replication complex assembly and virus replication.

66 leted from the virus genome without reducing virus replication.

67 uld otherwise restrict protein synthesis and virus replication.

68 enous Rint1 expression enhances E2-dependent virus replication.

69 autophagy and cell cycle arrest and benefits virus replication.

70 rements for host gene suppression versus RNA virus replication.

71 without significantly impacting the level of virus replication.

72 ing cells, demonstrating early inhibition of virus replication.

73 cells, but only VP35 IID appeared to promote virus replication.

74 biquitination and is important for efficient virus replication.

75 ed pigs); however, ISG15 is not required for virus replication.

76 port of RRE-containing RNAs, as required for virus replication.

77 spiratory syndrome)-CoV, we show that robust virus replication accompanied by delayed type I interfer

78 s and monitored in detail how suppression of virus replication affected the main virological and immu

79 es in SIV-infected SMs, thus suggesting that virus replication affects immune function even in the co

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

81 Suppression of virus replication after pregnancy was also strongly infl

82 ction and point toward a novel mechanism for virus replication among arthropod-borne viruses.

83 existing ADCC-Abs were associated with lower virus replication and a significant reduction in total s

84 these drugs have been associated with higher virus replication and accelerated disease progression as

85 e fibers are capable of productive influenza virus replication and are a potential tissue source of i

86 The same mutant virus in mice also enhanced virus replication and caused lethal infection.

87 at the duration of persistence is related to virus replication and cell-killing capacity.

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

89 We study the dynamics of virus replication and cytotoxic T lymphocytes (CTLs) wit

90 pathogenic determinant that is important for virus replication and disease progression in horses.

91 The stepwise pattern of virus replication and dissemination described here sugge

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

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

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

95 fluenza A virus protein PA-X plays a role in virus replication and inhibition of host antiviral respo

96 sting of 248 residues with a crucial role in virus replication and interference with the host innate

97 l host partner co-opted to support influenza virus replication and is a candidate host target for nov

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

99 insight into the mechanism of control of BK virus replication and may allow for future patient risk

100 factor 1 (vIRF-1) is targeted to mDRM during virus replication and negatively regulates the mitochond

101 ility of IFIT1 to inhibit negative-sense RNA virus replication and pathogenesis both in vitro and in

102 hat phosphorylation of M2-1 is essential for virus replication and pathogenesis in vivo Recombinant h

103 ll Ca(2+) homeostasis, which is critical for virus replication and pathogenesis.

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

105 (PKR) is activated by dsRNA produced during virus replication and plays a major role in the innate i

106 AMs support both active virus replication and production of infectious virions.

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

108 found a major role for NLRC5 in restricting virus replication and promoting viral clearance.

109 clusion that these cells are a major site of virus replication and raised the possibility that, like

110 Irf2(-/-) mice fail to control virus replication and recruit immune infiltrates into th

111 HIV-1 integrase (IN) is essential for virus replication and represents an important multifunct

112 of vpu-deleted HIV-1 recombinants, enhanced virus replication and resistance to antibody-dependent c

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

114 high capacity for mismatch extension during virus replication and revealed dramatic differences in a

115 upted DMV formation and result in changes in virus replication and RNA synthesis.

116 H9N2 viruses causes significant increases in virus replication and severity of infection in human cel

117 of which are associated with some control of virus replication and slower disease progression.

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

119 e a significant restriction of Vpr-deficient virus replication and spread in MDDCs alone and in cell-

120 s as well as modifying host cells to promote virus replication and spread.

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

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

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

124 any correlation between the level of primary virus replication and the level of viral DNA during late

125 These results suggest that increased virus replication and the local immune response to MERS-

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

127 tein synthesis by their host cell to enhance virus replication and to antagonize antiviral defense me

128 culoviruses could be related to accelerating virus replication and to protecting the virus genome fro

129 with the viral proteins that are central to virus replication and transcription, with a view to prov

130 Increased virus replication and type I IFN specifically inhibited

131 nces of herpes simplex virus 1 (HSV-1) gK on virus replication and viral pathogenesis, we constructed

132 We found significant inhibition of virus replication and viral protein expression in cells

133 iruses shown to alter fidelity and attenuate virus replication and virulence.

134 thin the glycoprotein that are important for virus replication and virulence.

135 acytoid (pDCs) dendritic cells on control of virus replication and virus-induced pathology caused by

136 n in MDDCs was observed in a single round of virus replication and was rescued by the expression of V

137 arge number of cellular proteins that affect virus replication and, in some cases, viral genetic reco

138 mTORC1 is believed to be important for virus replication, and HCMV maintains high mTORC1 activi

139 gen expression in intestinal cells restricts virus replication, and infectivity is abrogated by inact

140 t included delayed midgut infection, delayed virus replication, and reduced virus accumulation in sal

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

142 that spherules generated during Flock House virus replication are dynamic, protect double-stranded R

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

144 alphaviral encephalomyelitis should inhibit virus replication as well as neuroinflammatory damage.

145 of NOD1 and RIPK2 determined the outcome of virus replication, as evidenced by enhanced virus growth

146 Furthermore, MST-312 treatment inhibited virus replication, as measured by adsorption assays and

147 ets had lower viral titers and delayed or no virus replication at all following natural exposure to i

148 on in acute hepacivirus infection can dampen virus replication but also regulate acute and chronic li

149 in disease was not dependent on decrease in virus replication but did correspond to a decrease in pu

150 This did not affect virus replication but increased the F-specific antibody

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

152 es (NNAbs) were not associated with enhanced virus replication, but rather with promoted antigen pres

153 interferon (IFN) response in host control of virus replication, but this remains unclear for HuNoVs.

154 VP35, an important viral protein involved in virus replication by acting as an essential cofactor of

155 Instead, they inhibit virus replication by binding and regulating the function

156 a small molecule that can suppress influenza virus replication by disrupting the polymerase assembly.

157 hrough IFN receptor was necessary to inhibit virus replication by MOV10.

158 RNA virus replication by plant viral RdRPs occurs inside ves

159 us can manipulate cellular miRNAs to enhance virus replication by regulating antiviral responses foll

160 whether Zika virus antibodies enhance dengue virus replication, by exposing C57Bl/6 mice to Zika viru

161 Cell culture systems reproducing virus replication can serve as unique models for the dis

162 2, and specifically the enzyme that mediates virus replication, can be inhibited by a panel of drugs

163 echanistic insights into positive-strand RNA virus replication compartment structure, assembly, funct

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

165 unctionality of specific proteins within the virus replication complex.

166 Assembly of virus replication complexes for all known positive-stran

167 ization and microenvironment of plant (+)RNA virus replication complexes.

168 ls into numerous anucleate vesicles in which virus replication continues as these grow in the blood.

169 yme integrase plays an essential role in the virus replication cycle by catalyzing the covalent inser

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

171 l RNA genome in virion particles late in the virus replication cycle to promote particle maturation.

172 tion kinetics to determine what stage of the virus replication cycle was inhibited as a function of f

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

174 remodels keratinocytes for completion of the virus replication cycle.

175 at drives the persistence of otherwise acute viruses.Replication defective viral genomes (DVGs) can f

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

177 ExoN(-) virus replication did not result in IFN-beta gene expres

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

179 p65-specific response, suggesting that local virus replication drives antigen-specific CD8 T cells in

180 ractions between protein VI and hexon during virus replication, driving hexon nuclear accumulation an

181 e virus replication, we found that increased virus replication drove increased effector CD8(+) T cell

182 n host cells to provide, to support vaccinia virus replication during a host shutoff.IMPORTANCE Many

183 on plays an important role in the control of virus replication during acute infection in vivo.

184 of CD8 T cells with the potential to control virus replication during chronic infection or after reac

185 onstrated that CD8(+) T lymphocytes suppress virus replication during human immunodeficiency virus (H

186 els can activate RNase L and thereby inhibit virus replication early in infection upon exposure to vi

187 The role of virus replication, Env glycoprotein phenotype, and immun

188 l tract, indicating that the primary site of virus replication had shifted from the genital lymph nod

189 most 40 years ago, how m(6)A editing affects virus replication has remained unclear.

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

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

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

193 tion of IFITMs during the very late stage of virus replication, i.e., virion assembly.

194 t cells, which was inversely correlated with virus replication.IMPORTANCE The detection of viral RNA

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

196 These NS proteins together are required for virus replication in a host cell-dependent manner.

197 act of the PLK inhibitor BI2536 on influenza virus replication in a human lung tissue culture model a

198 s-derived NS segments necessarily attenuates virus replication in a mammalian host, although the alle

199 functions in vivo, thereby preventing Junin virus replication in a mouse model, opening the possibil

200 king IFN-I signaling on T cell responses and virus replication in a murine model of chronic HIV infec

201 Viral quasispecies evolution upon long-term virus replication in a noncoevolving cellular environmen

202 bachia on cholesterol homeostasis and dengue virus replication in Aedes aegypti.

203 Pathobiological features and systemic virus replication in all species tested were consistent

204 anced, HIV-1 protein and RNA expression, and virus replication in CD4+ T cells.

205 Favipiravir suppressed Lassa virus replication in cell culture by 5 log10 units.

206 iviral factor that potently inhibits Sindbis virus replication in cell culture.

207 t field isolate Georgia/2007, did not affect virus replication in cell cultures and did not affect di

208 f these, DP148R, is transcribed early during virus replication in cells and can be deleted from the v

209 To better understand the role of virus replication in determining the main features of SI

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

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

212 model for determining how ISGylation affects virus replication in human cells.

213 s of hantavirus infection fail to combat the virus replication in infected cells.

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

215 ous dual miRNA targeting led to silencing of virus replication in live Ixodes ricinus ticks and aboli

216 e host cellular immunity to reduce influenza virus replication in lungs, thereby providing a novel me

217 Whether influenza virus replication in macrophages is productive or aborti

218 Deletion of this gene did not reduce virus replication in macrophages, showing that it is not

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

220 es harboring 190V in the HA exhibit enhanced virus replication in mice.

221 on as evidenced by elevated infection rates, virus replication in multiple tissue types, and earlier

222 nd PA is necessary for efficient influenza A virus replication in new host species.

223 4, virus entry into cells bearing rhCD4, and virus replication in primary rhCD4 T cells without appre

224 n of the five cytokines suppressed R5 and X4 virus replication in resting CD4(+) T cells, and individ

225 AKAV and SBV, at least in vitro, to promote virus replication in susceptible cells.IMPORTANCE AKAV a

226 Virus replication in TBPCs in vitro dysregulates key pro

227 ced viral protein expression, and diminished virus replication in the absence of both pTRS1 and pIRS1

228 role for the immune response, but not local virus replication in the development of HSV-1-induced ne

229 M2 macrophages, was associated with reduced virus replication in the eye and reduced latency and red

230 Virus replication in the eye, latency in trigeminal gang

231 arding the interrelationship between primary virus replication in the eye, the level of latency in TG

232 lity of an interrelationship between primary virus replication in the eye, the level of viral DNA in

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

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

235 bias-inducing adjuvant, and protection from virus replication in the lower respiratory tract.IMPORTA

236 host response required to control varicella virus replication in the lung and provide insight into m

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

238 -CoV, human DPP4 knockin (KI) mice supported virus replication in the lungs, but developed no illness

239 eatment with 81.39a significantly suppressed virus replication in the lungs, prevented dramatic body

240 vels required for protection and with no/low virus replication in the lungs.

241 WT-infected mice, despite the lower level of virus replication in the lungs.

242 Homologous vaccination reduced H5N1 virus replication in the olfactory mucosa and prevented

243 rophylactic oseltamivir did not prevent H5N1 virus replication in the olfactory mucosa sufficiently,

244 gD27 provided better inhibition of challenge virus replication in the vagina than when the virus was

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

246 e initial challenge results in no detectable virus replication, indicating protective immunity agains

247 nvironment, organ, and system in controlling virus replication, inflammation, and disease progression

248 viruses, I highlight how distinct stages of virus replication initiate signaling pathways that elici

249 Successful virus replication is in large part achieved by the abili

250 of NA-specific antibodies on NA activity and virus replication is likely to depend on where the antib

251 ontrol and it has been suggested that dengue virus replication is regulated by Dnmt2-mediated DNA met

252 ve immune response can be protective only if virus replication is suppressed during the first several

253 ze and morphology.IMPORTANCE A key aspect in virus replication is virus particle assembly, which is a

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

255 ion of VZV induced multinuclear cells and in virus replication kinetics and spread.

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

257 their effects on RNA polymerase activity and virus replication kinetics at various temperatures.

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

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

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

261 nning of the 1980s, research on the vaccinia virus replication mechanism has basically stalled due to

262 xpected, CD8 depletion resulted in increased virus replication, more prominently in controllers than

263 nd swine with a swine FLUDV, which supported virus replication only in the upper respiratory tract an

264 r factors involved in supporting or limiting virus replication, opening up new avenues for antiviral

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

266 protection through the direct inhibition of virus replication or the modulation of the acute immune

267 dney recipients had a higher incidence of BK virus replication (P = 0.04) and nephropathy (P = 0.01)

268 and to have mutations associated with higher virus replication rates and illness severity.

269 with both protein families strongly affects virus replication rates.

270 Also, how CTD affects virus replication remains unclear.

271 Extrapulmonary loci of virus replication seem possible.

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

273 1 were observed, particularly in LN-draining virus replication sites already described.

274 ially increase the inhibition of influenza A virus replication, so that the PB1 interface with ZAPL i

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

276 as avian reovirus sigmaNS, are essential for virus replication, the mechanism by which they assist pa

277 ion of two enzymatic activities critical for virus replication, the methyltransferase and RNA-depende

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

279 thesis of monocistronic F mRNA or F protein, virus replication, virion morphogenesis, and immunogenic

280 In addition, ExoN(-) virus replication was attenuated in wild-type bone marro

281 Virus replication was determined by viral RNA quantifica

282 e caspase activation and recruitment domain, virus replication was enhanced, but in cells overexpress

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

284 ogous and heterologous H5 viruses, challenge virus replication was reduced in the respiratory tract.

285 However, the efficiency of infectious virus replication was still dependent on the presence of

286 Virus replication was strongly dependent on the preserva

287 for at least 3 months after rechallenge, but virus replication was suppressed, as revealed by the abs

288 rtant role these structures play during SFTS virus replication, we conducted live cell imaging studie

289 o the antiviral drug famciclovir to modulate virus replication, we found that increased virus replica

290 ted with maturation-dependent restriction of virus replication, we studied AP-7 rat olfactory bulb ne

291 ting virus proteins, and characterization of virus replication were subsequently examined.

292 ogenous SPL expression inhibited influenza A virus replication, which correlated with an increase in

293 ally infected animals transiently suppresses virus replication, which invariably returns to pre-treat

294 ly SDF-1beta, CCL14, and CCL27 suppressed R5 virus replication, while SDF-1beta, CCL21, and CCL14 sup

295 ture model and observed strong inhibition of virus replication with no measurable toxicity.

296 Attenuating virus replication with one or more doses of exogenous IF

297 volutionarily conserved sequence facilitates virus replication with the assistance of N in eukaryotic

298 gies are able to reduce or prevent influenza virus replication within the olfactory mucosa and subseq

299 ately 1% of people infected with HIV control virus replication without taking antiviral medications.

300 play a critical role in limiting peripheral virus replication, yet how they locate virus-infected ce