ライフサイエンスコーパス: viral replication

1 ction of apoptosis as mechanisms to restrict viral replication.

2 letion of which is associated with increased viral replication.

3 with the lack of pyroptosis or inhibition of viral replication.

4 d supports IFN gamma-mediated suppression of viral replication.

5 thesis was also observed as a sign of active viral replication.

6 diating both virus-induced cell toxicity and viral replication.

7 tinal mucosa served as major target sites of viral replication.

8 ) interacts with the Zika genome and enables viral replication.

9 but are unlikely to be phosphorylated during viral replication.

10 virus, acting directly or indirectly against viral replication.

11 nate immune response to facilitate efficient viral replication.

12 ore protein is involved in multiple steps of viral replication.

13 erferon-stimulated genes function to inhibit viral replication.

14 nable to suppress IFN induced in response to viral replication.

15 hancing viral growth, or directly inhibiting viral replication.

16 A deletion of these residues blocks viral replication.

17 ns, and the role played by viral genetics in viral replication.

18 t, we hypothesized that PKD played a role in viral replication.

19 d inflammation driven by years of continuous viral replication.

20 infected cells, each at a different stage of viral replication.

21 pport both full transcriptional activity and viral replication.

22 denosylmethionine (SAM) enzyme that inhibits viral replication.

23 impact on the ability of antibodies to halt viral replication.

24 odified by acylation whose removal abrogates viral replication.

25 persistent virus despite relative control of viral replication.

26 ons and fibroblasts that is likely to reduce viral replication.

27 es, resulting in enhanced beta-oxidation and viral replication.

28 ion, whereas inhibition of autophagy impairs viral replication.

29 posttranscriptional level in the control of viral replication.

30 ducing gammadelta T cells, without affecting viral replication.

31 ether result in increased fusion and reduced viral replication.

32 lates microRNA (miRNA) expression to support viral replication.

33 of cellular proteins that are important for viral replication.

34 n and aptamers have been reported to inhibit viral replication.

35 LY is required for cholangiocyte binding and viral replication.

36 ns and plays an essential role in regulating viral replication.

37 to identify cellular proteins necessary for viral replication.

38 ion by modulating inflammatory responses and viral replication.

39 for phosphatidylethanolamine and sterols in viral replication.

40 zing cellular pathways that support or limit viral replication.

41 can occur even in the absence of productive viral replication.

42 amic actin network during the early steps of viral replication.

43 al drugs that target viral genomes and block viral replication.

44 a specialized structure to compartmentalize viral replication.

45 of negative strand viral genome, indicating viral replication.

46 nd is thus essential to initiate and sustain viral replication.

47 of this PI4K isoform leads to the arrest of viral replication.

48 oss and myositis, but did not affect in vivo viral replication.

49 ndent, but it was dependent on the extent of viral replication.

50 gonism of innate immune signaling to enhance viral replication.

51 is and identifies the initiation platform of viral replication.

52 contains all of the genetic information for viral replication.

53 nus (p12 PM13 to PM15) block early stages in viral replication.

54 DNA to cell progeny in the absence of active viral replication.

55 h antibody playing a key role in controlling viral replication.

56 halation and the primary site of respiratory viral replication.

57 factors are a class of proteins that inhibit viral replication.

58 l polymerase function and attenuates overall viral replication.

59 gger antiviral immune responses and restrict viral replication.

60 tolbutamide decreases survival and increases viral replication.

61 lishment of latent EBV infection and enhance viral replication.

62 on or from those who require ART to suppress viral replication.

63 ABC59) and Nigerian (IBH30656) and analyzing viral replication.

64 in particular was able to improve control of viral replication.

65 hese factories aids efficient and controlled viral replication.

66 uence the transition into the lytic phase of viral replication.

67 crease in viral capsid production and robust viral replication.

68 functional yet appeared ignorant of ongoing viral replication.

69 rols are essential as proviral lipids during viral replication.

70 -33 boosted antiviral immunity and decreased viral replication.

71 onic infection but also functions to repress viral replication.

72 limiting polymerase activity and subsequent viral replication.

73 at both the efferent and afferent phases of viral replication.

74 ndicating that this pathway is important for viral replication.

75 ic CD8 T cell function, and led to decreased viral replication.

76 evels of CHK1, which plays a central role in viral replication.

77 V71 replication that involves host ACBD3 for viral replication.

78 duction in DENV-infected cells and decreases viral replication.

79 ut antiviral therapy, which prevents de novo viral replication.

80 -acetylation at these sites has no effect on viral replication.

81 arious means in order to establish efficient viral replication.

82 morbid mice died as a result of uncontrolled viral replication.

83 argely ineffective during the early steps of viral replication.

84 lls in the latent reservoir, or from ongoing viral replication?

85 of dengue virus infection, the mechanism of viral replication, a process commonly targeted by antivi

86 235 phosphorylation that correlated with the viral replication activity.

87 diagnosed individuals with ART, and suppress viral replication among 90% of treated individuals, for

88 gly inhibited VEEV pathogenesis in mice, and viral replication analyses suggest that the TF protein i

89 neration sequencing, patient viral load, and viral replication analysis with surveillance of RSV to i

90 code a helicase enzyme that is essential for viral replication and assembly (nonstructural protein 3

91 cellular immunization for preventing chronic viral replication and can be a way to prevent HIV spread

92 Viral replication and cellular responses were measured u

93 of viral entry, gene and protein expression, viral replication and cytokine induction.

94 d Il1r1(-/-) mice evaluating the kinetics of viral replication and cytokine production revealed diffe

95 reate an environment conducive to productive viral replication and egress.IMPORTANCE HPV genome ampli

96 o specifically suppress NORE1A, facilitating viral replication and elevated Ras signaling.

97 itate reallocation of cellular resources for viral replication and evasion of host antiviral immune r

98 nthesis should facilitate understanding both viral replication and fundamental cell biology.

99 s (HBV) HBx protein plays a critical role in viral replication and hepatocarcinogenesis.

100 l protein 1 (NS1) plays an essential role in viral replication and immune evasion.

101 initiating an ongoing cascade of persistent viral replication and inflammation, that causes irrevers

102 of cellular processes in order to facilitate viral replication and inhibit antiviral defenses.

103 otein secreted at high concentrations during viral replication and is a biomarker for DENV infection.

104 ron response and sex hormones can alter both viral replication and lethality.

105 Further, HO-1 induction also decreased viral replication and lung inflammation, as evidenced by

106 tain the EBOV nucleocapsids and are sites of viral replication and nucleocapsid maturation.

107 nhance host autophagic machinery to increase viral replication and pathogenesis.

108 d be considered in investigations of enteric viral replication and pathogenesis.

109 inations of markers synergistically enhanced viral replication and polymerase activity in human cell

110 pe I interferon (IFN-I) response that limits viral replication and promotes host defenses.

111 ons of antiretroviral drugs usually suppress viral replication and reduce viral RNA to undetectable l

112 producing cells, were measured to quantified viral replication and reservoirs.

113 e singular, dead-end events or can result in viral replication and spread in the new species.

114 show that NORE1A colocalizes to sites of HCV viral replication and suppresses the replication process

115 bility of the host immune system to suppress viral replication and the ability of a virus to countera

116 of EBV-specific antibodies in the control of viral replication and the evolution of sequence diversit

117 enetic modifications of cccDNA contribute to viral replication and the outcome of chronic HBV infecti

118 sion of PKR as well as its redistribution to viral replication and transcription factories.

119 he strategy of packaging dimeric RNA affects viral replication and viral evolution.

120 H10 viruses and combining this analysis with viral replication and weight loss findings, we identifie

121 or investigating roles of essential genes in viral replication and will better enable future developm

122 IV-infected cells survive infection, silence viral replication, and can reactivate viral production u

123 tant roles in metabolism, tumor progression, viral replication, and skin barrier formation.

124 hat HIV-2 RT exhibits higher fidelity during viral replication, and taken together, these findings de

125 By combining data on weight loss, viral replication, and the cross-reactive antibody respo

126 glutamine dependence, which is required for viral replication, and, importantly, that glutamine addi

127 Infection and viral replication are disassociated in lysogens until an

128 sease, but intestinal factors that influence viral replication are understudied.

129 its antiviral effect mainly at the level of viral replication, as opposed to functioning as a mechan

130 ical signs of disease but in relatively high viral replication, as visualized by luminescence, for 2

131 and these cells showed interference with HIV viral replication, assayed by virus capsid protein p24 p

132 erminal domain of CA and were found to block viral replication at low micromolar concentrations.

133 t study demonstrated that autophagy enhances viral replication at the late stage of infection, and th

134 llenge, demonstrating rapid sequestration of viral replication away from T cells.

135 lymerase inhibitors can efficiently suppress viral replication but are unable to eradicate the infect

136 HBeAg is not required for viral replication but is implicated in establishing immu

137 uxiliary proteins that are not essential for viral replication but provide them with a selective adva

138 The second block is downstream of viral replication but upstream of late protein synthesis

139 provide an advantageous microenvironment for viral replication, but it is unknown how the host immune

140 d discover host genes that are essential for viral replication, but not for host cell survival.

141 n and a mutant that significantly attenuates viral replication by abrogating hnRNP A1 interactions.

142 slowly, even during prolonged suppression of viral replication by antiretroviral therapy (ART).

143 Vif molecules contribute to viral replication by inactivating host antiviral factors

144 sponse, while the later treatment suppresses viral replication by inhibiting reverse transcriptase, w

145 A tight control of viral replication by the host innate immune defense migh

146 mission of consensus-like viruses with lower viral replication capacities.IMPORTANCE Understanding th

147 We addressed the role of viral replication capacity driven by Gag, a major struct

148 determine the impact of Gag-protease-driven viral replication capacity on mother-to-child transmissi

149 We show that viral replication capacity, but not viral infectivity, c

150 Gag-protease is a significant contributor to viral replication capacity.

151 All these changes were independent of viral replication, CD4 counts, inflammation, and type of

152 for the first time that HRVs enter and form viral replication centers in B lymphocytes and induce th

153 ISH that HRVs can enter B cells, form their viral replication centers, and the newly formed virions

154 of the cell nucleus including formation of a viral replication compartment and chromatin marginalizat

155 n to elicit the formation of a large nuclear viral replication compartment and marginalization of the

156 Our data showed that the formation of the viral replication compartment at late infection resulted

157 d PK generates high levels of ATP within the viral replication compartment at the expense of a reduct

158 We also show that enrichment of PE in the viral replication compartment is assisted by actin filam

159 In addition, the number of viral replication compartments is significantly higher i

160 In sequence, the ND10 bodies become viral replication compartments, and ICP0, a viral E3 lig

161 (MNV) NS3 is intimately associated with the viral replication complex and dsRNA.

162 number of the host proteins involved in the viral replication complex have been identified, includin

163 ctors and play critical roles in assembly of viral replication complexes (vRCs).

164 rt is considered to be the bottleneck of the viral replication cycle and therefore represents a promi

165 The model does not encompass other viral replication cycle steps such as entry, processing,

166 e crucial virus-host interactions during the viral replication cycle still remain incomplete.

167 es new molecular details about events in the viral replication cycle that contribute to the induction

168 ritical role that these proteins play in the viral replication cycle, but it also identifies a key in

169 ions that destabilize this region impair the viral replication cycle.

170 eins that function at multiple stages of the viral replication cycle.

171 n plays essential roles in many steps of the viral replication cycle.

172 nel and pH regulator that is involved in the viral replication cycle.

173 ural proteins during different phases of the viral replication cycle.

174 ement of PLK activity to early stages of the viral replication cycle.

175 Intriguingly, productive viral replication decreased phagocytosis of IgG-opsonize

176 narily constrained at the macro level due to viral replication defects.

177 (MAIT) cells might play a role in control of viral replication during chronic hepatitis B (cHBV) infe

178 or variant calling thresholds and stochastic viral replication dynamics within recipient hosts.

179 characterized by reduced ability to suppress viral replication ex vivo These data suggest that the co

180 ated, probably due to a stabilization of the viral replication factor E2.

181 er, we show that the binding of cellular and viral replication factors to viral RNA is conserved desp

182 increases survival of bees while decreasing viral replication following infection with FHV, whereas

183 ntenance of cellular functions necessary for viral replication if continuous protein synthesis is req

184 anctuaries and potentially suppress residual viral replication.IMPORTANCE AIDS virus persistence in i

185 oopt cellular translation factors to enhance viral replication.IMPORTANCE Human tRNA(Lys3), the prime

186 would otherwise have a detrimental effect on viral replication.IMPORTANCE Tumor viruses are known to

187 Inhibition of the JNK pathway blocked viral replication in a manner distinct from that of acyc

188 pression of microRNA-122 promoted persistent viral replication in B cells.

189 system might play a key role in controlling viral replication in bats.

190 nce, the viral host cell tropism and whether viral replication in carrier stallions occurs in the pre

191 iral entry into the cytoplasm and persistent viral replication in cell culture.

192 e effective CD8 T-cell responses can control viral replication in conjunction with drug therapy or in

193 iviral immunity, specifically in controlling viral replication in EBV-infected B cells.

194 Viral replication in eukaryotes is a process inherently

195 he fact that persistence involves continuous viral replication in fibrocytes (possibly including tiss

196 s contribute to liver disease and control of viral replication in HDV infection.

197 a protective effect against cytotoxicity and viral replication in HIV-1-infected macrophages.

198 Antiretroviral therapy (ART) suppresses viral replication in HIV-infected individuals but does n

199 Viral replication in lineage cells was determined by p24

200 s unclear whether treatment fully suppresses viral replication in lymphoid tissue reservoirs.

201 to viral replication within macrophages, how viral replication in macrophages might contribute to the

202 The deficiency in viral replication in microglial cells was associated wit

203 f 93 HHV8-seropositive recipients (2.1%) had viral replication in posttransplant period, one of whom

204 to other techniques currently used to assess viral replication in reactivation studies.

205 suggesting that in this model, efficiency of viral replication in select tissues early in infection m

206 hat the BTV nonstructural protein NS4 favors viral replication in sheep, the animal species most affe

207 Furthermore, comparable levels of early viral replication in spleen and liver were observed in M

208 s) maintain CD4(+) T cell counts and control viral replication in the absence of antiretroviral thera

209 anctuary site for latent virus and low-level viral replication in the absence of neuro-disease.

210 antiretroviral therapy can effectively block viral replication in the host, human immunodeficiency vi

211 ected to naive cell, resulting in productive viral replication in the naive cells.

212 moderate weight loss (5 to 15%), with robust viral replication in the nasal tissues and variable repl

213 ct lower levels of antigen production and/or viral replication in the persistent HIV reservoir.

214 , and those that do fail to robustly control viral replication in the TFH population.

215 was observed in these three cell types, and viral replication in the tonsil/gut was associated with

216 ealing a role for NS1 and characteristics of viral replication in the URT that were associated with a

217 in the draining lymph node had no impact on viral replication in this organ, suggesting that WNV may

218 This caused selective attenuation of viral replication in tick-derived cells.

219 of antibody titer has been shown to enhance viral replication in vitro and severe disease in animal

220 5, ORF132, ORF136, ORF148, or ORF149 affects viral replication in vitro, and deletion of ORF25, ORF64

221 ssion, the evidence that macrophages support viral replication in vivo, the animal models where macro

222 munity can control both early and persistent viral replication independently of adaptive immune effec

223 al hydrolysis activity significantly reduced viral replication, indicating that virions utilized the

224 y involved in a novel cytopathology in which viral replication induces nuclear lysis followed by cell

225 infected cells with a STAT3 inhibitor and a viral replication inhibitor, ganciclovir, represents a p

226 ted with the MNV replication complex and the viral replication intermediate double-stranded RNA (dsRN

227 s, activation of the ATM-CHK2 pathway during viral replication is a cell line-specific event, indicat

228 th epidermodysplasia verruciformis, beta-HPV viral replication is associated with skin keratosis and

229 TANCE In chronic, untreated HIV-1 infection, viral replication is concentrated in secondary lymphoid

230 tors are involved, it is largely unclear how viral replication is controlled.

231 As such, viral replication is impeded.

232 Because cellular resistance to viral replication is marked by expression of antiviral r

233 ication of additional proteins essential for viral replication is necessary to develop improved thera

234 ntiviral signalling in the absence of KHSRP, viral replication is reduced when KHSRP expression is kn

235 undamentally change our understanding of how viral replication is regulated.

236 en if the portion of viremia attributable to viral replication is significant, our model predicts (1)

237 initiation of replication compartments, (ii) viral replication is significantly less affected by IFN-

238 athways, but whether daily rhythms impact on viral replication is unknown.

239 he virus by relocating cellular resources to viral replication, it also poses a challenge to the main

240 lysis to create an environment favorable for viral replication, it predisposes the cell to transforma

241 have uncovered an unprecedented mechanism of viral replication: Kaposi's sarcoma-associated herpesvir

242 Viral replication leads to prolonged local immune activa

243 Interestingly, the transient activation of viral replication led to HIV-1 reservoir reduction after

244 However, outside of viral replication, little is known about the dependence

245 ence include replenishment through low-level viral replication, longevity and homeostatic proliferati

246 his process requires de novo assembly of the viral replication machinery, large ribonucleoprotein com

247 Treatment effectively controlled viral replication, mediating up to 4 log10 reductions af

248 ppressed viremia (ART), 42 with uncontrolled viral replication (noncontrollers [NCs]), and 48 HIV-uni

249 ded DNA (ssDNA) genome to the nucleus, where viral replication occurs.

250 vation whereby lytic genes are activated and viral replication occurs.

251 K77, K113 and K229 impacts multiple steps in viral replication of influenza A viruses.

252 To investigate the question of ongoing viral replication on current ART regimens, we analyzed H

253 ortantly, no evidence was found for residual viral replication or deficient tissue drug penetration t

254 rentiate ECs from subjects with uncontrolled viral replication or from those who require ART to suppr

255 tracellular signaling networks that regulate viral replication or innate antiviral response pathways.

256 ids from the pUL33 C terminus did not affect viral replication or the interaction of pUL33 with pUL28

257 D), there was no direct impact of the TBD on viral replication or virulence in mice.

258 ecular mechanism through which PKD regulates viral replication, our data suggest that this is not due

259 cal manifestations, disease course including viral replication patterns, and outcomes of critically i

260 This review describes the viral replication process based on tombusviruses, highli

261 promoted the temporal expression of ORF59, a viral replication protein.

262 through cellular SCF E3 ligase targeting of viral replication proteins is a unique form of latency t

263 t the local enrichment of sterols around the viral replication proteins that is critical for TBSV rep

264 Viral replication proteins were detected in both epithel

265 The known viral replication proteins, a telomere binding protein,

266 assays has led to treatments that target HCV viral replication proteins.

267 uppressed splenocyte proliferation, although viral replication rate increased only in the chronic cor

268 ng chronic SIVagm infection resulted in high viral replication rates in follicles and the T cell zone

269 on the permissiveness of malignant cells to viral replication rather than on receptor specificity, w

270 es in cell RNA splicing.IMPORTANCE Efficient viral replication requires that the virus create favorab

271 effect of an antiviral treatment that blocks viral replication, showing that the median time to undet

272 immunodeficiency virus (HIV)-1 and a site of viral replication, similar to lymphoid tissue, gut-assoc

273 9 is substantially more potent at inhibiting viral replication than HLA-B*14-DA9.

274 Because of its importance in viral replication, the M2 proton channel of the influenz

275 sites are associated with better control of viral replication, thereby likely reducing SIV morbidity

276 ntiretroviral therapies effectively suppress viral replication, they do not eliminate integrated prov

277 These proteins repress viral replication through mechanisms that rely on SUMO s

278 in protease (M(pro)), which is essential for viral replication through proteolytic processing of RNA

279 xonuclease activity of UL12 is essential for viral replication through the analysis of a nuclease-def

280 dividual miRNAs may be capable of inhibiting viral replication through their effects on host proteins

281 s of apoptosis are expressed first, enabling viral replication to proceed, after which the SfAV-1a ca

282 ic cells, which display a robust decrease in viral replication upon infection with Vpr-deficient HIV-

283 n coordinating the intercellular movement of viral replication vesicles.

284 (TuMV), in the intercellular movement of the viral replication vesicles.

285 everse transcription.APOBEC3G inhibits HIV-1 viral replication via catalytic and non-catalytic proces

286 To facilitate viral replication, Vpx has evolved to induce SAMHD1 degr

287 d capable of expressing reporter genes while viral replication was blocked.

288 vere neurological signs within 2 months, and viral replication was detected only in central nervous s

289 Viral replication was determined by RT-qPCR and virion r

290 The consequence of this was that viral replication was elevated, probably due to a stabil

291 proteins might act as key factors to control viral replication we cloned Mx1 cDNAs from three bat fam

292 , such as the microbiota, that alter enteric viral replication, we sought to investigate coxsackievir

293 responsiveness (AHR), and lung histology and viral replication were assessed.

294 uclear cells collected during episodes of BK viral replication were evaluated by multiparameter flow

295 s 50 to 60 or residues 110 to 120) precluded viral replication, whereas the truncation of the last 10

296 Although this coordination is crucial in viral replication, whether a DNA/RNA hybrid can simultan

297 f its exonuclease activity negatively impact viral replication, while in contrast, knockdown of Ku80

298 ivo, pathologies thought to be attributed to viral replication within macrophages, how viral replicat

299 ulations that are able to support high-level viral replication without causing a loss of CD4(+) T cel

300 ll subsets and anatomical sites that support viral replication without disrupting immune homeostasis