ライフサイエンスコーパス: productive infection

1 ning all three kinetic classes, and suppress productive infection.

2 linear viral cDNA into the host genome for a productive infection.

3 tion to a CXCR5(+)PD-1(low) phenotype during productive infection.

4 roduce an immune response to HuNoV, implying productive infection.

5 ly binding gangliosides are not required for productive infection.

6 r the transition from latency to reactivated productive infection.

7 al binding to LSTc, and only LSTc mediates a productive infection.

8 P1 is subverted by many viruses to promote a productive infection.

9 e that the viral DNA reaches the nucleus for productive infection.

10 y plays an indispensable role required for a productive infection.

11 (IAV) is only rarely sufficient to initiate productive infection.

12 of specific replicative steps, they promote productive infection.

13 avirus (HPV) gene expression is required for productive infection.

14 and infects underlying immune cells during a productive infection.

15 (SKI-1)/site 1 protease (S1P) is crucial for productive infection.

16 sal autophagy levels mostly unchanged during productive infection.

17 -A, mediates an efficient HIV-1 X4 entry and productive infection.

18 wn whether viruses use M cells to initiate a productive infection.

19 viral copy number, to levels associated with productive infection.

20 host cellular defence proteins that inhibit productive infection.

21 wn whether viruses use M cells to initiate a productive infection.

22 is substantially reduced relative to that in productive infection.

23 ne of ~50 virions in infected cells leads to productive infection.

24 nsmitted/founder HIV genomes responsible for productive infection.

25 one of the regions known to be essential for productive infection.

26 cell countermeasures in order to establish a productive infection.

27 human oral epithelial cells without causing productive infection.

28 iciently enter into hepatocytes to establish productive infection.

29 n hepatoma Huh7.5.1 cells and establishing a productive infection.

30 oped HSV-1 virions were observed, indicating productive infection.

31 es demonstrated that progesterone stimulated productive infection.

32 advantage of endocytic pathways to establish productive infection.

33 and the progesterone receptor (PR) stimulate productive infection.

34 RSV G and DC- or L-SIGN are not required for productive infection.

35 ads to lytic cycle viral gene expression and productive infection.

36 at traverse early and late endosomes yield a productive infection.

37 ic regions was detected during both types of productive infection.

38 fuse with endosomal membranes to initiate a productive infection.

39 vantage of caveolar endocytosis to establish productive infection.

40 hen complete the subsequent steps to achieve productive infection.

41 at this interaction is needed to establish a productive infection.

42 e infection more closely resembled that of a productive infection.

43 and compared the doses needed to establish a productive infection.

44 of viral transcription that is required for productive infection.

45 thelial system by which Listeria establishes productive infection.

46 uman cytomegalovirus (HCMV) is essential for productive infection.

47 two populations are cellular reservoirs for productive infection.

48 the bICP0 early promoter and stimulation of productive infection.

49 ere assessed for relative permissiveness for productive infection.

50 crophage populations in lesion formation and productive infection.

51 machinery to initiate and maintain a highly productive infection.

52 rogated, indicating that DCI is required for productive infection.

53 ctions in viremia after the establishment of productive infection.

54 UL21a is required to establish an efficient productive infection.

55 med bone marrow-derived macrophages during a productive infection.

56 ion of IE transcripts and establishment of a productive infection.

57 r stabilizing a DNA hairpin structure during productive infection.

58 ion partners among other HCV proteins during productive infection.

59 s receptor, H-F dissociation is required for productive infection.

60 nts and uninfected donors to HIV-1 entry and productive infection.

61 domain formation is not essential for HSV-1 productive infection.

62 diverse bunyaviruses require polyamines for productive infection.

63 tudies have also concluded that LAT inhibits productive infection.

64 number assay did not demonstrate evidence of productive infection.

65 explains the necessity for IRS1 or TRS1 for productive infection.

66 activation cycle by inhibiting apoptosis and productive infection.

67 8 locus with early-late gene kinetics during productive infection.

68 is required for HCMV to establish efficient productive infection.

69 either adenovirus (Ad) or herpesvirus, for a productive infection.

70 at maintains bICP0 protein expression during productive infection.

71 g to the delineation of kinetic class in HSV-productive infection.

72 thus maintaining a stoichiometry optimal for productive infection.

73 nterococcal polysaccharide antigen (Epa) for productive infection.

74 d they stimulate certain viral promoters and productive infection.

75 this host RNA decay machinery to establish a productive infection.

76 ly regulated and sequentially ordered during productive infection.

77 X-2 activation and does not result in a full productive infection.

78 ients and adenosine triphosphate (ATP) for a productive infection.

79 even a single virus particle can initiate a productive infection.

80 bs this balance has the potential to block a productive infection.

81 lex virus 1 (HSV-1) results in a delayed but productive infection.

82 m, which is essential for establishment of a productive infection.

83 Furthermore, GR and KLF4 stimulated productive infection.

84 gamma irradiated the cells to prevent their productive infection.

85 vate in order to establish persistent and/or productive infections.

86 and the induction of autophagy to establish productive infections.

87 modulate host immune defenses and establish productive infections.

88 ment proteins that enable gene expression in productive infection?

89 PLZF or Slug stimulated productive infection 20- or 5-fold, respectively, and Sl

90 To establish productive infection, a retrovirus must insert a DNA rep

91 During productive infection, a virus must simultaneously redire

92 We demonstrate that productive infection also triggers ATR-dependent Chk1 ac

93 nuclear translocation pattern that promotes productive infection and avoids viral degradation, sugge

94 , these studies suggest that E2F1 stimulates productive infection and bICP0 early promoter activity,

95 nduced transcription factors also stimulated productive infection and certain viral promoters.

96 n of humans with these viruses can lead to a productive infection and elicit a neutralizing antibody

97 antagonist, A438079, had a limited effect on productive infection and fusion.

98 these inflammatory receptors can block HIV-1 productive infection and HIV-1-associated inflammation.

99 ng reactivation and cooperatively stimulated productive infection and IEtu1 GREs in mouse neuroblasto

100 on factor 15 (KLF15) cooperated to stimulate productive infection and IEtu1 promoter activity.

101 a regulator of HIV-1 replication during both productive infection and induction from latency.

102 is known about the function of ICP22 during productive infection and latency.

103 of trigeminal ganglia (TG), cycling between productive infection and latency.

104 dhesive contacts greatly enhance the rate of productive infection and may be central to the spread of

105 Furthermore, GR and dexamethasone stimulate productive infection and promoters that drive expression

106 the glucocorticoid receptor (GR) stimulates productive infection and promoters that drive expression

107 Notch1 intercellular domain (ICD) stimulated productive infection and promoters that encode the viral

108 Alveolar macrophages undergo productive infection and release infectious virions.

109 MPCCs maintain prolonged, productive infection and represent a facile platform for

110 f viral infection are therefore required for productive infection and resultant viral disease.

111 hment could explain this apparent absence of productive infection and sought to determine its role in

112 However, these particles interfere with productive infection and stimulate antiviral signaling p

113 fection model was developed to support HIV-1 productive infection and stimulated the inflammatory cyt

114 e that the TRIM5 alleles can be a barrier to productive infection and that this should be taken into

115 stress, we tested whether the GR influences productive infection and the promoter that drives infect

116 e cleavage at this site was not required for productive infection and this sequence performs a critic

117 ost cell factors and compartments to mediate productive infection and to produce infectious progeny v

118 embryo implantation, cooperate to stimulate productive infection and two viral promoters that drive

119 n encoded by bovine herpesvirus 1 stimulates productive infection and viral gene expression but inhib

120 sight into how stress can directly stimulate productive infection and viral gene expression.

121 -mediated activation of the GR can stimulate productive infection and viral gene expression.

122 ed that the PR and/or progesterone regulates productive infection and viral transcription.

123 ticoid receptor (GR), cooperate to stimulate productive infection and viral transcription.

124 suggesting that E2F family members stimulate productive infection and/or reactivation from latency.

125 RNA sequences also inhibit bICP0 expression, productive infection, and cell growth.

126 ecific small interfering RNA (siRNA) reduced productive infection approximately 5-fold.

127 transcript was also detected in vitro during productive infection as early as 1 day postinfection.

128 The Notch3 ICD did not stimulate productive infection as efficiently as the Notch1 ICD an

129 +) T cells, can control HIV transcription in productive infection as well as during reactivation from

130 NF279 and NF449 blocked productive infection at the level of viral membrane fusi

131 NA profile could be the result not only of a productive infection but also of the exposure to HIV-1 p

132 vely with host factors to not only establish productive infection but also trigger unique pathologica

133 encode the means to circumvent this block to productive infection but relies on coinfecting helper vi

134 at these six serines was not essential for a productive infection but was required for optimal viral

135 All drugs limited HIV-1 productive infection, but P2X-selective antagonists (NF4

136 V-1 miR-H1, which is highly expressed during productive infection, but we did detect abundant express

137 A hallmark of productive infection by DNA viruses is the coupling of v

138 These RNAs are expressed during productive infection by either bacterial artificial chro

139 s cooperate on the virion surface to mediate productive infection by HIV-1.

140 Viral modulation of RNA granules supports productive infection by inhibiting their gene-silencing

141 i.r. inoculation was followed by productive infection by one or a few viruses (median 1;

142 virus type 1 (HIV-1) generally results from productive infection by only one virus, a finding attrib

143 Because productive infection by parvoviruses requires cell divis

144 Here, we find that CGCC primarily allow productive infection by preventing HIV-1 triggering of a

145 rmined how impairment of endocytosis affects productive infection by prion strains 22L and RML.

146 eloped sophisticated mechanisms to establish productive infections by counteracting host innate immun

147 Productive infections by human papillomaviruses (HPVs) a

148 nd viral proteins throughout the course of a productive infection could provide dynamic insights into

149 he association of LANA to chromatin during a productive infection cycle is controlled by a new regula

150 expressed, and transcriptional activity and productive infection demonstrated.

151 g entry of the HIV-1 core into target cells, productive infection depends on the proper disassembly o

152 r (GR), stimulates viral gene expression and productive infection during reactivation from latency.

153 egration of viral DNA (vDNA) is required for productive infection, efficient vDNA detection is crucia

154 particles entering the host cell results in productive infection, emphasizing the importance of iden

155 n and how these changes in the virus lead to productive-infection events.

156 (GREs) that have the potential to stimulate productive infection following stressful stimuli.

157 oop that activates viral gene expression and productive infection following stressful stimuli.IMPORTA

158 op that stimulates viral gene expression and productive infection following stressful stimuli.IMPORTA

159 cay consistent with RAL-mediated blockade of productive infection from preintegration complexes.

160 s (HCMV) entry into cells where it initiates productive infection has been well studied, but its entr

161 lity of progesterone and the PR to stimulate productive infection has the potential to promote virus

162 During productive infection, herpes simplex virus type 1 (HSV-1

163 To establish a productive infection, HIV-1 must counteract cellular inn

164 in both the cytoplasm and the nucleus during productive infection; however, the mechanism(s) involved

165 To establish a productive infection, human immunodeficiency virus type

166 infected in vivo, but evidence of widespread productive infection (ie, presence of viral RNA and prot

167 ctivity to support glycolytic activation and productive infection.IMPORTANCE Viruses are obligate par

168 h is necessary for viral internalization and productive infection.IMPORTANCE Viruses usurp cellular f

169 r the transcription start site that promotes productive infection in A5+ neurons and a second element

170 nimals were completely protected compared to productive infection in all seven DM-vaccinated animals.

171 34.5 expression is capable of establishing a productive infection in at least one normal mouse brain

172 We conclude that N. gonorrhoeae causes a productive infection in BALB/c mice that is characterize

173 HIVSGD-1 encoded full-length Tag, underwent productive infection in both human salivary gland cells

174 expression in mouse neuroblastoma cells and productive infection in bovine cells.

175 us particles to T cells without establishing productive infection in DCs, a mechanism of HIV-1 trans

176 is a ubiquitous human pathogen, which enters productive infection in human epithelial and many other

177 usively showed that MERS-CoV can establish a productive infection in human macrophages.

178 To establish a productive infection in humans, DENV uses different stra

179 and a second element in exon 1 that inhibits productive infection in KH10+ neurons.

180 ve provided clear evidence of papillomavirus productive infection in lymphocytes, placenta, and bovin

181 V-1, these mice showed decreased viremia and productive infection in lymphoid organs and preserved nu

182 Both influenza A-like viruses established a productive infection in MDCK II cells; however, HL18NL11

183 st (CORT-108297) significantly reduced HSV-1 productive infection in mouse neuroblastoma cells (Neuro

184 progeny virus generated an indistinguishable productive infection in naive PHK raft cultures as befor

185 Herpes simplex virus 1 (HSV-1) can undergo a productive infection in nonneuronal and neuronal cells s

186 HSV-2 is capable of developing a productive infection in RPE cells by using nectin-1 as a

187 ults suggest that Ct struggles to generate a productive infection in Sertoli cells, limiting its diss

188 cells containing viral genomes that lead to productive infection in SIV-infected macaques and assess

189 ritic cells (DCs) en route to establishing a productive infection in T lymphocytes but fails to induc

190 ensure subsequent reverse transcription and productive infection in target cells.

191 ilitate subsequent reverse transcription and productive infection in target cells.

192 hment of host-specific viral populations and productive infection in the central nervous system (CNS)

193 roduct in the survival of S. haematobium and productive infection in the host.

194 nically infected partner from establishing a productive infection in the naive host.

195 pithelial cells to establish a predominantly productive infection in the suprabasal layers of stratif

196 olate of HSV-2 was sufficient to establish a productive infection in the vagina of 75% +/- 17% and in

197 lia, results which correlate with restricted productive infection in these neurons in vitro.

198 ted against SARS-CoV-2, further evidencing a productive infection in this animal.

199 ble of transmitting infection and triggering productive infection in tissue.

200 interfere with bICP0 protein expression and productive infection in transient-transfection assays.

201 ed, contrasting with the 45% observed during productive infection in vitro.

202 DNA and was the most efficient in supporting productive infection in vitro.

203 hepatitis B virus (HBV) is essential for HBV productive infection in vivo.

204 were inhibited in their ability to establish productive infections in DC-T-cell cocultures.

205 or understanding how baculoviruses establish productive infections in the organism.IMPORTANCE Baculov

206 be more resistant to doxycycline than normal productive infections in vitro.

207 During productive infections (in the absence of drugs), RLuc wa

208 DENV-2 productive infection induces activation and release of h

209 urons; and this differential distribution of productive infection is determined at or before the expr

210 of Epstein-Barr virus (EBV) from latency to productive infection is infrequent, making its analysis

211 In the course of productive infection, it is localized during the first 5

212 strategy for lifelong persistence, involving productive infection, latency, and intermittent reactiva

213 stically stimulate viral gene expression and productive infection may be critical for the ability of

214 e gene promoters indicated that the block to productive infection occurred before IE gene expression.

215 tted most efficiently from cell to cell, and productive infection occurs mainly in activated CD4 T ce

216 ng the majority of sensory neurons in vitro; productive infection occurs within a subset of these neu

217 Coculture of HIV-exposed MEC resulted in productive infection of activated CD4(+) T cells.

218 lmark of infection by respiratory viruses is productive infection of and the subsequent destruction o

219 we identified IE1 domains that contribute to productive infection of Autographa californica multicaps

220 tectable in BM within 24 h of infection, and productive infection of BM cells was evident, peaking at

221 ed the bICP0 E promoter at late times during productive infection of bovine cells.

222 CD4 T cells are susceptible HIV targets, and productive infection of CCR7(hi) memory T cells did not

223 s of infected pigtailed macaques, suggesting productive infection of CD169(+) cells in vivo Treatment

224 calization of p27(gag) and CD169, suggesting productive infection of CD169(+) myeloid cells in vivo W

225 oplasmic effect of HDAC inhibitors promoting productive infection of CD4(+) T cells that is distinct

226 Endocytosed virus led to productive infection of cells, except when cells were cu

227 rse transcribed into double-stranded DNA for productive infection of cells.

228 For example, the capacity for efficient productive infection of cultured cells by herpes simplex

229 BocaSR genes, HBoV1 NS2 is required for the productive infection of HEK293 and HeLa cells by AAV2, w

230 eratinocytes, we have recapitulated a highly productive infection of HPV-18 in organotypic epithelial

231 IV-associated dementia (HAD) despite lack of productive infection of human brain microvascular endoth

232 Productive infection of iNKT cells was however not requi

233 inants of the macropinocytic entry route and productive infection of KSHV.

234 rapid transfer of Ags to DCs, in contrast to productive infection of LCs, suggests that this might be

235 binostat, romidepsin, and vorinostat) on the productive infection of macrophages.

236 While productive infection of monocyte-derived DCs activated a

237 Productive infection of mucosal leukocytes, predominantl

238 Quantitative analyses revealed preferential, productive infection of neural progenitors with either A

239 At least one VZV sncRNA was expressed in productive infection of neurons and fibroblasts that is

240 The lack of productive infection of neurons by HIV suggests that vir

241 The lack of productive infection of neurons by HIV-1 suggests that t

242 ex virus type 1 (HSV-1) transcriptome during productive infection of primary cells.

243 ) express HIV-1 transcripts, suggesting that productive infection of renal epithelial cells precipita

244 Productive infection of T cells by HIV is dependent upon

245 Because productive infection of T cells with HIV requires T cell

246 rus (SIV) virion-like particles enhanced the productive infection of T(SCM) cells, indicating that SA

247 Importantly, the CCCM HCV transfer leads to productive infection of target cells.

248 at a high dose, only the An/13 virus led to productive infection of the lower respiratory tract of g

249 and dissemination of the disease depends on productive infection of this critical organ.

250 2 target a common set of substrates vital to productive infection of this large cytoplasmic DNA virus

251 Here, we examine the effect on productive infection of triacsin C and YIC-C8-434, which

252 Productive infection of Trichoplusia ni cells by the bac

253 During the productive infection of tumor-associated gammaherpesviru

254 ks retain their cytoarchitecture and support productive infection of various pathogens without exogen

255 We observed low-level productive infection on exposure of these cells to prima

256 virus (PRV) throughout a 12-hour interval of productive infection on PK-15 cells.

257 terventions to inhibit this process to block productive infection or to trigger it in incompletely di

258 Following productive infection, p91 was expressed during the mid-d

259 ment of quiescently infected neurons induced productive infection preferentially from non-A5(+) neuro

260 en viral and host factors that regulates the productive infection process remains poorly understood.

261 zoites target their host cell and facilitate productive infection remains largely unknown.

262 A productive infection requires the virus to penetrate fem

263 The results for productive infection shed further light on the nature of

264 During a productive infection, species C adenovirus reprograms th

265 is prevented, reovirus fails to establish a productive infection, suggesting proteolytic priming is

266 d broadly neutralizing antibody PG9 to block productive infection, suggesting that these drugs may an

267 es of these are the long-term persistence of productive infection, sustained by the absence of cell d

268 high) CD4(+) T cells are more susceptible to productive infection than are alpha(4)beta(7)(low-neg) C

269 However, it appears desirable for productive infection that fusion should proceed before t

270 tion but also reverses latency, resulting in productive infection that generally leads to cell death.

271 cell receptors, dengue virus causes a highly productive infection that has the potential to increase

272 During productive infection, the genes of HSV-1 are transcribed

273 However, during a productive infection, the HS moieties on parent cells ca

274 During productive infection, the viral >230,000-bp dsDNA genome

275 abolic regulatory kinase subunits to support productive infection, thereby providing insight into how

276 al tenofovir can induce SIV immunity without productive infection, this has not been documented in hu

277 c through the endoplasmic reticulum (ER) for productive infection to occur; however, it is unknown ho

278 ection to non-TFH cells, with restriction of productive infection to TFH cells resuming upon CD8(+) T

279 latently infected tissue M s can reestablish productive infection upon treatment interruption.

280 ce loops are responsible for Sf6 binding and productive infection using a combination of in vivo and

281 analyzed in viral binding, transmission, and productive infection using monocyte-derived DCs (MDDCs),

282 e that HHV-8 can target both LC and iDDC for productive infection via different receptors and alter t

283 In productive infection, viral genes must be sequentially d

284 Thus, to establish a productive infection, virions must be stable in the envi

285 To establish productive infections, viruses must counteract numerous

286 The frequency of productive infection was also compared by assessing GFP

287 No productive infection was detected, but endocytosed virus

288 viral variants were present, suggesting that productive infection was initiated by a very small numbe

289 Additionally, virus transfer, fusion, or productive infection was not blocked by dynasore, dynami

290 -1 particles from early entry events through productive infection, we developed a method to visualize

291 ecipients of four HCV-positive donor organs, productive infection with a highly diverse viral populat

292 Productive infection with BV was possible only with nect

293 t cord blood CD34(+) cell precursors support productive infection with HHV-8.

294 s to establishment of systemic, disseminated productive infection with HIV after sexual exposure and

295 ndritic cells (DCs) are largely resistant to productive infection with HIV-1, they have a unique abil

296 Productive infection with HSV was restricted, and only 4

297 HSV-2 but were selectively nonpermissive for productive infection with HSV-1, a phenomenon that was n

298 A5(+) neurons supported productive infection with HSV-2 but were selectively non

299 The Egyptian rousette develops subclinical productive infection with MARV but is refractory to EBOV

300 i virulence determinant that is required for productive infection within vertebrate, but not tick, ho