ライフサイエンスコーパス: productive infection

1 nsmitted/founder HIV genomes responsible for productive infection.

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

3 ly regulated and sequentially ordered during productive infection.

4 cell countermeasures in order to establish a productive infection.

5 human oral epithelial cells without causing productive infection.

6 iciently enter into hepatocytes to establish productive infection.

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

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

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

10 advantage of endocytic pathways to establish productive infection.

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

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

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

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

15 fuse with endosomal membranes to initiate a productive infection.

16 vantage of caveolar endocytosis to establish productive infection.

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

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

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

20 of viral transcription that is required for productive infection.

21 thelial system by which Listeria establishes productive infection.

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

23 two populations are cellular reservoirs for productive infection.

24 the bICP0 early promoter and stimulation of productive infection.

25 ere assessed for relative permissiveness for productive infection.

26 crophage populations in lesion formation and productive infection.

27 machinery to initiate and maintain a highly productive infection.

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

29 UL21a is required to establish an efficient productive infection.

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

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

32 r stabilizing a DNA hairpin structure during productive infection.

33 ion partners among other HCV proteins during productive infection.

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

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

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

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

38 tudies have also concluded that LAT inhibits productive infection.

39 number assay did not demonstrate evidence of productive infection.

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

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

42 activation cycle by inhibiting apoptosis and productive infection.

43 8 locus with early-late gene kinetics during productive infection.

44 is required for HCMV to establish efficient productive infection.

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

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

47 ucial for activating viral transcription and productive infection.

48 -1 to autologous CD4(+) T cells resulting in productive infection.

49 responses in order to help them establish a productive infection.

50 ed for expression of most HSV-1 genes during productive infection.

51 immortalized B cells but fails to establish productive infection.

52 lper virus, such as adenovirus, to achieve a productive infection.

53 respect to disarming the IFN response during productive infection.

54 APC, which underscores its importance for a productive infection.

55 requires activated CCR5(+) CD4(+) cells for productive infection.

56 generated uninfected cells are refractory to productive infection.

57 pathogens, and helps to set a threshold for productive infection.

58 the cell in order to establish an efficient, productive infection.

59 phagocytic or direct fusion), entry leads to productive infection.

60 lates all viral promoters and, consequently, productive infection.

61 allow immune evasion and establishment of a productive infection.

62 sponse is critical to the establishment of a productive infection.

63 d they stimulate certain viral promoters and productive infection.

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

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

66 gamma irradiated the cells to prevent their productive infection.

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

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

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

70 ly binding gangliosides are not required for productive infection.

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

72 r the transition from latency to reactivated productive infection.

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

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

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

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

77 of specific replicative steps, they promote productive infection.

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

79 and infects underlying immune cells during a productive infection.

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

81 sal autophagy levels mostly unchanged during productive infection.

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

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

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

85 host cellular defence proteins that inhibit productive infection.

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

87 is substantially reduced relative to that in productive infection.

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

89 anced, the ability of parasites to establish productive infections.

90 cted cell could produce approximately 22 new productive infections.

91 modulate host immune defenses and establish productive infections.

92 ment proteins that enable gene expression in productive infection?

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

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

95 During productive infection, a virus must simultaneously redire

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

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

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

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

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

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

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

103 ns and neuropilin-1 and results in long-term productive infection and interleukin-2-independent trans

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

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

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

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

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

112 blood DCs in HIV-1 pathogenesis: to support productive infection and to evade the direct induction o

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

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

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

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

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

118 lack of expression of genes associated with productive infection, and that this occurs through chang

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

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

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

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

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

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

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

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

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

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

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

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

131 type dendritic cells (LC) are susceptible to productive infection by human CMV (HCMV).

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

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

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

135 Because productive infection by parvoviruses requires cell divis

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

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

138 t ex vivo-cultured tonsillar tissue supports productive infection by the New York City Board of Healt

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

140 Productive infections by human papillomaviruses (HPVs) a

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

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

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

144 ing passage from Langerhans cells, and overt productive infection ensued.

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

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

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

148 Productive infections have been achieved recently with g

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

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

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

152 To establish a productive infection, human immunodeficiency virus type

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

154 tors that restrict a virus from establishing productive infection in a new host species are important

155 on enzymes may explain why AAV is capable of productive infection in a wide variety of species with s

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

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

158 34.5 expression is capable of establishing a productive infection in at least one normal mouse brain

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

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

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

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

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

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

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

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

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

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

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

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

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

172 There was no evidence of productive infection in recipient baboons for up to 6 mo

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

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

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

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

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

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

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

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

181 somewhat surprisingly, C1q was required for productive infection in the spleen but not for developme

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

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

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

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

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

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

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

189 o examine how these properties contribute to productive infection in vivo, rhesus macaques were inocu

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

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

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

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

194 ) infected cell protein 0 (bICP0) stimulates productive infection, in part by activating viral gene e

195 wing for detailed study of the mechanisms of productive infection, including attachment and entry, in

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

197 In the context of productive infection, IRF3 and IRF7 are detected in the

198 by at least two distinct mechanisms and that productive infection is dependent upon the activation of

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

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

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

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

203 accessory V protein also establishes highly productive infections like wild-type (WT) SV5 but that c

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

205 administration of antibodies to RSV prevents productive infection normally accompanied by viral relea

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

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

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

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

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

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

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

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

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

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

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

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

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

219 R demonstrated viral replication and hence a productive infection of CF by HSV-1.

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

221 s retroviral Envelope (FeLV Env) protein for productive infection of feline AH927 cells.

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

223 patitis B virus X (HBX) is essential for the productive infection of hepatitis B virus (HBV) in vivo

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

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

226 1), this inhibition is insufficient to block productive infection of human cells.

227 the yield of infectious virions during KSHV productive infection of HUVEC.

228 Productive infection of iNKT cells was however not requi

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

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

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

232 Productive infection of mucosal leukocytes, predominantl

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

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

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

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

237 he central nervous system resulting from the productive infection of oligodendrocytes by the opportun

238 Productive infection of oligodendrocytes, which are resp

239 Productive infection of PERV or PLHV-1 could not be demo

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

241 Productive infection of rLCMV-LASVGP was only mildly aff

242 Productive infection of T cells by HIV is dependent upon

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

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

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

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

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

248 2 target a common set of substrates vital to productive infection of this large cytoplasmic DNA virus

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

250 Productive infection of Trichoplusia ni cells by the bac

251 During the productive infection of tumor-associated gammaherpesviru

252 Productive infection of varicella-zoster virus (VZV) in

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

254 63(+) vesicles (exosomes) and could initiate productive infections of CD4(+) target cells.

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 t this massive viral transfer contributes to productive infection or viral dissemination through the

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 Activated cells facilitate productive infections; quiescent cells enable the virus

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

263 A productive infection requires the virus to penetrate fem

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

265 During a productive infection, species C adenovirus reprograms th

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

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

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

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

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

271 the peaks and durations of a single round of productive infection that reflect envelope-specific diff

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

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

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

278 m is transcriptionally active and results in productive infection, unintegrated DNA is also capable o

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

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

281 disruption, and concomitantly they initiate productive infection very inefficiently.

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 lated into WHV-susceptible woodchucks, and a productive infection was demonstrated.

288 No productive infection was detected, but endocytosed virus

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

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

291 -1 particles from early entry events through productive infection, we developed a method to visualize

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