ライフサイエンスコーパス: cell-to-cell spread

1 nduce actin polymerization leading to direct cell to cell spread.

2 suggest an additional function in epithelial cell-to-cell spread.

3 e viral envelope glycoprotein H in entry and cell-to-cell spread.

4 -free entry/spread, is also required for the cell-to-cell spread.

5 Both motility pathways facilitate cell-to-cell spread.

6 c Ca2+ stores and was impaired for entry and cell-to-cell spread.

7 +) stores and contributes to viral entry and cell-to-cell spread.

8 l-free infectious virus, is not required for cell-to-cell spread.

9 ostentry, reduced plaque size, and prevented cell-to-cell spread.

10 n and an interferon-independent reduction in cell-to-cell spread.

11 mbranes and functions during virus entry and cell-to-cell spread.

12 ering its movement within cells and enabling cell-to-cell spread.

13 signaling, activation, and cell death during cell-to-cell spread.

14 diated actin polymerization to enhance their cell-to-cell spread.

15 phagosomal escape, intracellular growth, and cell-to-cell spread.

16 g antibodies, we show that EGCG inhibits HCV cell-to-cell spread.

17 ), therefore inhibiting entry and subsequent cell-to-cell spread.

18 in some anatomical sites and cell types, and cell-to-cell spread.

19 by two main routes: by cell-free virus or by cell-to-cell spread.

20 ications for the role of UL11 in gE-mediated cell-to-cell spread.

21 mulation of cell-free virus progeny and poor cell-to-cell spread.

22 I form a heterodimer that mediates efficient cell-to-cell spread.

23 us budding, and the gE-mediated mechanism of cell-to-cell spread.

24 ting that the mutation specifically inhibits cell-to-cell spread.

25 s results in increased viral replication and cell-to-cell spread.

26 irions but were defective in virus entry and cell-to-cell spread.

27 ograde and retrograde directional spread and cell-to-cell spread.

28 ating M. marinum escape from the vacuole and cell-to-cell spread.

29 as associated with larger plaques and better cell-to-cell spread.

30 egulating virus replication and facilitating cell-to-cell spread.

31 bacterial movement within the host cell and cell-to-cell spread.

32 raffic to cell junctions and did not mediate cell-to-cell spread.

33 o bacterial escape from vacuoles formed upon cell-to-cell spread.

34 essary, and sufficient, for gE/gI to promote cell-to-cell spread.

35 e host macrophage aggregation and subsequent cell-to-cell spread.

36 promote gE/gI traffic to cell junctions and cell-to-cell spread.

37 d to cell junctions, a process that enhances cell-to-cell spread.

38 rmation, maximal intracellular motility, and cell-to-cell spread.

39 r handle on the poorly understood process of cell-to-cell spread.

40 domain of gE is indispensable for efficient cell-to-cell spread.

41 microtubules, plays an important role in MDV cell-to-cell spread.

42 ficiencies of escape from a phagosome and in cell-to-cell spread.

43 (ET) domains of gE/gI might be important in cell-to-cell spread.

44 bution to bacterial intracellular growth and cell-to-cell spread.

45 modulates Shigella actin-based motility and cell-to-cell spread.

46 a deletion of mogR reduced the capacity for cell-to-cell spread.

47 mal compartments to promote virus egress and cell-to-cell spread.

48 ndary double-membrane vacuoles formed during cell-to-cell spread.

49 tions, gE/gI receptors which can promote HSV cell-to-cell spread.

50 , in the trans-Golgi network, did not reduce cell-to-cell spread.

51 known to bind virus receptors, also blocked cell-to-cell spread.

52 mains of gE/gI also appear to be involved in cell-to-cell spread.

53 al cells but is also necessary for efficient cell-to-cell spread.

54 othesis that US9 plays a direct role in HCMV cell-to-cell spread.

55 f BST2 demonstrated that BST2 restricts HCMV cell-to-cell spread.

56 as less efficient than wild-type Shigella at cell-to-cell spread.

57 ting motifs and are essential for epithelial cell-to-cell spread.

58 through host tissues using a process called cell-to-cell spread.

59 to neutralize HCMV and also to prevent virus cell-to-cell spread.

60 ation of HCMV infection, and attenuate viral cell-to-cell spread.

61 tiation of infection, viral replication, and cell-to-cell spread.

62 ors or gene silencing reduced MDV titers and cell-to-cell spread.

63 lation to resume actin-mediated motility and cell-to-cell spread.

64 aining mouse serum, which did not affect HCV cell-to-cell spread.

65 and SR-BI were found to modestly promote HCV cell-to-cell spread.

66 tal machinery inside nanotubes for efficient cell-to-cell spread.

67 exploitation by pathogens to enhance direct cell-to-cell spread.

68 ize and number, indicating a role for Lpd in cell-to-cell spread.

69 ny released into culture supernatants and in cell-to-cell spread.

70 y members significantly influenced bacterial cell-to-cell spread.

71 virus secretion/spread, is not required for cell-to-cell spread.

72 gE2 blocked gE2-mediated IgG Fc binding and cell-to-cell spread.

73 ired not in intracellular growth rate but in cell-to-cell spreading.

74 SV-1 infection at the entry stage and during cell-to-cell spreading.

75 by Listeria at membrane protrusions used for cell-to-cell spreading.

76 y (mAb hu2c) that completely abrogates viral cell-to-cell spread, a key mechanism by which HSV-1/2 es

77 To examine the role of gG in cell-to-cell spread, a nonsense mutation in the gG signa

78 The ActA- mutant, which is impaired in cell-to-cell spread and attenuated in maternal organs, i

79 the donor cells influence the efficiency of cell-to-cell spread and CD81 transfer between neighborin

80 V-1) is a critical mediator of virus-induced cell-to-cell spread and cell-cell fusion.

81 that DB C404/C439 and T401 are important for cell-to-cell spread and efficient entry of PrV.

82 virus 1 (HSV-1) glycoprotein E (gE) mediates cell-to-cell spread and functions as an IgG Fc receptor

83 (HSV-1) gene, glycoprotein E, which mediates cell-to-cell spread and immune evasion.

84 pes simplex virus 1 plays important roles in cell-to-cell spread and in virus assembly in the cytopla

85 al to seed and establish infection, and that cell-to-cell spread and increased CD4+ T cell activation

86 the trans-Golgi network and are required for cell-to-cell spread and pathogenesis.

87 Extracellular virions are required for cell-to-cell spread and pathogenesis.

88 ore, both viruses were severely defective in cell-to-cell spread and produced fewer DNA-containing ca

89 As such, elucidating the dynamics of cell-to-cell spread and quantifying the effect of blocki

90 ems were permissive for listerial growth and cell-to-cell spread and revealed that L. monocytogenes d

91 l cells and macrophages but caused defective cell-to-cell spread and strong attenuation in mice.

92 e of continuous but inefficient hepadnavirus cell-to-cell spread and superinfection during chronic in

93 bits HSV-2 by a unique mechanism of blocking cell-to-cell spread and support its further development

94 een the virus and the cell and also inhibits cell-to-cell spread and syncytium formation.

95 nuclear egress but also profoundly inhibits cell-to-cell spread and trafficking of gE.

96 ithelial cells and fibroblasts and prevented cell-to-cell spread and viral dissemination from endothe

97 ycoprotein E (gE) of HSV plays a key role in cell-to-cell spread and virus-induced cell fusion.

98 hyphae of the giv2 mutant were defective in cell-to-cell spreading and mainly grew intercellularly i

99 ghly specialized for either for cell-free or cell-to-cell spread, and these phenotypes are determined

100 , displayed reduced abilities to mediate HSV cell-to-cell spread, and W174R and A261D exhibited no sp

101 tants lacking pUS27 rely primarily on direct cell-to-cell spread, and we conclude that the viral GCPR

102 1 or RL13 loci.IMPORTANCE Both cell-free and cell-to-cell spread are likely important for the natural

103 r and efavirenz whereas infections involving cell-to-cell spread are markedly less sensitive to the d

104 -PMO reduced virus-induced cytopathology and cell-to-cell spread as a consequence of decreasing viral

105 s that will further investigate hepadnavirus cell-to-cell spread as a potential regulator of the chro

106 gies for their ability to limit cell-free or cell-to-cell spread as independent processes.

107 cted cells occurred in clusters, pointing to cell-to-cell spread as the predominant mode of HCV trans

108 y can have dramatic impacts on cell-free and cell-to-cell spread as well as on antibody neutralizatio

109 ria with respect to intracellular growth and cell-to-cell spread as well as virulence in mice.

110 Results from intracellular growth and cell-to-cell spread assays showed that the plcBDelta pro

111 type 1 (HSV-1) glycoprotein E (gE) promotes cell-to-cell spread at basolateral surfaces of epithelia

112 During cell-to-cell spread, bacteria become temporarily confine

113 Notably, the model predicts that cell-to-cell spread becomes increasingly effective as in

114 imeric glycoprotein, gE/gI, that facilitates cell-to-cell spread between epithelial cells and neurons

115 E and I (gE and gI), which are critical for cell-to-cell spread between epithelial cells.

116 ntibody, we also showed that FQ inhibits HCV cell-to-cell spread between neighboring cells.

117 t with the peptide inhibited viral entry and cell-to-cell spread both in vitro and in vivo using a mo

118 onsidered absolutely essential for entry and cell-to-cell spread, both in cultured cells and in vivo.

119 mer gE/gI plays a critical role in promoting cell-to-cell spread but does not obviously function duri

120 oprotein E was found to be important for HCV cell-to-cell spread, but very-low-density lipoprotein (V

121 Both initial infection and cell-to-cell spread by herpes simplex virus type 1 (HSV-

122 ion to enhancing T cell activation, promotes cell-to-cell spread by inducing LFA-1 clustering on T ce

123 by the Timd4 gene) contributes to efficient cell-to-cell spread by L. monocytogenes in macrophages i

124 e to type I IFN and leads to 1) promotion of cell-to-cell spread by L. monocytogenes, 2) defective le

125 SV-1) facilitates virus entry into cells and cell-to-cell spread by mediating fusion of the viral env

126 e expected if the virus is limited to direct cell-to-cell spread by neutralization of extracellular v

127 virulence genes associated with invasion and cell-to-cell spread by Shigella flexneri, including mult

128 Direct evidence for cell-to-cell spread by wild-type M. marinum was obtained

129 previously unappreciated impact blocking HCV cell-to-cell spread can have on the efficacy of HCV comb

130 These data indicate that efficient cell-to-cell spread can overcome the decreased infectivi

131 us, had a significant negative impact on the cell-to-cell spread capabilities of the virus, which was

132 We also show that Nef157 inhibits VV cell-to-cell spread, causing formation of atypical plaqu

133 SV was increased by activation of LFA-1, and cell-to-cell spread could be inhibited by antibodies to

134 wild-type virus, both mutants showed slower cell-to-cell spread; decreased yields of infectious viru

135 The cell-to-cell spread defect associated with the pUL51 mut

136 the intracellular Brucella lifecycle and for cell-to-cell spreading, demonstrating that Brucella sele

137 Cell-to-cell spread did not occur in cell cultures, but

138 indings suggest that the mechanism(s) of HCV cell-to-cell spread differs from that of cell-free infec

139 attachment to heparan sulfate or gE-mediated cell-to-cell spread, do not account for the reduced viru

140 toskeleton by using actin-based motility for cell to cell spread during infection.

141 ther bacteria that use similar strategies of cell-to-cell spread during infection.

142 ogenes, can exploit efferocytosis to promote cell-to-cell spread during infection.

143 esulted in a significant defect in bacterial cell-to-cell spread during intracellular infection and a

144 these studies show that UL21 is required for cell-to-cell spread even in the absence of syncytial mut

145 We concluded that cell-to-cell spread facilitates maternal-to-fetal transm

146 tute the first demonstration of VS-dependent cell-to-cell spread for a predominantly nonlymphotropic

147 determined that MDV CHPK is not required for cell-to-cell spread, for disease induction, and for onco

148 of individual accessory proteins will block cell-to-cell spread, forcing the virus to transmit in a

149 and the indirect ActA-mediated infection by cell-to-cell spread from adjacent phagocytic cells.

150 ls occurred much more efficiently via direct cell-to-cell spread from infected fibroblasts than by ce

151 ere was a strong correlation between loss of cell-to-cell spread function and binding of immunoglobul

152 uncoupling of the replication, release, and cell-to-cell spread functions of HSV-1 pUL51 in two ways

153 If cell-to-cell spread has the same properties in vivo, it

154 The underlying mechanisms of cell-to-cell spread, however, remain to be fully elucida

155 distinct roles for gH/gL/gO in cell-free and cell-to-cell spread, (ii) gO isoforms can differentially

156 is and cholesterol trafficking to facilitate cell-to-cell spread in a LAMP-1-dependent mechanism.IMPO

157 viral genes, UL51, has an important role in cell-to-cell spread in addition to its previously demons

158 could localize to cell junctions and mediate cell-to-cell spread in ARPE-19 retinal epithelial cells.

159 resulted in increased syncytia and enhanced cell-to-cell spread in cells infected with wild-type HSV

160 dimer gE/gI plays an important role in virus cell-to-cell spread in epithelial and neuronal tissues.

161 ased yields of cell-free virus and increased cell-to-cell spread in fibroblasts but reduced the abund

162 ted virulence in mice and impaired bacterial cell-to-cell spread in host cells.

163 ditional requirement for LLO in facilitating cell-to-cell spread in L2 fibroblasts, a nonprofessional

164 replication and spread in MDDCs alone and in cell-to-cell spread in MDDC-CD4(+) T cell cocultures.

165 e MeV fusion complex that promote fusion and cell-to-cell spread in the absence of known MeV receptor

166 sceptible hosts, the virus is transmitted by cell-to-cell spread in the body and in vitro.

167 la spp. and facilitating cellular egress and cell-to-cell spread in the case of Brucella spp.

168 We examine replication from cell-to-cell spread in the presence of clinical drug con

169 understand and quantify the dynamics of HCV cell-to-cell spread in vitro and determined the degree t

170 individuals, we examined the dynamics of HCV cell-to-cell spread in vitro and quantified the effect o

171 in orally infected mice and were impaired in cell-to-cell spread in vitro.

172 levels of proteins required for invasion and cell-to-cell spread, including Ipa, Mxi, and Ics protein

173 ; little is known about how it transits from cell to cell, spreading infection.

174 One mechanism by which gE/gI facilitates cell-to-cell spread involves selective sorting of nascen

175 h TRDeltagO particles could not enter cells, cell-to-cell spread involving epithelial and endothelial

176 Cell-to-cell spread is a conserved ability of herpesviru

177 Cell-to-cell spread is a conserved property of herpesvir

178 understanding the mechanisms and kinetics of cell-to-cell spread is fundamental to elucidating the dy

179 , our results indicate that L. monocytogenes cell-to-cell spread is heterogeneous, and that rare pion

180 rast, viral spread assays indicated that HCV cell-to-cell spread is less dependent on TfR1.

181 s cell-to-cell transmission is the idea that cell-to-cell spread is more than the sum of the processe

182 nt at cell-to-cell spread, whereas TB and TR cell-to-cell spread is poor.

183 cell junctions, but the mechanism of direct cell-to-cell spread is poorly understood.

184 in vitro and determined the degree to which cell-to-cell spread is reduced when individual HCV entry

185 s virus, (i) hepadnavirus superinfection and cell-to-cell spread likely continue to occur and (ii) th

186 Because direct cell-to-cell spread likely contributes importantly to pa

187 While L. monocytogenes virulence hinges on cell-to-cell spread, little is known about the dynamics

188 ns that produce Syn variants dysregulate the cell-to-cell-spread machinery in unique ways and provide

189 A better understanding of the mechanism of cell-to-cell spread may enable the development of drugs

190 t infectivity, suggesting that the efficient cell-to-cell spread mechanism of ME depends on features

191 This cell-to-cell spread mechanism requires the viral fusion

192 only modestly reduced, further supporting a cell-to-cell spread mechanism.

193 Here, two divergent cell-to-cell spread mechanisms are exemplified: firstly

194 or are indicative of particularly efficient cell-to-cell spread mechanisms.

195 alteration in the viral cycle, which reduces cell-to cell spread of HSV-1.

196 ession comparably reduced both cell-free and cell-to-cell spread of all three strains, suggesting tha

197 ll conclude by comparing and contrasting the cell-to-cell spread of animal and plant viruses.

198 GBPs inhibit actin-dependent motility and cell-to-cell spread of bacteria but are antagonized by I

199 ation of Listeria protrusions and subsequent cell-to-cell spread of bacteria.

200 Here we present evidence that cell-to-cell spread of BDV required neither the expressi

201 The findings reported here (i) confirm that cell-to-cell spread of CMV is sensitive to antibody inhi

202 The cell-to-cell spread of cytoplasmic constituents such as

203 that during chronic hepadnaviral infection, cell-to-cell spread of hepadnavirus is at least very ine

204 Both entry and cell-to-cell spread of herpes simplex virus (HSV) involv

205 helper type 17, that have been implicated in cell-to-cell spread of HIV and enhanced restoration of C

206 We then examine the drug sensitivity of cell-to-cell spread of HIV, a mode of HIV transmission t

207 release, viral entry, plaque formation, and cell-to-cell spread of HSV-1 and HSV-2 in human cervical

208 the US9 gene, which plays a critical role in cell-to-cell spread of HSV-1 in neurons.

209 The participation of MAL in the cell-to-cell spread of HSV-1 may shed light on the invol

210 V-1 to A5-positive neurons,(ii) differential cell-to-cell spread of HSV-1 to A5-positive neurons, (ii

211 quent studies indicated that Spm8CHAS blocks cell-to-cell spread of HSV.

212 However, the mechanism of cell-to-cell spread of HTLV-I is not understood.

213 The mechanisms that control cell-to-cell spread of human adenoviruses (Ad) are not w

214 cid and indomethacin, markedly reduce direct cell-to-cell spread of human cytomegalovirus in cultured

215 Direct cell-to-cell spread of human immunodeficiency virus type

216 Furthermore, the efficiency of cell-to-cell spread of iLLO bacteria in L2 cells was IPT

217 ynthesis and release of infectious HSV-1 and cell-to-cell spread of infection were all impaired in ch

218 al migration efficiency, leading to impaired cell-to-cell spread of infection.

219 Cholesterol was also critical for cell-to-cell spread of infection.

220 for Lpd in the actin-based movement and the cell-to-cell spread of L. monocytogenes.

221 n network that is critically involved in the cell-to-cell spread of L. monocytogenes.

222 a1, mDia2, and mDia3 substantially decreased cell-to-cell spread of L. monocytogenes.

223 question about the mechanism involved in the cell-to-cell spread of MDV.

224 n UL128-131 was transcriptionally repressed, cell-to-cell spread of ME was still more efficient than

225 Thereafter, lateral cell-to-cell spread of MV led to the formation of large

226 This cell-to-cell spread of NMDA-induced oxidative injury was

227 The critical role of NSP1 in promoting cell-to-cell spread of rotavirus was demonstrated by usi

228 on the bacterial surface and contributes to cell-to-cell spread of S. flexneri in cell culture.

229 is, is involved in the uptake, motility, and cell-to-cell spread of Shigella organisms within the hum

230 the protein product of which is required for cell-to-cell spread of the bacterium, is expressed at lo

231 Yields of progeny virus and cell-to-cell spread of the DeltaM25 mutant in vitro were

232 could promote syncytium formation and direct cell-to-cell spread of the infection.

233 ng toxin that mediates phagosomal escape and cell-to-cell spread of the intracellular pathogen Lister

234 Under passage conditions where cell-to-cell spread of the virus is required to complete

235 N-WASP to generate actin tails that promote cell-to-cell spread of the virus.

236 cate that gB is required for virus entry and cell-to-cell spread of the virus.

237 zyme (IDE) and facilitates VZV infection and cell-to-cell spread of the virus.

238 This is associated with slower cell-to-cell spread of the virus.

239 eutralizing antibody, cell-virus fusion, and cell-to-cell spread of the virus.

240 articles most likely are responsible for the cell-to-cell spread of the virus.

241 e factors required for cellular invasion and cell-to-cell spread of this pathogen.

242 e, CaLCuV systemic infection is delayed, and cell-to-cell spread of TMV and CaLCuV movement proteins

243 e p30 movement protein (MP) is essential for cell-to-cell spread of tobacco mosaic virus in planta.

244 Efficient cell-to-cell spread of vaccinia virus and other orthopox

245 r multiple retrograde pathway components for cell-to-cell spread of vaccinia virus.

246 A36-driven super-repulsion in promoting the cell-to-cell spread of vaccinia.

247 Their loss, however, reduces the cell-to-cell spread of vaccinia.

248 The gE-gI heterodimer has been implicated in cell-to-cell spread of virus and is a receptor for the F

249 In the absence of inducer, cell-to-cell spread of virus did not occur, despite the

250 e integrity of HA protein trimers, inhibited cell-to-cell spread of virus in culture, and protected m

251 Cell-to-cell spread of virus was also impaired by blocki

252 Silymarin also blocked cell-to-cell spread of virus.

253 not due to a host response activated by the cell-to-cell spread of virus.

254 concentrations of anti-HSV IgG also enhance cell-to-cell spread of wild-type HSV-1 but not of gE del

255 logical synapses, which facilitate efficient cell-to-cell spreading of HIV-1.

256 Cell-to-cell spreading of misfolded alpha-synuclein (alp

257 fied MBs enabled real-time monitoring of the cell-to-cell spreading of viral infection.

258 ssive waves of intracellular replication and cell-to-cell spread, parasites drain via local lymphatic

259 ns in E1 and E2 responsible for the enhanced cell-to-cell spread phenotype of clone 2 rendered cell-f

260 there was no correlation between defects in cell-to-cell spread (plaque size) and loss of expression

261 odeling to demonstrate that L. monocytogenes cell-to-cell spread proceeds anisotropically in an epith

262 this study advances our understanding of HCV cell-to-cell spread, provides mechanistic insight into t

263 ostattachment receptors in HCV infection and cell-to-cell spread remains controversial.

264 nhibited bacterial escape from a vacuole and cell-to-cell spread, resulting in greatly reduced virule

265 ial for viral replication and is involved in cell-to-cell spread, secondary envelopment, and entry.

266 Noting that HCV cell-free and cell-to-cell spread share some common factors but not ot

267 and thereby enable the process of bacterial cell-to-cell spread so critical for L. monocytogenes vir

268 se cell lysis and was dependent on bacterial cell-to-cell spread, suggesting that damage was localize

269 ion in vivo, the limitations of hepadnavirus cell-to-cell spread/superinfection (observed recently in

270 and G genes from SB exhibited more efficient cell-to-cell spread than a chimeric SN virus in which on

271 eminate through host tissues by a process of cell-to-cell spread that involves protrusion formation,

272 ediated endocytosis pathway and a subsequent cell-to-cell spread that is independent of the expressio

273 ially infect an adjacent cell to mediate the cell-to-cell spread that is observed.

274 or invasion, vacuolar escape, and subsequent cell-to-cell spread, the L. monocytogenes factors requir

275 sertions in the gG locus result in decreased cell-to-cell spread, the phenotype was not due to loss o

276 template-dependent reiterated short-distance cell-to-cell spread through the cells of the central ste

277 egions of Ena/VASP enhanced L. monocytogenes cell-to-cell spread to a similar degree, although the En

278 orts suggesting that some factors impact HCV cell-to-cell spread to different extents, modeling resul

279 Cell-to-cell spread to T cells did not require HSV glyco

280 V genome, clone 2, characterized by superior cell-to cell spread, to its parental genome, J6/JFH-1, w

281 ein E (apoE) is critically important for HCV cell-to-cell spread, unlike VLDL-containing mouse serum,

282 dvances in our understanding of animal virus cell-to-cell spread using examples from these two virus

283 ed that survival within phagocytic cells and cell-to-cell spread via actin protrusions is required fo

284 trafficking of B. mallei and may facilitate cell-to-cell spread via actin-based motility.

285 transport their cargos to plasmodesmata for cell-to-cell spread via an endocytic recycling pathway.

286 rs are components of transport complexes for cell-to-cell spread via plasmodesmata and systemic movem

287 issues than RSV, suggesting HMPV may promote cell-to-cell spread via these extensions.

288 t although HCV can lose SR-BI dependence for cell-to-cell spread, vulnerability to neutralizing antib

289 The reduced cell-to-cell spread was due to ICP27 since plaque sizes

290 Cell-to-cell spread was reduced when insertions were mad

291 in involved in intracellular trafficking and cell-to-cell spread, we constructed a panel of truncatio

292 e a hierarchy of efficacies for blocking HCV cell-to-cell spread when targeting different host factor

293 free spread but is particularly efficient at cell-to-cell spread, whereas TB and TR cell-to-cell spre

294 HCV is also thought to propagate via cell-to-cell spread, which allows highly efficient virio

295 Because repression of A28 inhibited cell-to-cell spread, which is mediated by extracellular

296 ous center assays indicated similar rates of cell-to-cell spread, which was approximately 1,000-fold

297 factor NPC1L1 as also being required for HCV cell-to-cell spread, while showing that the VLDL pathway

298 An understanding of viral cell-to-cell spreading will enhance our ability to inter

299 MPORTANCE The HSV-1 gI is required for viral cell-to-cell spread within the host, but the molecular m

300 Quasi-enveloped HAV (eHAV) mediates stealthy cell-to-cell spread within the liver, whereas stable nak