ライフサイエンスコーパス: cell-to-cell spread

1 from an infected cell to an uninfected cell (cell-to-cell spread).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 ain of L. monocytogenes that is incapable of cell-to-cell spread.

46 ry, survival, intracellular replication, and cell-to-cell spread.

47 indicative of decreased virus replication or cell-to-cell spread.

48 the double-membrane vacuole that forms upon cell-to-cell spread.

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

50 not affect accumulation at cell junctions or cell-to-cell spread.

51 ement, formation of cellular protrusions and cell-to-cell spread.

52 ntributes to lysis of host cell vacuoles and cell-to-cell spread.

53 red for intracellular bacterial motility and cell-to-cell spread.

54 erpesvirus genomes participate in egress and cell-to-cell spread.

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

56 the A33R protein is necessary for efficient cell-to-cell spread.

57 bably because gE and gI are also involved in cell-to-cell spread.

58 phage cell line, and in a plaquing assay for cell-to-cell spread.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 The mutant virus is inefficient at cell-to-cell spread and does not produce or release enve

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

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

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

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

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

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

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

92 Normal cell-to-cell spread and replication kinetics were restor

93 Normal cell-to-cell spread and replication kinetics were restor

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

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

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

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

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

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

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

101 seudorabies virus are important mediators of cell-to-cell spread and virulence in all animal models t

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

103 rocesses appear to have an important role in cell-to-cell spread, and MVeGFP was observed to utilize

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 gE and gI (gE/gI) is required for efficient cell-to-cell spread, especially between cells that form

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

147 owever, its role in intracellular growth and cell-to-cell spread events has not been testable by a ge

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

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

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

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

152 y direct invasion of endothelial cells or by cell-to-cell spread from infected phagocytes to endothel

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

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

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

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

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 nd neuronal tissues and also show defects in cell-to-cell spread in HaCaT cells, but not in other, no

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

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

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

166 blasts but were impaired in the capacity for cell-to-cell spread in polarized human retinal pigment e

167 ion of GCCM cells and to subsequently follow cell-to-cell spread in real time.

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

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

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

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

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

173 produced large plaques, indicating efficient cell-to-cell spread in vitro, and gradient centrifugatio

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

175 Heterogeneity was seen in cell-to-cell spread in what was expected to be a homogen

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

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

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

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

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

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

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

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

184 Bacterial cell-to-cell spread is mediated in part by two secreted

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

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

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

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

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

190 of lucifer yellow via gap junctions, whereas cell-to-cell spread of [Ca2+]i signals could be induced

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 f tobacco mosaic virus (TMV) facilitates the cell-to-cell spread of infection by altering the structu

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

211 MV) plays a critical role in virus entry and cell-to-cell spread of infection.

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

213 Additionally, cell-to-cell spread of L. monocytogenes throughout the m

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

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

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

217 Finally, isoproterenol increased cell-to-cell spread of lucifer yellow via gap junctions,

218 lacking a virulence determinant involved in cell-to-cell spread of M. tuberculosis.

219 ssion of monocyte aggregation and diminished cell-to-cell spread of M. tuberculosis.

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

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

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

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

224 hin epithelial protrusions, in turn allowing cell-to-cell spread of S. flexneri.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 Cell-to-cell spread of tobacco mosaic virus (TMV) throug

240 Virus-encoded movement protein (MP) mediates cell-to-cell spread of tobacco mosaic virus (TMV) throug

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

242 Cell-to-cell spread of tobacco mosaic virus is facilitat

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

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

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

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

247 required for envelopment, translocation, and cell-to-cell spread of virions.

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

251 -fold compared to the rescued isolate, (iii) cell-to-cell spread of virus was not detected within gan

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 r a sufficient time to allow replication and cell-to-cell spread prior to eventual death due to necro

262 mutant, PRV157, failed to express gG yet had cell-to-cell spread properties indistinguishable from th

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

264 ovilli and for a role of these structures in cell-to-cell spread rather than in formation of extracel

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

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

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

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

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

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

271 cells are also highly resistant to entry by cell-to-cell spread, suggesting that the same cellular f

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

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

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

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

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

277 In assays for cell-to-cell spread, the H56Y and D4E mutants had close

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

293 MVeGFP infected the cells, and cell-to-cell spread was studied by virtue of the resulti

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

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

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

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

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

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

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