ライフサイエンスコーパス: VSV

1 VSV infection induced increased production of IFN-beta i

2 VSV tumor tropism is generally dependent on the permissi

3 VSV-p53wt and VSV-p53-CC encode a VSV matrix protein (M)

4 VSV-vectored influenza vaccines that express chimeric he

5 VSVs that include the VSV glycoprotein (G) gene, even in

6 ne (G) with the spike protein of SARS-CoV-2 (VSV-eGFP-SARS-CoV-2) and developed a high-throughput-ima

7 iratory syndrome coronavirus 2 (SARS-CoV-2) (VSV-SARS-CoV-2) elicited by Apilimod and Vacuolin-1, sma

8 VSV-p53wt and VSV-p53-CC encode a VSV matrix protein (M) with a DeltaM51 mutation (M-Delta

9 artite motif (TRIM) family of proteins, is a VSV(IND) inhibitor.

10 After VSV infection, HIPK2 was cleaved by active caspases, whi

11 Although VSV is effective against a majority of pancreatic ductal

12 Although VSV is effective against most PDAC cells, some are highl

13 ce were more susceptible to lethal HSV-1 and VSV infection, with decreased type I IFNs.

14 nerated a set of chimeras composed of gB and VSV-G or gp64, respectively.

15 the late endosome (recombinant VSV-Lassa and VSV-Junin), including an SFV point mutant with a lower p

16 Conversely, cell-free MLV and VSV virion yields and VSV spread to distal cells were dr

17 VSV-p53wt and VSV-p53-CC encode a VSV matrix protein (M) with a DeltaM

18 viruses, both SUIT-2-passaged VSV-p53wt and VSV-p53-CC showed improved replication in SUIT-2 and AsP

19 ed oncolytic VSV recombinants, VSV-p53wt and VSV-p53-CC, we generated novel oncolytic VSVs with an im

20 he cell cycle affects replication of VSV and VSV-DeltaM51.

21 ely, cell-free MLV and VSV virion yields and VSV spread to distal cells were dramatically reduced by

22 ncoding patient-derived Vif, human APOBEC3G, VSV-G, and a vif/env-deficient luciferase-reporter HIV-1

23 n, and survivability of intranasally applied VSV depends on both innate and adaptive immune mechanism

24 However, as VSV attachment to PDAC cells has never been tested befor

25 d negative-strand (NNS) RNA viruses, such as VSV, possess a fully methylated cap structure, which is

26 ular stomatitis virus (VSV), newly assembled VSV particles are released from the surface of infected

27 revious study in which we used an attenuated VSV-EBOV with no MLD that expressed green fluorescent pr

28 we generated rVSVs (wild-type and attenuated VSV with mutated matrix protein [VSVm] versions) that ex

29 We therefore generated a highly attenuated VSV that expresses MHBs and contains two attenuating mut

30 subsequent immunization with the attenuated VSV induced MHBs-specific CD8(+) T cell responses that c

31 Blocking REV-ERBalpha activity before VSV administration resulted in a significant increase in

32 apparent destruction of most tumor cells by VSV-EBOVDeltaMLD, the virus remained active within the S

33 if the building blocks - here exemplified by VSV M- and N-protein - are structurally closely related.

34 A chimeric VSV expressing the full-length EBOV GP (VSV-EBOV) contai

35 Using a recombinant chimeric VSV/SARS-CoV-2 reporter virus, we show that functional S

36 hat unlike neutralization-sensitive chimeric VSV, authentic filoviruses are highly resistant to neutr

37 Here, we compared chimeric VSVs in which EBOV GP replaces the VSV glycoprotein, the

38 These results suggest that while chimeric VSVs show promise, each must be tested with both intrana

39 Moreover, combining VSV with polycations and ruxolitinib (which inhibits ant

40 Moreover, combining VSV with ruxolitinib and Polybrene or DEAE-dextran succe

41 Additionally, replication-competent VSV-eGFP-SARS-CoV-2 provides a tool for testing inhibito

42 us (VSV), as well as a replication-competent VSV/SARS-CoV-2 chimeric virus.

43 Here, using complementary VSV and RABV systems, we show that the loop governs RNA

44 trate long-term genomic stability of complex VSV recombinants carrying large transgenes and support f

45 ating long-term genomic stability of complex VSV recombinants carrying large transgenes.IMPORTANCE Ve

46 In conclusion, VSV-EBOV remains a potent and fast-acting prophylactic v

47 In contrast, VSV-EBOV containing the MLD showed substantially better

48 In contrast, VSV-EBOV eliminated the tumors and showed relatively lit

49 d, more than one-third of subjects developed VSV-specific cytotoxic T-lymphocyte responses and antibo

50 g the envelope proteins of Zaire ebolavirus (VSV-ZEBOV) or severe acute respiratory syndrome coronavi

51 on of NRP2 or its N-terminal domain enhances VSV-LUJV infection, and cells lacking NRP2 are deficient

52 Two independently evolved VSVs obtained 2 identical VSV glycoprotein mutations, K1

53 We show that a three-stage model fits VSV single-particle fusion kinetics: (i) reversible, pH-

54 responses to internal VSV proteins following VSV-EBOV immunization.

55 e the circadian effect on survival following VSV infection.

56 chimeric viruses containing genes coding for VSV, together with a gene coding for the glycoprotein fr

57 Ebola virus and influenza virus, modest for VSV, and mild for measles virus, suggesting a greater ro

58 sruption of the viral machinery required for VSV(IND) RNA synthesis.IMPORTANCE Interferons are import

59 y distinct and phylogenetically distant from VSV.

60 Passive transfer of sera from VSV-eGFP-SARS-CoV-2-immunized animals also protects naiv

61 g vesicular stomatitis virus glycoprotein G (VSV-G) or baculovirus gp64.

62 h vesicular stomatitis virus glycoprotein G (VSV-G).

63 X4-tropic and vesicular stomatitis virus G (VSV-G)-pseudotyped viruses.

64 that syncytium formation of the fusogenic gB/VSV-G chimera can be significantly inhibited by only a s

65 ne in place of the native glycoprotein gene (VSV-eGFP-SARS-CoV-2).

66 t expressed green fluorescent protein (GFP) (VSV-EBOVDeltaMLD-GFP), VSV-EBOVDeltaMLD without GFP targ

67 escent protein (GFP) (VSV-EBOVDeltaMLD-GFP), VSV-EBOVDeltaMLD without GFP targeted glioma but yielded

68 itis virus expressing the EBOV glycoprotein (VSV-EBOV), a live-attenuated vector with marked preclini

69 e vesicular stomatitis virus G glycoprotein (VSV-G) efficiently, it could not pseudotype the full-len

70 ycoprotein (RABV-G) or its own glycoprotein (VSV-G), we created viruses that can transsynaptically la

71 Vesicular stomatitis virus glycoprotein (VSV-G)-pseudotyped viruses were generated by cotransfect

72 urprisingly, two identical VSV glycoprotein (VSV-G) mutations, K174E and E238K, were identified in bo

73 eric VSV expressing the full-length EBOV GP (VSV-EBOV) containing the MLD was substantially more effe

74 icular stomatitis virus expressing MACV GPC (VSV-MACV) as well as against authentic MACV.

75 ng anisotropy of approximately 3.7% with VSH>VSV.

76 on plaque-forming units (PFU) and homologous VSV-Ebola vaccine boost in healthy adult volunteers.

77 However, VSV attachment to HPAF-II cells was dramatically improve

78 However, VSV has some undesirable pathogenic properties, and the

79 ependently evolved VSVs obtained 2 identical VSV glycoprotein mutations, K174E and E238K.

80 Surprisingly, two identical VSV glycoprotein (VSV-G) mutations, K174E and E238K, wer

81 Here we examined if VSV attachment to cells was inhibited in resistant PDAC

82 Importantly, VSV-gp160G effectively exerted potent oncolytic activity

83 d LDLR expression levels but did not improve VSV attachment or LDL uptake in HPAF-II cells.

84 ted that these acquired G mutations improved VSV replication, at least in part due to improved virus

85 cated that the acquired G mutations improved VSV replication, at least in part due to improved virus

86 -II cells to VSV by simultaneously improving VSV attachment and replication.

87 -II cells to VSV by simultaneously improving VSV attachment and replication.IMPORTANCE Oncolytic viru

88 sed cell surface molecules playing a role in VSV attachment to host cells.

89 diminished IFNbeta expression and increased VSV replication.

90 as vesicular stomatitis virus (VSV) Indiana (VSV(IND)), is a model virus that is exceptionally sensit

91 tegy in West Africa, recombinant, infectious VSV encoding the Ebola virus glycoprotein effectively pr

92 TRIM69 potently inhibited VSV(IND) replication through a previously undescribed tr

93 sis of adaptive immune responses to internal VSV proteins following VSV-EBOV immunization.

94 Lassa-VSV was particularly effective, showed no adverse side e

95 ficient mice were more susceptible to lethal VSV disease than were wild-type mice.

96 of nonsegmented negative-strand viruses like VSV are assembled in the cytoplasm during genome RNA rep

97 e I interferon (IFN) response that can limit VSV spread at both the inoculation site and among synapt

98 l construct with an EBOV GP lacking the MLD (VSV-EBOVDeltaMLD).

99 In a murine VSV infection model, commensal-induced IFN-beta regulate

100 ious SIV vaccine trials, the present DNA-MVA-VSV-Ad5-RRV-DNA regimen resulted in comparable levels of

101 the polymerases of Mononegavirales, namely, VSV, RABV, HRSV, human metapneumovirus (HMPV), and human

102 ns gB, gD, gH, and gL but lacking the native VSV fusogen G.

103 Neither VSV-EBOV nor VSV-EBOVDeltaMLD showed substantive infecti

104 eta (IFNbeta)-sodium iodide symporter (NIS) (VSV-mIFNbeta-NIS) oncolytic virus has significant antile

105 Neither VSV-EBOV nor VSV-EBOVDeltaMLD showed substantive infection of the bra

106 transsynaptic tracer, or naturally occurring VSV-derived defective interfering particles (DIPs), into

107 The ability of VSV to induce a robust multispecific T cell response tha

108 However, LDLR-independent attachment of VSV to HPAF-II cells was dramatically improved by treati

109 ata show a dramatically weaker attachment of VSV to HPAF-II cells, the most resistant human PDAC cell

110 Our data show very inefficient attachment of VSV to the most resistant human PDAC cell line, HPAF-II.

111 These data support development of VSV-SARS-CoV-2 as an attenuated, replication-competent v

112 We treated groups of animals with 1 dose of VSV-EBOV either in a single injection at 1 or 24 hours a

113 We modified a safe form of VSV to express an immunogenic HBV protein and evaluated

114 into the existing structural information of VSV L.IMPORTANCE This study represents the first functio

115 Neonatal intravascular injection of VSV-G pseudotyped lentivirus resulted in almost exclusiv

116 The greatest limitation of VSV is that it is highly neurotropic and can be lethal w

117 virus (VSV), we show that microinjection of VSV particles leads to a dose-dependent, muscle tissue-t

118 crotubules were responsible for migration of VSV nucleocapsids to the plasma membrane for virus assem

119 We find that oligomerization of VSV P is not required for any step of viral mRNA synthes

120 infection on the progression and outcome of VSV-induced encephalitis and demonstrated a significant

121 racterized defective interfering particle of VSV (DI-T) that is only competent for RNA replication re

122 In this study, we analyzed the potential of VSV-EBOV for postexposure treatment of rhesus macaques i

123 A single-dose regimen of VSV-EBOV revealed a safe and immunogenic profile and dem

124 ed how the cell cycle affects replication of VSV and VSV-DeltaM51.

125 arrest strongly enhances the replication of VSV-DeltaM51 (but not of wild-type VSV) and Sendai virus

126 M phase strongly enhanced the replication of VSV-DeltaM51 in cells with functional antiviral signalin

127 we studied the pRNA acceptor specificity of VSV PRNTase using various GDP analogues and identified c

128 Our study of VSV now extends this description to "class III" viral fu

129 ents for engagement of the N-RNA template of VSV by its polymerase are provided by the C-terminal dom

130 n (OD) and the CTD were replaced by those of VSV P stimulated RABV RdRP activity on naked RNA but was

131 ion eliminated the normally broad tropism of VSV and restricted infection to primarily the transforme

132 Here, we test 4 chimeric viruses of VSV with glycoprotein genes from Nipah, chikungunya, and

133 with our two previously described oncolytic VSV recombinants, VSV-p53wt and VSV-p53-CC, we generated

134 rt further clinical development of oncolytic VSV recombinants as safe therapeutics for cancer.

135 and VSV-p53-CC, we generated novel oncolytic VSVs with an improved ability to replicate in virus-resi

136 ution approach, we generated novel oncolytic VSVs with an improved ability to replicate in virus-resi

137 Like other viruses of this order, VSV encodes a unique polymerase, a complex of viral L (l

138 aCa-2-passaged viruses, both SUIT-2-passaged VSV-p53wt and VSV-p53-CC showed improved replication in

139 al particles expressing SARS-CoV-2 spike (pp-VSV-SARS-CoV-2 spike) that served as a bona fide system

140 prevented adhesion of and infection with pp-VSV-SARS-CoV-2 spike.

141 he Michaelis constants for GDP and pppAACAG (VSV mRNA-start sequence) are 0.03 and 0.4 muM, respectiv

142 We produced VSV pseudotypes containing the prototypical X-31 (H3) HA

143 P as its sole attachment and fusion protein (VSV-LUJV), we demonstrate that infection is independent

144 sulate vesicular stomatitis virus G protein (VSV-G) with bioactive macromolecules via split GFP compl

145 Therefore, the EBOV GP pseudotyped VSV neutralisation assay reported here could be used to

146 ture resistance mutations into a recombinant VSV backbone resulted in the recovery of replication-com

147 ent epidemic demonstrated that a recombinant VSV where G protein is replaced with EBOV GP (rVSV-EBOV)

148 that fuse in the late endosome (recombinant VSV-Lassa and VSV-Junin), including an SFV point mutant

149 emerge when we serially passaged recombinant VSV encoding GP1,2 from these ebolaviruses.

150 Here, we show that recombinant VSV and DNA vaccines expressing NS1, alone, confer parti

151 iously described oncolytic VSV recombinants, VSV-p53wt and VSV-p53-CC, we generated novel oncolytic V

152 esicular stomatitis virus, Indiana serotype (VSV(IND)), a prototype negative-strand RNA virus.

153 We show VSV P lacking the OD (P(DeltaOD)) is monomeric but is in

154 inib and JAK inhibitor I) strongly stimulate VSV replication and oncolysis in all resistant cell line

155 (MV), Sendai (SV), or vesicular stomatitis (VSV) virus.

156 y pathway, we generated fluorescently tagged VSV G tsO45 with either the native G tail (G) or a cytop

157 ions where they cannot bind to their target VSV in absence of these cations.

158 duced substantially more progeny faster than VSV-EBOV.

159 s-reactive humoral immune responses and that VSV-cHA vaccine-induced protection varies by site of ino

160 Our data indicate that VSV-gp160G exerts potent oncolytic efficacy against CD4(

161 and Western blotting assessments showed that VSV-EBOVDeltaMLD produced substantially more progeny fas

162 rn is the neurotropic nature conveyed by the VSV glycoprotein.

163 luenza H5N1 viruses were substituted for the VSV glycoprotein gene.

164 Marburg virus, which was substituted for the VSV glycoprotein gene.

165 th the EBOV glycoprotein substituted for the VSV glycoprotein show greater safety and efficacy in tar

166 ive EBOV neutralisation were greater for the VSV-based pseudotyped virus system, which is particularl

167 ant difference in HeV G incorporation in the VSV vectors expressing either wt or codon-optimized HeV

168 quently impedes all downstream events in the VSV(IND) replication cycle.

169 VSVs that include the VSV glycoprotein (G) gene, even in most recombinant atte

170 Moreover, GFP-MxA condensates included the VSV nucleocapsid (N) protein, a protein previously shown

171 Like the VSV L-P structure, the RABV complex analyzed here repres

172 ack of impediments to the replication of the VSV core in eukaryotic cells allowed us to broadly surve

173 e glycoproteins HL17 or HL18 in place of the VSV glycoprotein were generated to identify cell lines t

174 control group received the same dose of the VSV-based Marburg virus vaccine at both time points; ano

175 was insufficient to permit initiation on the VSV N-RNA template.

176 Overall, the VSV(ENV) probe identified bNAb lineages with neutralizin

177 chimeric VSVs in which EBOV GP replaces the VSV glycoprotein, thereby reducing the neurotoxicity ass

178 To our knowledge, this is the first time the VSV pseudotyping system has been successfully extended b

179 neurotropism can be mostly attributed to the VSV G glycoprotein.

180 gated, limited human data on immunity to the VSV vector are available.

181 test a virus-like vesicle (VLV) in which the VSV glycoprotein gene is expressed from a replicon encod

182 an improved oligo-RNA capping assay with the VSV L protein, we showed that the Michaelis constants fo

183 cally, TRIM69 physically associates with the VSV(IND) phosphoprotein (P), requiring a specific peptid

184 ection, including the group treated with the VSV-based Marburg virus vaccine.

185 d on targeting human brain tumors with these VSV-EBOVs.

186 This VSV-CoV-2-S platform allows virus neutralization assays

187 lly broke the resistance of HPAF-II cells to VSV by simultaneously improving VSV attachment and repli

188 lly broke the resistance of HPAF-II cells to VSV by simultaneously improving VSV attachment and repli

189 1 (DRH-1), to display hypersusceptibility to VSV infection as evidenced by elevated infection rates,

190 e characterized the response of microglia to VSV infection and found that infected microglia produced

191 ove the susceptibility of resistant PDACs to VSV.

192 sity in susceptibility and permissibility to VSV.

193 to VSV) or MIA PaCa-2 (highly permissive to VSV) human PDAC cell lines.

194 n and TNF response and are more resistant to VSV infection.

195 n either the SUIT-2 (moderately resistant to VSV) or MIA PaCa-2 (highly permissive to VSV) human PDAC

196 ost PDAC cells, some are highly resistant to VSV, and the mechanisms are still unclear.

197 some PDAC cell lines are highly resistant to VSV, and the mechanisms of resistance are still unclear.

198 PDAC cell line also moderately resistant to VSV, while remaining highly attenuated in nonmalignant c

199 wever, some PDAC cell lines are resistant to VSV.

200 e novo production of IFN-beta in response to VSV plays a key role in antiviral defense during infecti

201 identification of cell lines susceptible to VSV chimeras allowed us to recover recombinant HL17NL10

202 such cells showed antiviral activity toward VSV.

203 ear bodies, showed antiviral activity toward VSV.

204 he same bullet shape appearance as wild-type VSV but had a modest increase in particle length, reflec

205 not stimulate the replication of a wild-type VSV that is more effective at evading antiviral response

206 Wild-type VSV was lethal when injected directly into the brain.

207 cation of VSV-DeltaM51 (but not of wild-type VSV) and Sendai virus (a paramyxovirus) via inhibition o

208 F+G was even more neurotropic than wild-type VSV, evoking a rapid lethal response in the adult brain.

209 Compared to wild-type VSV, the highly attenuated virus displayed markedly redu

210 the neurotoxicity associated with wild-type VSV.

211 When tested in vivo using VSV-MACV in a Stat2(-/-) mouse model, three MAbs signifi

212 virus (VSV) (a rhabdovirus) and its variant VSV-DeltaM51 are widely used model systems to study mech

213 virus (VSV) (a rhabdovirus) and its variant VSV-DeltaM51 are widely used model systems to study mech

214 ral RNAi response not only inhibits vertical VSV transmission but also promotes transgenerational inh

215 RNA transcription in vitro Recombinant virus VSV-P(DeltaOD) exhibits a pronounced kinetic delay in pr

216 of the DNA virus HSV-1 but not the RNA virus VSV.

217 bdovirus vesicular stomatitis Indiana virus (VSV), lentiviruses or gammaretroviruses with their envel

218 Vesicular stomatitis virus (VSV) (a rhabdovirus) and its variant VSV-DeltaM51 are wi

219 rrest.IMPORTANCE Vesicular stomatitis virus (VSV) (a rhabdovirus) and its variant VSV-DeltaM51 are wi

220 antiviral toward vesicular stomatitis virus (VSV) (a rhabdovirus).

221 (-)ssRNA viruses vesicular stomatitis virus (VSV) (Rhabdoviridae family) and Rift Valley fever virus

222 ses on oncolytic vesicular stomatitis virus (VSV) against pancreatic ductal adenocarcinoma (PDAC) cel

223 vesiculoviruses, vesicular stomatitis virus (VSV) and Chandipura virus (CHAV), which is responsible f

224 g infection with vesicular stomatitis virus (VSV) and lymphocytic choriomeningitis virus (LCMV).

225 viruses, such as vesicular stomatitis virus (VSV) and rabies virus (RABV), possess an unconventional

226 viruses, such as vesicular stomatitis virus (VSV) and rabies virus, catalyzes the transfer of 5'-phos

227 (G proteins) of vesicular stomatitis virus (VSV) and related rhabdoviruses (e.g., rabies virus) medi

228 viruses, such as Vesicular Stomatitis Virus (VSV) and Respiratory Syncytial Virus (RSV), without cyto

229 viruses such as vesicular stomatitis virus (VSV) are being considered as anticancer agents since the

230 Vesicular stomatitis virus (VSV) assembly requires condensation of the viral ribonuc

231 Vesicular stomatitis virus (VSV) based oncolytic viruses are promising agents agains

232 ious recombinant vesicular stomatitis virus (VSV) bearing the SARS-CoV-2 spike glycoprotein S as its

233 tion by chimeric vesicular stomatitis virus (VSV) containing the envelope proteins of Zaire ebolaviru

234 Recombinant vesicular stomatitis virus (VSV) encoding the hemagglutinin-like envelope glycoprote

235 cation-competent vesicular stomatitis virus (VSV) expressing a modified form of the SARS-CoV-2 spike

236 lecular clone of vesicular stomatitis virus (VSV) expressing eGFP as a marker of infection, we replac

237 ether a chimeric vesicular stomatitis virus (VSV) expressing the EBOV glycoprotein (GP) might selecti

238 with recombinant vesicular stomatitis virus (VSV) expressing the EBOV Zaire glycoprotein showed that

239 binant wild-type vesicular stomatitis virus (VSV) expressing the HBV middle surface glycoprotein (MHB

240 CoV-1 spike, and vesicular stomatitis virus (VSV) expressing the SARS-CoV-2 spike.

241 ting recombinant vesicular stomatitis virus (VSV) in which the glycoprotein was replaced by HERV-K EN

242 ormerly known as vesicular stomatitis virus (VSV) Indiana (VSV(IND)), is a model virus that is except

243 Vesicular stomatitis virus (VSV) infection downregulates NLRP12 expression to allow

244 acrophages after vesicular stomatitis virus (VSV) infection, and HIPK2-deficient mice were more susce

245 ges to withstand vesicular stomatitis virus (VSV) infection.

246 Vesicular stomatitis virus (VSV) is a promising oncolytic virus (OV).

247 Vesicular stomatitis virus (VSV) is an archetypical member of Mononegavirales, virus

248 structure of the vesicular stomatitis virus (VSV) L protein determined in 2015 and highlight multiple

249 ly resembles the vesicular stomatitis virus (VSV) L-P, the one other known full-length NNS-RNA L-prot

250 distribution of vesicular stomatitis virus (VSV) nucleocapsids in the cytoplasm of infected cells wa

251 tion with either vesicular stomatitis virus (VSV) or influenza was demonstrated to be dependent on th

252 ission of either vesicular stomatitis virus (VSV) or the retrovirus MoMLV.

253 Vesicular stomatitis virus (VSV) P is dimeric with an oligomerization domain (OD) se

254 virus (MLV), and vesicular stomatitis virus (VSV) particles.

255 ncorporated onto vesicular stomatitis virus (VSV) pseudoparticles and transduction efficiencies were

256 ys, and chimeric vesicular stomatitis virus (VSV) recombinants expressing the RABV glycoprotein (G) d

257 brain.IMPORTANCE Vesicular stomatitis virus (VSV) shows considerable promise both as a vaccine vector

258 inimally affects vesicular stomatitis virus (VSV) spread, to adjacent cells in a monolayer.

259 engineering the vesicular stomatitis virus (VSV) to encode a fluorophore and either the rabies virus

260 pe 1 (HIV-1) and vesicular stomatitis virus (VSV) to measure the neutralising ability of plasma from

261 5'ppp-dsRNA, and vesicular stomatitis virus (VSV) triggers IFN-I expression in overexpression systems

262 em, we generated vesicular stomatitis virus (VSV) virions pseudotyped with HSV-1 essential entry glyc

263 pseudotyping of vesicular stomatitis virus (VSV) with the SARS-CoV-2 spike.

264 terferon against vesicular stomatitis virus (VSV), a model virus that whose genome consists of a sing

265 We injected vesicular stomatitis virus (VSV), a transsynaptic tracer, or naturally occurring VSV

266 aired control of vesicular stomatitis virus (VSV), a virus sensed by STING that can cause an influenz

267 ia Ankara (MVA), vesicular stomatitis virus (VSV), adenovirus type 5 (Ad5), rhesus monkey rhadinoviru

268 influenza virus, vesicular stomatitis virus (VSV), and measles virus in GBA knockout cells.

269 e-1 (HIV-1), and vesicular stomatitis virus (VSV), as well as a replication-competent VSV/SARS-CoV-2

270 thic effect from Vesicular stomatitis virus (VSV), Encephalomyocarditis virus (EMCV), and Reovirus-3

271 rabies virus and vesicular stomatitis virus (VSV), expressing wild-type or codon-optimized HeV glycop

272 ter infection by vesicular stomatitis virus (VSV), newly assembled VSV particles are released from th

273 A virus (IAV) or vesicular stomatitis virus (VSV), respectively.

274 n infection with vesicular stomatitis virus (VSV), revealed diminished IFNbeta expression and increas

275 ted rhabdovirus, vesicular stomatitis virus (VSV), we demonstrate that both polymerases can copy the

276 gene expression, vesicular stomatitis virus (VSV), we determined the importance of P oligomerization.

277 tive-sense ssRNA vesicular stomatitis virus (VSV), we show that microinjection of VSV particles leads

278 Recombinant vesicular stomatitis virus (VSV)-based chimeric viruses that include genes from othe

279 6, a recombinant vesicular stomatitis virus (VSV)-based EBOV vaccine was clinically tested (NCT022830

280 genes.IMPORTANCE Vesicular stomatitis virus (VSV)-based oncolytic viruses are promising agents agains

281 ns, we devised a vesicular stomatitis virus (VSV)-based probe to display membrane-embedded Env trimer

282 Here, vesicular stomatitis virus (VSV)-based pseudovirions displaying distinct influenza v

283 dministration of vesicular stomatitis virus (VSV)-Ebola vaccine at 3 million, 20 million and 100 mill

284 hese vaccines is vesicular stomatitis virus (VSV)-EBOV, also known as rVSV-ZEBOV, a fast-acting vacci

285 In the vesicular stomatitis virus (VSV)-induced encephalitis model, the replication, caudal

286 In vesicular stomatitis virus (VSV)-infected Huh7 cells, the nucleocapsid (N) protein,

287 nstrate that the vesicular stomatitis virus (VSV)-murine interferon beta (IFNbeta)-sodium iodide symp

288 for the related Vesicular stomatitis virus (VSV).

289 virus (IAV); and vesicular stomatitis virus (VSV).

290 the L protein of vesicular stomatitis virus (VSV, a prototypic NNS RNA virus) to examine participatio

291 SINV, CHIKV, and vesicular stomatitis virus [VSV]), while viruses that fuse in the late endosome (rec

292 s are based on vesicular stomatitis viruses (VSV), but viral entry is mediated by HIV-1 Env proteins

293 4I mutation emerged within two passages when VSV-MAK-GP was grown on Vero E6, Vero, and BS-C-1 cells

294 th the start of the active cycle, ZT12, when VSV infection results in a more favorable outcome.

295 expressed human ACE2 and were immunized with VSV-eGFP-SARS-CoV-2 show profoundly reduced viral infect

296 following transduction of T cell lines with VSV-G-pseudotyped lentiviral or gammaretroviral particle

297 Immunization of mice with VSV-eGFP-SARS-CoV-2 elicits high antibody titers that ne

298 Additionally, we show that vaccination with VSV-cHAs generates greater stalk-specific and cross-reac

299 Here, we show that vaccination with VSV-eGFP-SARS-CoV-2 generates neutralizing immune respon

300 serum antibodies than does vaccination with VSV-vectored full-length HAs, confirming that cHA-based