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 is one oncolytic virus out of an arsenal of potentia

3 VSV tumor tropism is generally dependent on the permissi

4 VSV with Maraba G substituted or lentiviral vectors shou

5 VSV-FH infects cells expressing MV receptors and is fuso

6 VSV-FH is a hybrid vesicular stomatitis virus (VSV) with

7 VSV-FH is not fusogenic at low CD46 density but requires

8 VSV-gp160G was further noted to be highly attenuated and

9 VSV-infected BM-mDC triggered BM-pDC to mount significan

10 VSV-TMD primarily catalyzed initial intermediate formati

11 VSV-vectored influenza vaccines that express chimeric he

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

13 mucosal and T cell immunities triggered by a VSV-based human NoV vaccine.

14 We previously generated a VSV vaccine vector that incorporates two enhancing strat

15 Accordingly, VSV-gp160G did not elicit any evidence of neurotoxicity

16 e, IFN-alpha and -beta differentially affect VSV oncolysis, justifying the evaluation and comparison

17 ses and provided complete protection against VSV infection.

18 ated with VSV infection while still allowing VSV to effectively target ATL cells.

19 Although VSV is effective against a majority of pancreatic ductal

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

21 In contrast, in the wild-type mice, although VSV replicated equally well in the lymph node, infection

22 n, combining domains from gp160 of HIV-1 and VSV-G.

23 Lassa virus glycoprotein precursor (GPC) and VSV showed no adverse actions within or outside the brai

24 The influences of VSV-TMD, hexadecane, and VSV-TMD + hexadecane on the kinetics, activation thermod

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

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

27 inished susceptibility to both nonimmune and VSV-immune serum neutralization.

28 ng affinities between the selected SwAps and VSV and to determine the coefficient of switching (CoS)

29 Comparison of the parental VSV and VSV with Maraba G substituted revealed nearly identical

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

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

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

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

34 Viruses such as VSV that are used as vaccine vectors can induce protecti

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

36 lation can serve as an approach to attenuate VSV, and perhaps other nonsegmented negative-strand RNA

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

38 e, we demonstrate that IFN-lambda attenuates VSV replication and spread following intranasal virus de

39 at IFN-lambda expression severely attenuates VSV in cell culture.

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

41 derscoring the intimate relationship between VSV and the host cell.

42 alization and restricted replication of both VSV and an HSV-1 strain deficient in gamma34.5, while wi

43 nate immune mechanisms over those induced by VSV alone.

44 Susceptibility of HNSCC lines to killing by VSV varied.

45 improves the sensitivity of EBOV-GP carrying VSV detection compared to directly immobilized antibodie

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

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

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

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

50 A chimeric virus combining VSV genes with the gene coding for the Ebola virus glyco

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

52 ates virus-like vesicles (VLVs) that contain VSV G but no other viral structural proteins.

53 quiescent hCD34(+) cells, whereas high-dose VSV-G-LVs were insufficient.

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

55 nfection with enhanced GFP (eGFP)-expressing VSV (VSVeGFP) than BM-pDC.

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

57 mice did not mount IFN-I responses following VSV infection.

58 e the circadian effect on survival following VSV infection.

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

60 provide a curated list of genes required for VSV replication.

61 ore effective at protecting HNSCC cells from VSV oncolysis than was IFN-alpha2a.

62 otype L protein with their counterparts from VSV New Jersey and analyzed effects on virus polymerase

63 y distinct and phylogenetically distant from VSV.

64 expression or coadministration of HSP70 from VSV vector significantly enhanced human NoV-specific muc

65 however, interferon can protect neurons from VSV infection.

66 2, as the protein that protects neurons from VSV infection.

67 protects the peripheral nervous system from VSV infection as well.

68 Ifit2 protected only the nervous system from VSV infection; other tissues were well protected even in

69 not needed to protect other cell types from VSV.

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

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

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

73 the vesicular stomatitis virus glycoprotein (VSV G) has been described.

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

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-FH cytotoxic activity was reduced by pretreatment of

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

80 Importantly, VSV-FH, similar to MV, can discriminate between low- and

81 Importantly, VSV-gp160G effectively exerted potent oncolytic activity

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

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

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

85 Further analysis in VSV-FH-infected cell lines shows earlier and higher expr

86 The size of each syncytium is larger in VSV-FH-infected cells at a specific CD46 density.

87 produced faster and in higher quantities in VSV-FH-infected cells.

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

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

90 ncolytic VSV therapy for HNSCC by inhibiting VSV replication in normal cells without a corresponding

91 When mice had two brain tumors, intratumoral VSV-LASV-GPC injection in one tumor (glioma or melanoma)

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

93 marginally enhanced susceptibility to lethal VSV i.v. infection.

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

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

96 In vivo, IFN-lambda limits VSV replication in the mouse lung after intranasal admin

97 The live VSV vectors induced more HeV G-specific antibodies as we

98 In Ifit2(-/-) mice, VSV, injected subcutaneously into the footpad, entered t

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

100 al in the brain by replacing the neurotropic VSV glycoprotein with the glycoprotein from one of five

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

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

103 delivery but does not reduce the ability of VSV to induce potent protective immune responses.

104 pens a new door to widespread application of VSV-LASV-GPC as a safe and efficacious oncolytic chimeri

105 esolution of existing models for assembly of VSV.

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

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

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

109 rVSV vectors containing a full complement of VSV genes and expressing the Ebola virus (EBOV) GP from

110 We measured the dissociation constant of VSV polymerases from their whole genome template to be 2

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

112 The efficacy of VSV-based vaccines can be improved by engineering vector

113 tion with VSV could lead to the formation of VSV DNA.

114 The envelope glycoprotein (G) of VSV was replaced with a variant glycoprotein of the lymp

115 e hypothesis that the catalytic influence of VSV-TMD on the initial-intermediate- and pore-forming st

116 The influences of VSV-TMD, hexadecane, and VSV-TMD + hexadecane on the kin

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

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

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

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

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

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

123 ells through replacement of the G protein of VSV with a hybrid fusion protein, combining domains from

124 ng the fusion-active TMD of the G protein of VSV.

125 in-coated magnetic beads for purification of VSV.

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

127 ors that are required for specific stages of VSV entry and gene expression.

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

129 nidase proteins, expressed on the surface of VSV particles, allowed this vaccine to grow in cell cult

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

131 G protein is about 80% homologous to that of VSV, is relatively resistant to the neutralizing activit

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

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

134 These results are encouraging for the use of VSV for the treatment of prostate cancers that are resis

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

136 alpha2a may enhance selectivity of oncolytic VSV therapy for HNSCC by inhibiting VSV replication in n

137 Pairing VSV with IFN-alpha2a may enhance selectivity of oncolyti

138 rsus normal cells may be enhanced by pairing VSV with IFN-alpha2a.

139 Comparison of the parental VSV and VSV with Maraba G substituted revealed nearly id

140 Moreover, in contrast to the parental VSV, the VSV with Maraba G substituted was resistant to

141 ed survival of HNSCC cells during persistent VSV infection.

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

143 he transduction of cells that do not produce VSV DNA with the long interspersed nuclear element 1 and

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

145 ely, these results indicated that productive VSV infection was needed to trigger IFN responses of mDC

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

147 s used vesicular-stomatitis-virus-G protein (VSV-G)-LVs at high doses combined with strong cytokine-c

148 ted the efficacy and safety of a recombinant VSV that has been retargeted to specifically infect and

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

150 refore constructed and rescued a recombinant VSV whose G gene was replaced by the corresponding gene

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

152 d how IFN-lambda expression from recombinant VSV would influence vector replication, spread, and immu

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

154 reviously showed that a panel of recombinant VSVs carrying mutations at a predicted methyltransferase

155 In this study, we showed that recombinant VSVs (rVSVs) defective in mRNA cap methylation were atte

156 This was achieved by replacing the single VSV glycoprotein (G) with human immunodeficiency virus t

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

158 cribed here, we developed new tools to study VSV assembly by fusing fluorescent proteins to M and to

159 plasmacytoid dendritic cells and subsequent VSV infection, MyTrCa(-/-) mice displayed significantly

160 In summary, VSV-FH has significant advantages over MV as an oncolyti

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

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

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

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

165 This indicates that VSV-EBOV may protect humans against EBOV infections in W

166 Here, we provide the preclinical proof that VSV-EBOV completely protects macaques against lethal cha

167 Overall, our data suggest that VSV with Maraba G substituted should be further investig

168 The VSV DNA was detected in the cytoplasm as single-stranded

169 The VSV polymerase can initiate on both DNA and RNA and can

170 the rVSV-VP1 backbone further attenuates the VSV-based vaccine in vitro and in vivo, thus improving t

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

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

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

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

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

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

177 olavirus glycoproteins (GPs) in place of the VSV G protein demonstrated protection of nonhuman primat

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

179 filovirus glycoprotein (GP) in place of the VSV glycoprotein, have shown 100% efficacy against homol

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

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

182 In contrast, in BM-pDC the VSV variant M2 induced particularly high IFN responses t

183 However, as demonstrated in this report, the VSV infectious titer drops by 4 log units during the fir

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

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

186 (VSV), we detected DNA complementary to the VSV RNA.

187 reover, in contrast to the parental VSV, the VSV with Maraba G substituted was resistant to nonimmune

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

189 al proteins of Semliki Forest virus with the VSV glycoprotein has been described.

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

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

192 SwAps, four have exhibited high affinity to VSV and ability to switch upon elution and thus were fur

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

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

195 1 (DRH-1), to display hypersusceptibility to VSV infection as evidenced by elevated infection rates,

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

197 ove the susceptibility of resistant PDACs to VSV.

198 T1 in response to VSV, and were resistant to VSV infection.

199 o development of cells that are resistant to VSV infection.

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

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

202 cells that were susceptible and resistant to VSV.

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

204 factor STAT1, activated STAT1 in response to VSV, and were resistant to VSV infection.

205 n deletion, cells are primarily sensitive to VSV, but subsequent evolution in tumors leads to develop

206 ed primarily of cells that were sensitive to VSV.

207 rs in which cells are primarily sensitive to VSV.

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

209 poorly to interferon and were susceptible to VSV infection.

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

211 BM-pDC stimulated with wild-type VSV mounted TLR-dependent IFN responses that were indepe

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

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

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

215 otection against challenge with the virulent VSV.

216 In contrast, a novel chimeric virus (VSV-LASV-GPC) containing genes from both the Lassa virus

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

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

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

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

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

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

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

224 a on the DMFE of Vesicular stomatitis virus (VSV) and Tobacco etch virus (TEV), we found that increas

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

226 d here to purify vesicular stomatitis virus (VSV) as a model case, however this technique can be exte

227 n of pseudotyped vesicular stomatitis virus (VSV) as a model virus on SP-IRIS platform.

228 Using vesicular stomatitis virus (VSV) as a model, we coinfected BHK cells with VSV DIPs a

229 gy that utilizes vesicular stomatitis virus (VSV) as a vector for chimeric hemagglutinin (cHA) antige

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

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

232 VSVFH is a vesicular stomatitis virus (VSV) encoding the MV-Edm F and H entry proteins in place

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

234 Vesicular stomatitis virus (VSV) has been extensively studied as a vaccine vector an

235 Replication of vesicular stomatitis virus (VSV) has long served as a model for understanding host-v

236 seroprevalence, vesicular stomatitis virus (VSV) has promise as a systemic oncolytic agent for human

237 Vesicular stomatitis virus (VSV) has shown substantial promise, but a key problem is

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

239 endage region of vesicular stomatitis virus (VSV) Indiana serotype L protein with their counterparts

240 bust decrease of vesicular stomatitis virus (VSV) infection and a corresponding enhancement of type I

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

242 Vesicular stomatitis virus (VSV) is the prototype for negative sense non segmented (

243 structure of the vesicular stomatitis virus (VSV) L protein.

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

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

246 Assembly of vesicular stomatitis virus (VSV) particles requires the separate trafficking of the

247 n treatment with vesicular stomatitis virus (VSV) particles, plasmacytoid dendritic cells (pDC) are t

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

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

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

251 eered a chimeric vesicular stomatitis virus (VSV) that is devoid of its natural neurotoxicity while r

252 binant strain of vesicular stomatitis virus (VSV) that specifically targets transformed CD4(+) T cell

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

254 ls infected with vesicular stomatitis virus (VSV) to identify miRNAs that regulate viral-host interac

255 cation-defective vesicular stomatitis virus (VSV) vector backbone that lacks the native G surface gly

256 es an attenuated vesicular stomatitis virus (VSV) vector, to deliver and express influenza virus prot

257 Vesicular stomatitis virus (VSV) vectors that express heterologous antigens have sho

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

259 V-FH is a hybrid vesicular stomatitis virus (VSV) with a deletion of its G glycoprotein and encoding

260 ed a pseudotyped vesicular stomatitis virus (VSV) with a glycoprotein of Maraba virus, a closely rela

261 Work with vesicular stomatitis virus (VSV), a prototype, supports a model of RNA synthesis whe

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

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

264 oncolytic virus, vesicular stomatitis virus (VSV), and tested the hypothesis that the neurotoxicity a

265 and recombinant vesicular stomatitis virus (VSV), expressing either the codon-optimized or the wild-

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

267 us studied here, vesicular stomatitis virus (VSV), like its relative, rabies virus, can cause neuropa

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

269 otype RNA virus, vesicular stomatitis virus (VSV), was cultured for three passages on BHK host cells,

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

271 oblasts with the vesicular stomatitis virus (VSV), we detected DNA complementary to the VSV RNA.

272 Working with vesicular stomatitis virus (VSV), we previously showed that a panel of recombinant V

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

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

275 , we developed a vesicular stomatitis virus (VSV)-based human NoV vaccine candidate.

276 Using a vesicular stomatitis virus (VSV)-based pseudoparticle seroneutralization assay, we d

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

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

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

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

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

282 ant to oncolytic vesicular stomatitis virus (VSV).

283 virus (WNV), or vesicular stomatitis virus (VSV).

284 rom oncolysis by vesicular stomatitis virus (VSV).

285 er infected with vesicular stomatitis virus (VSV).

286 x (M) protein of vesicular stomatitis virus (VSV).

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

288 mbrane domain of vesicular stomatitis virus (VSV-TMD) promotes both initiation of fusion and formatio

289 w that both RNA (vesicular stomatitis virus [VSV]) and DNA (cytomegalovirus [CMV]) virus inoculations

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

291 The resultant virus, VSV-gp160G, was found to only target cells expressing CD

292 4I mutation emerged within two passages when VSV-MAK-GP was grown on Vero E6, Vero, and BS-C-1 cells

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

294 atly reduced neurotoxic risk associated with VSV infection while still allowing VSV to effectively ta

295 SV) as a model, we coinfected BHK cells with VSV DIPs and recombinant helper virus carrying a gene en

296 of IFN subtypes for use in combination with VSV therapy.

297 d nuclear element 1 and their infection with VSV could lead to the formation of VSV DNA.

298 ta receptor succumbed to the infection, with VSV spreading throughout the brain.

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

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