ライフサイエンスコーパス: SFV

1 SFV also serves as a model for studies of alphavirus mol

2 SFV can be zoonotically transmitted to humans who either

3 SFV E1 is the first virus fusion protein demonstrated to

4 SFV fusion and infection are blocked by agents such as a

5 SFV fusion is triggered by low pH, which releases E1 fro

6 SFV infection of mice provides a well-characterized mode

7 SFV integrase gene (int) and gag sequences were PCR ampl

8 SFV seropositivity for periods of 8 to 26 years (median,

9 SFV, however, believed to enter cells from the early end

10 SFV-RDR has a single amino acid change which disrupts th

11 SFV-RDR infection of mice lacking alpha/beta interferon

12 SFV-specific immunoglobulin G (IgG) antibodies, but not

13 SFVs possess a broad host range, and human infections ca

14 ed the utility of simian foamy virus type 1 (SFV-1) as a vector system by transient expression assay.

15 d proviral DNA of simian foamy virus type 1 (SFV-1) from linear unintegrated DNA (pSFV-1).

16 derived from the simian foamy virus type 1 (SFV-1) internal promoter.

17 vectors based on simian foamy virus type 1 (SFV-1) to define the minimum cis-acting elements require

18 mliki Forest virus vectors expressing IL-12 (SFV-IL-12) were shown to induce potent antitumor respons

19 to RNA sequences of transcriptionally active SFV from buccal swabs obtained from the same animals.

20 y and the in vivo infection model will allow SFV to serve as a prototype for aquatic flaviviruses.

21 An SFV mutant with an alanine substitution at this position

22 An SFV mutant, srf-3, shows efficient fusion and exit in th

23 infection and were used to select srf-3, an SFV mutant that is approximately 100-fold less cholester

24 with alanine (D188A) or lysine (D188K) in an SFV infectious clone.

25 inant VSV-Lassa and VSV-Junin), including an SFV point mutant with a lower pH threshold for fusion (S

26 We have previously isolated an SFV mutant, fus-1, that requires more acidic pH to trigg

27 lines represents a step toward the use of an SFV-1 vector delivery system that will allow scaled-up p

28 et cells infected with wild-type virus or an SFV vector encoding nucleocapsid proteins.

29 We selected an SFV mutant, srf-3, that was strikingly independent of ch

30 rized DIII and DI/II proteins from CHIKV and SFV.

31 en shown to inhibit E1 hairpin formation and SFV fusion and infection.

32 STLV tax and long terminal repeat (LTR), and SFV pol and LTR sequences revealed unique SIV and SFV st

33 The pH dependence of E1s production and SFV budding was unaffected by the stability of the spike

34 Both RRV and SFV glycoproteins considerably expand the host range of

35 Together, our data suggest that RRV and SFV glycoproteins might be suitable as alternatives to V

36 he transduction rates with VSV-G-, RRV-, and SFV-pseudotyped lentivirus vectors into adherent cell li

37 We compared the replication of SFV4 and SFV-RDR in adult mouse brain.

38 In BHK cells, SFV4 and SFV-RDR replicate to high titers, but SFV-RDR is less vi

39 Both SFV4 and SFV-RDR were neuroinvasive following intraperitoneal ino

40 The SIN and SFV variant replicons resulted from previously undescrib

41 two of the Old World alphaviruses, SINV and SFV, which belong to different serological complexes, de

42 ol and LTR sequences revealed unique SIV and SFV strains and a novel STLV lineage, each divergent fro

43 CHIKV DIII-stem and SFV DIII-stem showed efficient cross-inhibition of SFV,

44 Overall, chimpanzee samples had higher anti-SFV IgG titers than humans.

45 differences within the E1 226 region between SFV, srf-3, and SIN, we constructed six SIN mutants with

46 he fusion loop was previously shown to block SFV fusion and infection, although the mutant E1 protein

47 ts indicated that the D188K mutation blocked SFV fusion and infection.

48 V4 and SFV-RDR replicate to high titers, but SFV-RDR is less virulent in mice.

49 s suggest that persistent human infection by SFV and reduced transmissibility may be influenced by th

50 The signaling pathway triggered by SFV does neither involve death receptors nor the classic

51 in the establishment of persistent cellular SFV infections.

52 Thus, chimeric CHIKV/SFV provide insights on the role the alphavirus E2 prote

53 ediated hypermutation, and use it to compare SFV sequences from human and NHP hosts living in close p

54 Thus, under a variety of conditions, SFV-infected cells can produce a soluble form of E1 that

55 In contrast, SFV budding was independent of both ubiquitin and the ac

56 Conversely, SFVs may have influenced the evolution of TRIM5 variants

57 Depletion of TSPAN9 specifically decreases SFV membrane fusion in endosomes.

58 Surprisingly, a PCR assay failed to detect SFV infection in any of these participants.

59 he test set when classifying three different SFV winemakers.

60 erficial femoral vein (CFV), mid-SFV, distal SFV, and popliteal vein (PV).

61 recruitment to the encephalitic brain during SFV infection.

62 a specific stem sequence requirement during SFV fusion suggests that the interaction of domain III w

63 Efficient SFV-membrane fusion requires the presence of cholesterol

64 everal viruses that fuse in early endosomes (SFV, SINV, CHIKV, and vesicular stomatitis virus [VSV]),

65 ; for tracing origins, grape type, and even (SFV) winemakers.

66 The proposed salmon flavivirus (SFV) has a 10.3-kb genome that encodes a rare dual open

67 e describe a variety of sensitive assays for SFV isolation and detection which were developed with a

68 wners (an ethnic group called the Bedey) for SFV infection.

69 en position 6486 and 6975 to be critical for SFV-1 vector transduction.

70 s showed that these cells were essential for SFV-IL-12 antitumor activity.

71 10 of 187 persons (5.3%) tested positive for SFV antibodies by Western blot (WB) analysis.

72 We show that the last event is required for SFV mistranslation of inserted genes.

73 o important cis-acting elements required for SFV-1 vector construction, and the finding of a cis-acti

74 Selection for SFV zinc resistance identified a key histidine residue,

75 ll line was found to be highly sensitive for SFV production on the basis of various general and speci

76 primatologists tested were seropositive for SFV from a NWM, the spider monkey, none had detectable l

77 rived from Sindbis (SIN) and Semliki Forest (SFV) viruses have mutations in nsP2.

78 By contrast, all four SFV-SIVgp160-immunized animals and three of the four rgp

79 2 (DeltaDomA, DeltaDomB, and DeltaDomC) from SFV, but not VEEV, were successfully rescued.

80 The E1 fusion protein from SFV bound cholesterol, as detected by labeling with phot

81 mutant with a lower pH threshold for fusion (SFV E2 T12I), were relatively resistant.

82 macaques naturally infected with simian FV (SFV).

83 15 Cameroonian hunters infected with gorilla SFV (cases) to 15 controls matched for age and ethnicity

84 nd plasma biomarkers associated with gorilla SFV infection in humans.

85 st virus expressing the SIV-PBj14 Env gp160 (SFV-SIVgp160) or purified recombinant SIV-PBj14 gp120 (r

86 ealed three geographically-independent human SFV infections, each of which was acquired from a distin

87 To examine if persistent human SFV infection and apparent lack of secondary transmissio

88 Virions, pseudotyped with a class II, SFV E1 or VEEV E, or a class III protein, VSV G, were pr

89 e used a Semliki Forest virus encoding IL12 (SFV-IL12) based on its promise as an RNA viral vector fo

90 Viral strains, defined by differences in SFV gag sequences, from buccal mucosal specimens overlap

91 caused a decrease of approximately 5 logs in SFV fusion at the plasma membrane.

92 s demonstrated that the relevant mutation in SFV 4-2 was a change of E1 glycine 157 to arginine (G157

93 body production and earlier remyelination in SFV-infected KO (day 28 pi), than WT mice.

94 The Remyelination in SFV-infected WT mice started on day 15 and was completed

95 viously described cholesterol requirement in SFV exit was shown to be due to a block in budding in th

96 Here we test the co-speciation hypothesis in SFVs and their primate hosts by comparing the phylogenie

97 tify a potential region of neutralization in SFVs and demonstrate recombination between genetically d

98 During the low pH- induced SFV fusion reaction, the E1 subunit exposes new epitopes

99 The infecting SFV originated from an African green monkey (one person)

100 is not required for production of infectious SFV or Chikungunya virus.

101 gRNA-specific regions and promote infectious SFV production and gRNA packaging.

102 Internalized SFV particles colocalized with TSPAN9 in vesicles early

103 One virus isolate, SFV 4-2, showed reduced binding of three acid-specific M

104 Fusion studies of pyrene-labeled SFV with cholesterol-containing liposomes showed that C(

105 study, we compare DNA sequences from latent SFV proviruses found in blood cells of 30 Bangladesh rhe

106 izing the host cell translational machinery, SFV reduces levels of translation eukaryotic initiation

107 ver, where colon tumors usually metastasize, SFV-IL-12 efficacy was significantly reduced.

108 proximal superficial femoral vein (CFV), mid-SFV, distal SFV, and popliteal vein (PV).

109 s, the fusion peptide was shielded in native SFV particles and exposed when E1-E2 dimer dissociation

110 to NWM SFV, a nested PCR assay to detect NWM SFV DNA, and a beta-galactosidase-containing indicator c

111 icator cell line to assay replication of NWM SFV.

112 we conclude that while humans exposed to NWM SFV produce antibodies, there is no evidence for long-te

113 stern blot assay to detect antibodies to NWM SFV, a nested PCR assay to detect NWM SFV DNA, and a bet

114 notic transmission of New World monkey (NWM) SFV to humans and resulting infection.

115 Analysis of naturally occurring SFV infection in macaques indicated that analysis by a c

116 rm multiple hydrogen bonds to amino acids of SFV E1 for fusion to proceed.

117 IFNAR) abolished the therapeutic activity of SFV-IL12, as did a specific antibody-mediated blockade o

118 ce anisotropy-based assay for the binding of SFV DIII-stem to the core trimer and used it to demonstr

119 ovide links between the molecular biology of SFV and its biological properties and significantly incr

120 .0, conditions that inhibited the budding of SFV but not the budding of the rhabdovirus vesicular sto

121 ter low-pH-induced conformational changes of SFV E1 have occurred.

122 An infectious clone of SFV-1 which is distantly related to the human foamy viru

123 ere, for the first time, consensus clones of SFV strains were used to map virulence determinants.

124 E1 conformational changes in the control of SFV cholesterol dependence.

125 PAN9 depletion did not alter the delivery of SFV to early endosomes or change their pH or protease ac

126 ts provide a first comparative evaluation of SFV-specific host mucosal humoral immunity in infected h

127 Evidence of SFV infection included seropositivity, proviral DNA dete

128 er understanding of the potential impacts of SFV infection on ecologically and economically important

129 Incorporation of SFV glycoproteins into lentivirus vector is less efficie

130 II-stem showed efficient cross-inhibition of SFV, Sindbis virus, and CHIKV infections.

131 Intratumoral injection of SFV-IL12 induced production of IFN-I as detected in seru

132 An intermediate of SFV E1-induced fusion was created by transient acidifica

133 The level of SFV RNA in buccal swabs varied greatly between macaques,

134 We have examined the entry mode of SFV, Sindbis virus, HRV 14 and poliovirus using a method

135 Thus, the innocuous nature of SFV infection can be explained by replication that is li

136 n important role in the neuropathogenesis of SFV.

137 rimate hosts by comparing the phylogenies of SFV polymerase and mitochondrial cytochrome oxidase subu

138 the genetic basis of different properties of SFV strains has been studied using molecular clones, whi

139 librations revealed an extremely low rate of SFV evolution, 1.7 x 10(-8) substitutions per site per y

140 is extended trimer and to define a series of SFV fusion-block mutants.

141 ch were developed with a prototype strain of SFV serotype 2.

142 In agreement with the known structure of SFV and other alphaviruses, the fusion peptide was shiel

143 l good health, and secondary transmission of SFV was not observed in three wives available for WB and

144 heterologous gene, indicating the utility of SFV-1 as a vector.

145 polyprotein processing and the virulence of SFV.

146 lpha has potentially shaped the evolution of SFVs in NWM hosts.

147 cell lines for foamy virus vectors based on SFV-1.

148 hough occasional infection with SIV, SRV, or SFV in persons occupationally exposed to NHPs has been r

149 imeric cDNA clones between CHIKV and VEEV or SFV to probe the effect of each domain on pathogenicity

150 ted with SFV of African green monkey origin (SFV-3).

151 equences added to the 5' end of the original SFV 5' sequence or its "deleted" versions.

152 ut did not affect the replication of its own SFV.

153 Phylogenetic analysis places SFV in a basal position among a new subgroup of recently

154 can induce genetic changes that may prevent SFV replication in infected humans in vivo.

155 ped on the basis of the sequences in primary SFV isolates obtained from pig-tailed macaques (Macaca n

156 Compared to the prototype SFV-3 sequence, the LTR, internal promoter, and FV trans

157 Remarkably, SFV-IL-12 induced a high percentage of circulating tumor

158 Phylogenetic analysis showed SFV infection originating from chimpanzees (n = 8) and b

159 plicons were compared to wild-type (wt) SIN, SFV, and wt nsPs SIN replicons.

160 Among different simian species, SFV demonstrates significant sequence diversity within t

161 were available, demonstrating long-standing SFV infection.

162 We have studied SFV in free-ranging rhesus macaques in Bangladesh.

163 Budding of biotin-tagged SFV was continuous for at least 2 h, independent of micr

164 We found that SFV isolated from three different species of NWM replica

165 vid pathway of cell entry, it was found that SFV, Sindbis virus and HRV 14 require an active clathrin

166 Virus mutant studies indicate that SFV's cholesterol dependence is controlled by regions of

167 criptase, and integrase, it is possible that SFV-1 contains a promoter within the pol gene for initia

168 rical voltage-clamp measurements showed that SFV E1-induced cell-cell fusion occurred quickly after a

169 It has been previously shown that SFV in immunocompetent animals replicates to detectable

170 sterol-depleted insect cells have shown that SFV requires cholesterol in the cell membrane for both v

171 These results suggest that SFV-IL-12 therapy could benefit from the use of strategi

172 These results indicate that SFVs might have co-speciated with Old World primates for

173 The SFV 4-2 mutant was fully infectious, formed the E1 homot

174 The SFV ij loop contains a histidine residue at position 230

175 The SFV spike protein is composed of a dimer of E1 and E2 tr

176 The SFV-1 vector in the presence of vesicular stomatitis vir

177 94 completely abrogated gene transfer by the SFV-1 vector.

178 nes with the open reading frame encoding the SFV capsid, demonstrating that one function of the capsi

179 However, the location of the E1 stem in the SFV particle and its rearrangement and functional import

180 low-pH-induced conformational changes in the SFV spike protein.

181 as DNA target sites located elsewhere in the SFV-1 genome.

182 s response in vivo when substituted into the SFV-1 internal promoter context.

183 (v) Viruses of the SFV clade are the exception to the general rule.

184 ur data identify two separate regions of the SFV E1 ectodomain, one responsible for target membrane a

185 odies to the N- or C-terminal regions of the SFV E1 stem and used them to study the stem during fusio

186 Our results identify a region of the SFV E2 spike protein subunit that regulates the pH depen

187 ce identifying the source chimpanzees of the SFV infection in two workers.

188 stograms correctly differentiated all of the SFV samples from the other geographic regions in the tes

189 Fusion is mediated by the E1 subunit of the SFV spike protein.

190 ol of virus cholesterol dependence, once the SFV fusion peptide inserts in the target membrane it has

191 ed to the CFV in eight studies (61%), to the SFV in six studies (4.6%), and to the PV in 14 studies (

192 An E1 H230A mutant was constructed using the SFV infectious clone.

193 bited the replication of at least one of the SFVs associated with the other two species but did not a

194 n (1%) of 1099 individuals had antibodies to SFV.

195 This indicates that, in contrast to SFV, ALV-B is unable to fuse at the cellular surface, ev

196 SFVmcy-2 was highly related to SFV serotype 1 (SFVmcy-1), an isolate from the same spec

197 , which contained novel sequences related to SFV serotype 3 (SFVagm-3), isolated from an African gree

198 IN, an alphavirus quite distantly related to SFV.

199 AVS or caspase-8 expression are resistant to SFV-induced apoptosis.

200 active to STLV, and 97% were seroreactive to SFV.

201 Thus, similar to SFV, SIN was cholesterol dependent for both virus entry

202 esting a shift toward a phenotype similar to SFV.

203 l products, could minimize human exposure to SFVs by reducing the risk of potential retrovirus infect

204 onclude that treatment with, or antibody to, SFV E2 peptide2 triggers some mechanism that promotes re

205 at neither heat nor urea treatment triggered SFV-liposome fusion at neutral pH, although either treat

206 s persistently infected with chimpanzee-type SFV for an unknown length of time.

207 ion of the postfusion E1 trimer in wild-type SFV but not in an H333 mutant.

208 Surprisingly, the wild-type SFV-1 internal promoter Tas DNA binding site fails to co

209 usion and E1 trimer formation than wild-type SFV.

210 Unlike SFV DIII, both core trimer binding and fusion inhibition

211 wines produced in the Sao Francisco Valley (SFV) region to trace geographic origin, winemaker, and g

212 Pseudorevertants of various SFV-SIN chimeras were isolated, and suppressor mutations

213 survival following infection with a virulent SFV strain.

214 ly reduced mortality in response to virulent SFV infection.

215 to alanine (R50A) of the simian foamy virus SFV cpz(hu) inhibits proper capsid assembly and abolishe

216 rophic virus (STLV), and simian foamy virus (SFV) and for nucleic acids of these same viruses using g

217 Simian Foamy Virus (SFV) can be transmitted from non-human primates (NHP) to

218 Simian foamy virus (SFV) infection and the subsequent immune response are no

219 Recently, simian foamy virus (SFV) infection was reported in 4 of 231 individuals occu

220 Zoonotic infections with simian foamy virus (SFV), a retrovirus endemic in most Old World primates, w

221 D retrovirus (SRV), and simian foamy virus (SFV).

222 Semliki Forest virus (SFV) and Sindbis virus (SIN) are enveloped alphaviruses

223 on by the alphaviruses Semliki Forest virus (SFV) and Sindbis virus were strongly promoted by cholest

224 Alphaviruses such as Semliki Forest virus (SFV) are enveloped viruses that infect cells through a l

225 Alphaviruses such as Semliki Forest virus (SFV) are enveloped viruses whose surface is covered by a

226 River virus (RRV) and Semliki Forest virus (SFV) are two alphaviruses that have a high degree of ami

227 avirulent and virulent Semliki Forest virus (SFV) as well as West Nile virus infection and demonstrat

228 those belonging to the Semliki Forest virus (SFV) clade, have PSs which can be recognized by the caps

229 fine binding sites for Semliki Forest virus (SFV) Cp on the gRNA.

230 ponding regions of the Semliki Forest virus (SFV) E2 (domains A, B, and C) substituted into the CHIKV

231 ALV-B and pH-dependent Semliki Forest virus (SFV) entered cells with slower uptake kinetics than HIV-

232 licase protein nsP2 of Semliki Forest virus (SFV) has a 648RRR nuclear localization signal and is tra

233 ous DIII proteins from Semliki Forest virus (SFV) has been shown to inhibit E1 hairpin formation and

234 dies of the alphavirus Semliki Forest virus (SFV) here demonstrated that there was a strong requireme

235 endai virus (SeV), and Semliki Forest virus (SFV) infection and to the TLR3 agonist poly(I:C).

236 Semliki Forest virus (SFV) infects cells by an acid-dependent membrane fusion

237 The alphavirus Semliki Forest virus (SFV) infects cells through a low-pH-dependent membrane f

238 The alphavirus Semliki Forest virus (SFV) infects cells through low-pH-induced membrane fusio

239 e enveloped alphavirus Semliki Forest virus (SFV) infects cells via a low pH-triggered membrane fusio

240 The alphavirus Semliki Forest virus (SFV) infects cells via a low-pH-dependent membrane fusio

241 e enveloped alphavirus Semliki Forest virus (SFV) infects cells via a low-pH-triggered membrane fusio

242 e enveloped alphavirus Semliki Forest virus (SFV) infects cells via a membrane fusion reaction mediat

243 tein of the alphavirus Semliki Forest virus (SFV) is a class II fusion protein that mediates low pH-t

244 Semliki Forest virus (SFV) is an enveloped alphavirus that infects cells by a

245 Semliki Forest virus (SFV) is an enveloped alphavirus that infects cells throu

246 Semliki Forest virus (SFV) is an enveloped alphavirus that infects cells via a

247 Semliki Forest virus (SFV) is an enveloped alphavirus that infects cells via a

248 Semliki Forest virus (SFV) is an enveloped alphavirus that requires cellular m

249 Semliki Forest virus (SFV) is an enveloped alphavirus whose membrane fusion is

250 Semliki Forest virus (SFV) provides a well-characterized model system to study

251 itis virus (VSV) and a Semliki Forest virus (SFV) replicon (SFVG) that propagates through expression

252 riants of both SIN and Semliki Forest virus (SFV) replicons encoding the neomycin resistance gene tha

253 Semliki Forest virus (SFV) requires RNA replication and Bax/Bak for efficient

254 ar stomatitis (VSV) or Semliki Forest virus (SFV) that require delivery to acidic endosomes to penetr

255 ed influenza virus and Semliki Forest virus (SFV) to define a role for protein kinase C betaII (PKCbe

256 ike protein subunit of Semliki Forest virus (SFV) triggers membrane fusion upon exposure to mildly ac

257 The alphavirus Semliki Forest virus (SFV) uses a membrane fusion reaction to infect host cell

258 cells infected with a Semliki Forest virus (SFV) vector.

259 lls were infected with Semliki Forest virus (SFV) vectors containing the rat NCS-1 gene.

260 ng genes inserted into Semliki Forest virus (SFV) vectors generate a large fraction of defective ribo

261 l fusion protein E1 of Semliki Forest virus (SFV) were fused to target cells.

262 2 envelope proteins of Semliki Forest virus (SFV) were fused to voltage-clamped planar lipid bilayer

263 r alphaviruses such as Semliki Forest virus (SFV), acidic pH initiates a series of conformational cha

264 monitor the budding of Semliki Forest virus (SFV), an enveloped alphavirus that buds from the plasma

265 Semliki Forest virus (SFV), an enveloped alphavirus, is a well-characterized p

266 s widely accepted that Semliki Forest virus (SFV), an enveloped virus, requires this pathway there ar

267 Sindbis virus (SINV), Semliki Forest virus (SFV), and chikungunya virus (CHIKV).

268 litis virus (VEEV) and Semliki Forest virus (SFV), can cause encephalitic disease.

269 ly related alphavirus, Semliki Forest virus (SFV), resulted in nonviable chimeras.

270 tudies have shown that Semliki Forest virus (SFV)-infected delta-knock-out (KO) mice did not exhibit

271 SV) and the alphavirus Semliki Forest virus (SFV).

272 ndbis virus (SINV) and Semliki Forest virus (SFV).

273 E1 from the alphavirus Semliki Forest virus (SFV).

274 fusion domain of E1 of Semliki Forest virus (SFV).

275 tion of the alphavirus Semliki Forest virus (SFV).

276 The A7(74) strain of Semliki Forest virus (SFV; genus Alphavirus) is avirulent in adult mice, while

277 Simian and human foamy viruses (SFV and HFV) encode a transcriptional transactivator, Ta

278 .8%) of infection with simian foamy viruses (SFV) among humans occupationally exposed to nonhuman pri

279 Simian foamy viruses (SFV) are complex retroviruses that are ubiquitous in non

280 ssion of Old World NHP simian foamy viruses (SFV) has been documented, leading to nonpathogenic persi

281 Simian foamy viruses (SFVs) are highly prevalent in a variety of nonhuman prim

282 Simian foamy viruses (SFVs) are ubiquitous, non-pathogenic retroviruses that i

283 Zoonotic simian foamy viruses (SFVs) establish persistent infections in humans, for who

284 We studied simian foamy viruses (SFVs) from common marmosets, spider monkeys, and squirre

285 spread rapidly throughout the brain, whereas SFV-RDR infection was confined to small foci of cells.

286 the tissue, are the major cell type in which SFV replicates.

287 esults indicate that while immunization with SFV-SIVgp160 and rgp120 did not protect against virus in

288 CTL lysis of target cells infected with SFV encoding nucleocapsid was major histocompatibility c

289 cantly different between cells infected with SFV expressing green fluorescent protein (GFP) or GFP pl

290 lear cell samples from a human infected with SFV of African green monkey origin (SFV-3).

291 n central Africa are currently infected with SFV.

292 the first time, that chronic infection with SFV is associated with T lymphocyte differentiation and

293 study documents more frequent infection with SFV than with other simian retroviruses in persons worki

294 after intratumoral injection of WT mice with SFV-IL12, this did not occur in mice where IFNAR was ina

295 revealed only minimal cross-reactivity with SFV-3.

296 holesterol and sphingolipid dependent for wt SFV and strikingly less cholesterol dependent for srf-3.

297 had growth properties similar to those of wt SFV and showed modest change or no change in the pH depe

298 wing that superinfection of PI cells with wt SFV triggered the shutdown of minus-strand synthesis, wh

299 tidines by mutagenesis of the wild-type (wt) SFV infectious clone to create virus mutants with E1 H3A

300 e the public health implications of zoonotic SFV infections.