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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.
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.
22 infection and were used to select srf-3, an SFV mutant that is approximately 100-fold less cholester
24 inant VSV-Lassa and VSV-Junin), including an SFV point mutant with a lower pH threshold for fusion (S
26 lines represents a step toward the use of an SFV-1 vector delivery system that will allow scaled-up p
32 STLV tax and long terminal repeat (LTR), and SFV pol and LTR sequences revealed unique SIV and SFV st
36 he transduction rates with VSV-G-, RRV-, and SFV-pseudotyped lentivirus vectors into adherent cell li
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
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
49 s suggest that persistent human infection by SFV and reduced transmissibility may be influenced by th
53 ediated hypermutation, and use it to compare SFV sequences from human and NHP hosts living in close p
61 a specific stem sequence requirement during SFV fusion suggests that the interaction of domain III w
63 everal viruses that fuse in early endosomes (SFV, SINV, CHIKV, and vesicular stomatitis virus [VSV]),
64 peak titers prior to challenge, 1:1,700 for SFV-SIV gp 160 and 1:10,500 for rgp120), but neither neu
65 e describe a variety of sensitive assays for SFV isolation and detection which were developed with a
71 o important cis-acting elements required for SFV-1 vector construction, and the finding of a cis-acti
73 ll line was found to be highly sensitive for SFV production on the basis of various general and speci
74 primatologists tested were seropositive for SFV from a NWM, the spider monkey, none had detectable l
81 st virus expressing the SIV-PBj14 Env gp160 (SFV-SIVgp160) or purified recombinant SIV-PBj14 gp120 (r
82 ealed three geographically-independent human SFV infections, each of which was acquired from a distin
85 e used a Semliki Forest virus encoding IL12 (SFV-IL12) based on its promise as an RNA viral vector fo
86 Viral strains, defined by differences in SFV gag sequences, from buccal mucosal specimens overlap
88 s demonstrated that the relevant mutation in SFV 4-2 was a change of E1 glycine 157 to arginine (G157
91 viously described cholesterol requirement in SFV exit was shown to be due to a block in budding in th
92 Here we test the co-speciation hypothesis in SFVs and their primate hosts by comparing the phylogenie
93 tify a potential region of neutralization in SFVs and demonstrate recombination between genetically d
99 study, we compare DNA sequences from latent SFV proviruses found in blood cells of 30 Bangladesh rhe
100 izing the host cell translational machinery, SFV reduces levels of translation eukaryotic initiation
103 s, the fusion peptide was shielded in native SFV particles and exposed when E1-E2 dimer dissociation
104 to NWM SFV, a nested PCR assay to detect NWM SFV DNA, and a beta-galactosidase-containing indicator c
106 we conclude that while humans exposed to NWM SFV produce antibodies, there is no evidence for long-te
107 stern blot assay to detect antibodies to NWM SFV, a nested PCR assay to detect NWM SFV DNA, and a bet
111 IFNAR) abolished the therapeutic activity of SFV-IL12, as did a specific antibody-mediated blockade o
112 ce anisotropy-based assay for the binding of SFV DIII-stem to the core trimer and used it to demonstr
113 ovide links between the molecular biology of SFV and its biological properties and significantly incr
114 .0, conditions that inhibited the budding of SFV but not the budding of the rhabdovirus vesicular sto
117 ere, for the first time, consensus clones of SFV strains were used to map virulence determinants.
119 PAN9 depletion did not alter the delivery of SFV to early endosomes or change their pH or protease ac
120 ts provide a first comparative evaluation of SFV-specific host mucosal humoral immunity in infected h
131 rimate hosts by comparing the phylogenies of SFV polymerase and mitochondrial cytochrome oxidase subu
132 the genetic basis of different properties of SFV strains has been studied using molecular clones, whi
133 librations revealed an extremely low rate of SFV evolution, 1.7 x 10(-8) substitutions per site per y
136 In agreement with the known structure of SFV and other alphaviruses, the fusion peptide was shiel
137 l good health, and secondary transmission of SFV was not observed in three wives available for WB and
142 hough occasional infection with SIV, SRV, or SFV in persons occupationally exposed to NHPs has been r
143 imeric cDNA clones between CHIKV and VEEV or SFV to probe the effect of each domain on pathogenicity
148 ped on the basis of the sequences in primary SFV isolates obtained from pig-tailed macaques (Macaca n
158 vid pathway of cell entry, it was found that SFV, Sindbis virus and HRV 14 require an active clathrin
160 criptase, and integrase, it is possible that SFV-1 contains a promoter within the pol gene for initia
161 rical voltage-clamp measurements showed that SFV E1-induced cell-cell fusion occurred quickly after a
163 sterol-depleted insect cells have shown that SFV requires cholesterol in the cell membrane for both v
171 nes with the open reading frame encoding the SFV capsid, demonstrating that one function of the capsi
172 However, the location of the E1 stem in the SFV particle and its rearrangement and functional import
177 ur data identify two separate regions of the SFV E1 ectodomain, one responsible for target membrane a
178 odies to the N- or C-terminal regions of the SFV E1 stem and used them to study the stem during fusio
182 ol of virus cholesterol dependence, once the SFV fusion peptide inserts in the target membrane it has
183 ed to the CFV in eight studies (61%), to the SFV in six studies (4.6%), and to the PV in 14 studies (
185 bited the replication of at least one of the SFVs associated with the other two species but did not a
189 , which contained novel sequences related to SFV serotype 3 (SFVagm-3), isolated from an African gree
195 l products, could minimize human exposure to SFVs by reducing the risk of potential retrovirus infect
196 onclude that treatment with, or antibody to, SFV E2 peptide2 triggers some mechanism that promotes re
197 at neither heat nor urea treatment triggered SFV-liposome fusion at neutral pH, although either treat
206 to alanine (R50A) of the simian foamy virus SFV cpz(hu) inhibits proper capsid assembly and abolishe
207 rophic virus (STLV), and simian foamy virus (SFV) and for nucleic acids of these same viruses using g
211 Zoonotic infections with simian foamy virus (SFV), a retrovirus endemic in most Old World primates, w
214 on by the alphaviruses Semliki Forest virus (SFV) and Sindbis virus were strongly promoted by cholest
215 Alphaviruses such as Semliki Forest virus (SFV) are enveloped viruses that infect cells through a l
216 Alphaviruses such as Semliki Forest virus (SFV) are enveloped viruses whose surface is covered by a
217 River virus (RRV) and Semliki Forest virus (SFV) are two alphaviruses that have a high degree of ami
218 avirulent and virulent Semliki Forest virus (SFV) as well as West Nile virus infection and demonstrat
219 those belonging to the Semliki Forest virus (SFV) clade, have PSs which can be recognized by the caps
220 ponding regions of the Semliki Forest virus (SFV) E2 (domains A, B, and C) substituted into the CHIKV
221 ALV-B and pH-dependent Semliki Forest virus (SFV) entered cells with slower uptake kinetics than HIV-
222 licase protein nsP2 of Semliki Forest virus (SFV) has a 648RRR nuclear localization signal and is tra
223 ous DIII proteins from Semliki Forest virus (SFV) has been shown to inhibit E1 hairpin formation and
224 dies of the alphavirus Semliki Forest virus (SFV) here demonstrated that there was a strong requireme
229 e enveloped alphavirus Semliki Forest virus (SFV) infects cells via a low pH-triggered membrane fusio
231 e enveloped alphavirus Semliki Forest virus (SFV) infects cells via a low-pH-triggered membrane fusio
232 e enveloped alphavirus Semliki Forest virus (SFV) infects cells via a membrane fusion reaction mediat
233 tein of the alphavirus Semliki Forest virus (SFV) is a class II fusion protein that mediates low pH-t
241 itis virus (VSV) and a Semliki Forest virus (SFV) replicon (SFVG) that propagates through expression
242 riants of both SIN and Semliki Forest virus (SFV) replicons encoding the neomycin resistance gene tha
244 ar stomatitis (VSV) or Semliki Forest virus (SFV) that require delivery to acidic endosomes to penetr
245 ed influenza virus and Semliki Forest virus (SFV) to define a role for protein kinase C betaII (PKCbe
246 ike protein subunit of Semliki Forest virus (SFV) triggers membrane fusion upon exposure to mildly ac
250 ng genes inserted into Semliki Forest virus (SFV) vectors generate a large fraction of defective ribo
252 2 envelope proteins of Semliki Forest virus (SFV) were fused to voltage-clamped planar lipid bilayer
253 r alphaviruses such as Semliki Forest virus (SFV), acidic pH initiates a series of conformational cha
254 monitor the budding of Semliki Forest virus (SFV), an enveloped alphavirus that buds from the plasma
256 s widely accepted that Semliki Forest virus (SFV), an enveloped virus, requires this pathway there ar
260 tudies have shown that Semliki Forest virus (SFV)-infected delta-knock-out (KO) mice did not exhibit
266 The A7(74) strain of Semliki Forest virus (SFV; genus Alphavirus) is avirulent in adult mice, while
268 .8%) of infection with simian foamy viruses (SFV) among humans occupationally exposed to nonhuman pri
270 ssion of Old World NHP simian foamy viruses (SFV) has been documented, leading to nonpathogenic persi
274 spread rapidly throughout the brain, whereas SFV-RDR infection was confined to small foci of cells.
276 esults indicate that while immunization with SFV-SIVgp160 and rgp120 did not protect against virus in
277 CTL lysis of target cells infected with SFV encoding nucleocapsid was major histocompatibility c
278 cantly different between cells infected with SFV expressing green fluorescent protein (GFP) or GFP pl
281 study documents more frequent infection with SFV than with other simian retroviruses in persons worki
282 after intratumoral injection of WT mice with SFV-IL12, this did not occur in mice where IFNAR was ina
284 holesterol and sphingolipid dependent for wt SFV and strikingly less cholesterol dependent for srf-3.
285 had growth properties similar to those of wt SFV and showed modest change or no change in the pH depe
286 wing that superinfection of PI cells with wt SFV triggered the shutdown of minus-strand synthesis, wh
287 tidines by mutagenesis of the wild-type (wt) SFV infectious clone to create virus mutants with E1 H3A
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