ライフサイエンスコーパス: EIAV

1 EIAV and HIV vectors transduced equivalent numbers of pr

2 EIAV causes a uniquely dynamic disease that is character

3 EIAV encoding enhanced green fluorescent protein (eGFP)

4 EIAV NC mutants lost interactions with Bro1 and failed t

5 EIAV Rev is characterized by a high rate of genetic vari

6 EIAV vectors are able to efficiently transduce rod and c

7 EIAV(17SU), containing only the TM/Rev region from the a

8 EIAV(vMA-1c) superinfection of ED cells results in a bui

9 EIAV-based gene transfer of eGFP is highly efficient and

10 EIAV-derived vectors devoid of S2 are less susceptible t

11 al neutralizing domain variants of groups 1 (EIAV(PND-1)) and 5 (EIAV(PND-5)), respectively; however,

12 studies of equine infectious anemia virus-1 (EIAV) reverse transcriptase (RT) showed two effects of D

13 However, in contrast to HIV-1, EIAV Gag release is insensitive to TSG101 depletion and

14 Similarly, expression of the HIV-1/EIAV Gag-binding domain of Alix (Alix-V) did not disrupt

15 in variants of groups 1 (EIAV(PND-1)) and 5 (EIAV(PND-5)), respectively; however, the neutralization-

16 determine if proteasome inactivation affects EIAV release from chronically infected cells.

17 PTAP or PPPY dependent; (iii) budding of all EIAV clones is blocked by dominant negative Vps4; and (i

18 Although EIAV provides an important animal model for lentivirus d

19 , VPS28, can restore efficient release of an EIAV Gag late-domain mutant.

20 all three proteins bound both the HIV-1 and EIAV nucleocapsid protein specifically in vitro.

21 nd L domain-defective particles of HIV-1 and EIAV to examine whether the HIV-2 Env EVR function was a

22 ev-response element [RRE]) used by HIV-1 and EIAV with the hepatitis B virus posttranscriptional regu

23 The LTRs of EIAV(19) and EIAV(17) differ by 16 nucleotides in the transcriptional

24 ats (LTRs) and produce viruses (EIAV(19) and EIAV(17), respectively) of dramatically different virule

25 dependency ranking of SIV > HIV-1 > BIV and EIAV > MLV, RSV, and FIV.

26 Concerted BIV and EIAV integration resulted in 5 bp duplications of the ta

27 mutation in the virulent proviral clone, and EIAV(PR)DeltaS2 derived from a reference avirulent provi

28 lease is insensitive to TSG101 depletion and EIAV particles do not contain significant levels of TSG1

29 l for sufficient ribosomal frameshifting and EIAV replication, while concomitant alterations in the a

30 AIP1 also binds the HIV-1 p6(Gag) and EIAV p9(Gag) proteins, indicating that it can function d

31 tinct region in the L domain of HIV-1 p6 and EIAV p9 to ESCRT-III.

32 y proteasome inhibitors, while EIAV/PTAP and EIAV/PPPY release is strongly disrupted by these compoun

33 Retroviruses, including HIV-1, SIV, and EIAV, bind and recruit ALIX through YPX(n)L late-domain

34 omparative study of three related attenuated EIAV proviral vaccine strains: the previously described

35 binant HIV-1 CA-NC proteins and to authentic EIAV core particles.

36 uggests either that equine cells infected by EIAV in vivo do not express active A3 proteins or that E

37 ic lentivirus and indicate that infection by EIAV may be mediated by a single receptor, in contrast t

38 the mechanism of resistance that is used by EIAV to prevent superinfection and explored the means by

39 We found that the cellular receptor used by EIAV, equine lentivirus receptor 1 (ELR1), remains on th

40 with a reference virulent biological clone, EIAV(PV).

41 ference infectious molecular proviral clone, EIAV(uk).

42 taS2 derived from a virulent proviral clone, EIAV(UK)DeltaS2/DU containing a second gene mutation in

43 virion budding from a replication-competent EIAV variant with its L domain replaced by the HIV PTAP

44 In contrast, EIAV Gag polyproteins synthesized from mRNA exported via

45 In contrast, EIAV-resistant human, murine, and simian cells were nega

46 rates of evolution of the previously defined EIAV gp90 variable domains demonstrated distinct differe

47 re revealed in human cells for Rev-dependent EIAV and HIV-1 Gag polyproteins.

48 al vaccine strains: the previously described EIAV(UK)DeltaS2 derived from a virulent proviral clone,

49 production and processing to provirus during EIAV infection, in addition to its previously defined ro

50 on PTAP; (ii) the release of wild-type EIAV (EIAV/WT) is insensitive to TSG-3', whereas this C-termin

51 n contrast, a superinfecting strain of EIAV, EIAV(vMA-1c), utilizes two mechanisms of entry.

52 An activity that enables EIAV to tolerate exposure to proteasome inhibitors was m

53 gion of helix alpha1 constituted an expanded EIAV-CA(N) oligomeric interface and overlapped with the

54 early and late endocytic proteins facilitate EIAV production mediated by either YPDL or PTAP L domain

55 entedly, in the presence of the host factor, EIAV IN almost exclusively catalyzed concerted integrati

56 n oligomerization, independent to the faster EIAV-CA(C) domain dimerization.

57 ntify specific motifs that are essential for EIAV Rev activity.

58 In addition, the data define a function for EIAV p9 in the infectivity of virus particles, indicatin

59 sly shown that these sites are important for EIAV LTR activity in primary macrophages.

60 nants of Gag-Pol frameshifting necessary for EIAV replication, reveal novel aspects relative to frame

61 elements within the enhancer are needed for EIAV replication in macrophages.

62 essed in various equine cells permissive for EIAV replication in vitro, including monocytes and macro

63 ntified and cloned a functional receptor for EIAV, designated equine lentivirus receptor-1 (ELR1), re

64 We found that a low-pH step was required for EIAV infection of tissue culture cell lines as well as p

65 ntry, we examined the entry requirements for EIAV into two different cells: equine dermal (ED) cells

66 g is monoubiquitinated, the requirements for EIAV release are somewhat different from those for retro

67 time, differential levels of restriction for EIAV and human immunodeficiency virus type 1 (HIV-1) rep

68 imal PU.1 site is the most critical site for EIAV LTR activity in the presence of Tat, other elements

69 s evident in SU sequences obtained from four EIAV-infected immunocompetent foals.

70 data indicate that transgene expression from EIAV vectors is limited by the instability of vector-der

71 rovirus glycoGag, the accessory protein from EIAV is an example of a retroviral virulence determinant

72 Furthermore, Tat from EIAV functions in equine and canine cells but not in hum

73 Finally, we demonstrate that fusing EIAV Gag directly with another cellular component of the

74 Subretinal injections of EIAV-CMV-GFP, EIAV-RK-GFP (photoreceptor specific), EIAV-CMV-MYO7A (Us

75 erarchy: FIV, HIV-1, and BIV > SIV and MLV > EIAV.

76 ID), followed by challenge with a homologous EIAV stock.

77 AIP1 also binds to the L domain in EIAV p9, and this binding correlates perfectly with L do

78 low-pH constraint implicates endocytosis in EIAV entry.

79 however, no corresponding loss was found in EIAV-transduced equine cells.

80 Photoreceptor function in EIAV-CMV-MYO7A treated eyes was determined by evaluating

81 o identify the endocytic pathway involved in EIAV entry, we examined the entry requirements for EIAV

82 revealed new functional properties of p9 in EIAV replication, not previously elucidated by Gag polyp

83 ly unrecognized role for this Gag protein in EIAV replication.

84 o determine the role of these three sites in EIAV LTR activity.

85 A self-inactivating EIAV minimal lentiviral vector that expresses tyrosine h

86 ck organelle acidification failed to inhibit EIAV entry into the same target cells.

87 as hA3G, although only the latter inhibited EIAV infectivity.

88 d AIP-1/ALIX depletion specifically inhibits EIAV YPDL-type L-domain function.

89 risingly, eA3F1 and eA3F2 were packaged into EIAV and HIV-1 virions as effectively as hA3G, although

90 blocked by dominant negative Vps4; and (iv) EIAV/WT release is not impaired by proteasome inhibitors

91 Like EIAV RT, HIV RT showed lower burst amplitudes on CTS-con

92 into common cellular processes that mediate EIAV budding and infectivity, respectively.

93 vealed additive suppression of YPDL-mediated EIAV budding.

94 subunit specifically inhibited YPDL-mediated EIAV budding; (iii) virion budding from a replication-co

95 or SIVagm, whilst AGM cells restrict N-MLV, EIAV, HIV-1, HIV-2 and SIVmac.

96 relaxation time ratios T1/T2 for a monomeric EIAV-CA in the presence of oligomerization equilibrium.

97 ults show a dominant population of monomeric EIAV MA at a concentration of 63 microM and 20 degrees C

98 pressed, including in cells that are natural EIAV targets.

99 Neither EIAV(17SU) nor EIAV(17TM) produced lethal disease when a

100 Neither EIAV(17SU) nor EIAV(17TM) produced lethal disease when administered at

101 ulatory element (PRE) altered HIV-1, but not EIAV, Gag assembly sites and budding efficiency in human

102 s where no detectable superinfection occurs, EIAV(vMA-1c) entry that is low-pH dependent occurs throu

103 ls but only modestly affected the ability of EIAV(vMA-1c) to enter and kill previously infected ED ce

104 ancer that was associated with adaptation of EIAV to endothelial cells and fibroblasts.

105 Our analysis of EIAV assembly demonstrates that EIAV Gag release is bloc

106 CRD1 as essential for functional binding of EIAV gp90 and for virus infection of transduced Cf2Th ce

107 teasome inhibitors to disrupt the budding of EIAV particles bearing each of the three types of L doma

108 101 fragment potently impairs the budding of EIAV when it is rendered PTAP or PPPY dependent; (iii) b

109 so examined the role of NC in the budding of EIAV, a retrovirus relying exclusively on the (L)YPX(n)L

110 better understand the critical components of EIAV vaccine efficacy, we examine here the relationship

111 Long-term culture of EIAV-transduced human cells showed a significant decreas

112 Subretinal delivery of EIAV-CMV-MYO7A (UshStat) rescues photoreceptor phenotype

113 phenotypes and to define the determinants of EIAV envelope neutralization specificity.

114 further define the envelope determinants of EIAV neutralization specificity, we examined the neutral

115 to identifying potential Env determinants of EIAV vaccine efficacy and demonstrating the profound eff

116 animals, while a similar infectious dose of EIAV(17TM) (which derives SU from the avirulent parent)

117 e assembly sites and budding efficiencies of EIAV and HIV-1 Gag in both human and rodent cells.

118 ernal vesicles inhibited productive entry of EIAV.

119 ric clones indicate that both LTR and env of EIAV(17) are required for the development of severe acut

120 ains are contained within the second exon of EIAV Rev.

121 ticipates in the initial trimer formation of EIAV MA, but more importantly, the concentration effect

122 then identified the envelope glycoprotein of EIAV as a determinant that also modulates retroviral sus

123 The observed inhibition of EIAV entry was shown not to be related to cytotoxicity.

124 microscopy confirmed that the inhibition of EIAV production correlated temporally over several days

125 both eA3F1 and eA3F2 are weak inhibitors of EIAV.

126 Subretinal injections of EIAV-CMV-GFP, EIAV-RK-GFP (photoreceptor specific), EIAV

127 omains and suggest that the insensitivity of EIAV to proteasome inhibitors is conferred by the L doma

128 ng utilized, the internalization kinetics of EIAV is rapid with 50% of cell-associated virions intern

129 The LTRs of EIAV(19) and EIAV(17) differ by 16 nucleotides in the tr

130 ) RNA copies/ml) and a similar maturation of EIAV envelope-specific antibody responses as determined

131 Thus, the mechanism of EIAV budding may not be substantially different from tha

132 medium dramatically decreased the number of EIAV antigen-positive cells.

133 yclin T1 supported productive replication of EIAV and produced infectious virions at levels similar t

134 Bro1-mediated rescue of EIAV release required the wild-type NC.

135 To elucidate further the role of EIAV p9 in virus assembly and replication, we have exami

136 e immunity primarily drives the selection of EIAV SU variants, but also they demonstrate that other s

137 ed the replication properties of a series of EIAV proviral mutants in which the parental YPDL L domai

138 The specificity of EIAV entry into these various cells was determined by as

139 duction, we have examined the specificity of EIAV p9 binding to endocytic factors and the effects on

140 summary, in vitro selection for a strain of EIAV that rapidly killed cells resulted in the generatio

141 In contrast, a superinfecting strain of EIAV, EIAV(vMA-1c), utilizes two mechanisms of entry.

142 d from an avirulent, noncytopathic strain of EIAV, MA-1.

143 A superinfecting variant strain of EIAV, vMA-1c, did not require a low-pH step for producti

144 ed the entry mechanism of several strains of EIAV and found that both macrophage-tropic and tissue cu

145 prevented entry of the wild-type strains of EIAV into two permissive cell populations.

146 re, we demonstrate that wild-type strains of EIAV require a low-pH step for productive entry.

147 ine fibroblasts compared to other strains of EIAV.

148 growth curves and relative fitness scores of EIAVs of principal neutralizing domain variants of group

149 titrated by coinfections with FIV, HIV-1, or EIAV virus-like particles.

150 eptor specific), EIAV-CMV-MYO7A (UshStat) or EIAV-CMV-Null (control) vectors were performed in shaker

151 viral gene expression, suggesting that other EIAV proteins can at least in part mediate late budding

152 eplication-competent E32 mutant and parental EIAV(UK) viruses.

153 ld higher than a lethal dose of the parental EIAV(17).

154 uses that replicated as well as the parental EIAV(uk) in transfected ED cells.

155 rus that spontaneously arose during passage, EIAV(vMA-1c), can circumvent this mechanism in some cell

156 Cathepsin inhibitors did not prevent EIAV entry, suggesting that the low-pH step required by

157 these same interference treatments prevented EIAV(vMA-1c) infection of endothelial cells but only mod

158 ubretinally delivered UshStat, a recombinant EIAV-based lentiviral vector expressing human MYO7A, on

159 ed SU sequences from an immune-reconstituted EIAV-infected SCID foal.

160 ively; however, the neutralization-resistant EIAV(PND-5) variant was less infectious in single-round

161 neutralization phenotypes of the sequential EIAV envelope variants, we determined the sensitivity of

162 However, specific EIAV nucleotide or amino acid changes that are responsib

163 V-GFP, EIAV-RK-GFP (photoreceptor specific), EIAV-CMV-MYO7A (UshStat) or EIAV-CMV-Null (control) vect

164 nduced by a homologous Env challenge strain (EIAV(PV)) was recently tested in ponies to determine the

165 MR spectroscopy is perfectly suited to study EIAV-CA that dimerizes weaker than HIV-1-CA.

166 for the EIAV slippery sequence in supporting EIAV replication.

167 omoted transfers with higher efficiency than EIAV RT.

168 It therefore appears that EIAV has evolved a novel mechanism to specifically neutr

169 In cells such as ED cells that EIAV(vMA-1c) is able to superinfect, viral entry is pH i

170 e results of these studies demonstrated that EIAV entry into all cell types was substantially inhibit

171 analysis of EIAV assembly demonstrates that EIAV Gag release is blocked by inhibition of the VPS pat

172 We found that EIAV late budding defects were rescued by overexpression

173 These findings indicate that EIAV(vMA-1c) retains the ability to use ELR1 for entry a

174 l susceptibility to SERINC5, indicating that EIAV has a bimodal ability to counteract the host factor

175 vo do not express active A3 proteins or that EIAV has developed a novel mechanism to avoid inhibition

176 These findings suggest that EIAV Rev utilizes a bipartite RNA-binding domain.

177 Thus, these data suggest that EIAV variation can be associated predominantly with ongo

178 surface-exposed helix of Ub, suggesting that EIAV Gag may have captured a function that allows it to

179 observations reveal for the first time that EIAV p9 is not absolutely required for virus budding in

180 e experiments reveal for the first time that EIAV receptor-mediated entry into target cells is via a

181 The EIAV-CMV-MYO7A vector protected the shaker1 mouse photor

182 It allowed the EIAV RT to make a distribution of cuts, greatly stimulat

183 logenetic analysis of the same data, and the EIAV rev variants were partitioned into two overlapping

184 ning the functional interactions between the EIAV SU protein (gp90) and its ELR1 receptor, we mapped

185 red a functional late (L) domain, either the EIAV YPDL L-domain or the proline-rich L domains derived

186 emonstrate that NIH 3T3 cells expressing the EIAV receptor ELR1 and equine cyclin T1 supported produc

187 visna virus were able to substitute for the EIAV slippery sequence in supporting EIAV replication.

188 agrees with the atomic coordinates from the EIAV MA crystal structure.

189 of the functions of the YPDL L domain in the EIAV life cycle can be replaced by replacement of the pa

190 detail the role of the YPDL L domain in the EIAV life cycle, we have examined the replication proper

191 Loop region between Helix2 and Helix3 in the EIAV MA.

192 results indicated that the evolution of the EIAV envelope sequences observed during sequential febri

193 in sequences in the C-terminal region of the EIAV MA protein.

194 1) motif and potential ubiquitination of the EIAV p9 protein, mutations of these lysine residues to m

195 embly, but not infectivity, functions of the EIAV proviral YPDL substitution mutants can be partially

196 The specificity of the EIAV SU binding domain identified for the ELR1 receptor

197 derived RNA transcripts and silencing of the EIAV vectors over time.

198 In the context of the EIAV(17) LTR, SU appears to have a greater impact on vir

199 Additional investigations of the EIAV(wyo) LTR were performed in vivo to determine if LTR

200 r1 mice following subretinal delivery of the EIAV-CMV-GFP/MYO7A vectors.

201 ater levels of EGFP protein and RNA than the EIAV-transduced cells.

202 vations indicate for the first time that the EIAV Gag p9 protein performs a critical role in viral DN

203 These results indicated that the EIAV gp90 V3 and V4 domains individually conferred serum

204 Thus, these data demonstrate that the EIAV S2 gene provides an optimal site for modification t

205 together, these results demonstrate that the EIAV vectors transduced human cells with efficiencies si

206 en together, these data demonstrate that the EIAV YPDL L domain mediates distinct functions in viral

207 R over that time period, indicating that the EIAV(wyo) LTR was evolutionarily stable in vivo.

208 -(409-715) was sufficient for binding to the EIAV YPDL motif; (ii) overexpression of AIP1/Alix or AP-

209 cro-millisecond exchange kinetics due to the EIAV-CA(N) domain oligomerization, independent to the fa

210 n of binding and functional assays using the EIAV SU gp90 protein and various chimeric receptor prote

211 oreover, insensitivity was observed when the EIAV Gag protein was expressed in the absence of all the

212 old higher with the HIV vector than with the EIAV vector.

213 fectious anemia virus reverse transcriptase (EIAV RT), was evaluated by pre-steady-state kinetic tech

214 dence on PTAP; (ii) the release of wild-type EIAV (EIAV/WT) is insensitive to TSG-3', whereas this C-

215 Additionally, interference of wild-type EIAV binding to ELR1 by the addition of either anti-ELR1

216 nfected with EIAV, suggesting that wild-type EIAV interferes with superinfection by masking ELR1.

217 g that the low-pH step required by wild-type EIAV is not required to activate cellular cathepsins.

218 efore, a dopamine replacement strategy using EIAV has been investigated as a treatment in the 6-hydro

219 uine infectious anemia virus (EIAV) vaccine (EIAV(D9)) capable of protecting 100% of horses from dise

220 an experimental attenuated proviral vaccine, EIAV(UK)deltaS2, based on inactivation of the S2 accesso

221 previously defined panel of natural variant EIAV envelope isolates from sequential febrile episodes

222 the disease potential of the highly virulent EIAV(17).

223 orses challenged with the reference virulent EIAV(PV) by using a low-dose multiple-exposure protocol

224 ly immunized horses by our standard virulent EIAV(PV) strain by using a low-dose multiple exposure pr

225 virulent, macrophage-tropic strain of virus EIAV(wyo) to identify LTR changes associated with altera

226 pseudotyped equine infectious anaemia virus (EIAV) based vectors encoding a marker gene to the rat st

227 n encoded by equine infectious anemia virus (EIAV) acts by recruiting AIP-1/ALIX and expression of a

228 roteins from equine infectious anemia virus (EIAV) as an example, demonstrates a linear extrapolation

229 inhibitors, equine infectious anemia virus (EIAV) budding is not affected by these agents.

230 el strain of equine infectious anemia virus (EIAV) called vMA-1c that rapidly and specifically killed

231 L domain of equine infectious anemia virus (EIAV) contains a Yxxtheta motif that interacts with AP-2

232 c strains of equine infectious anemia virus (EIAV) contains three PU.1 binding sites, namely an invar

233 19/wenv17 of equine infectious anemia virus (EIAV) differ in env and long terminal repeats (LTRs) and

234 y pathway of equine infectious anemia virus (EIAV) during infection of its natural target, equine mac

235 e lentivirus equine infectious anemia virus (EIAV) encodes the small protein S2, a pathogenic determi

236 patterns of equine infectious anemia virus (EIAV) envelope variation during a 2.5-year period in exp

237 e budding of equine infectious anemia virus (EIAV) from infected equine cells is largely unaffected b

238 eal that the equine infectious anemia virus (EIAV) Gag p9 protein provides a late assembly function m

239 tem based on equine infectious anemia virus (EIAV) gives rise to highly efficient and sustained trans

240 mechanism of equine infectious anemia virus (EIAV) has yet to be examined.

241 , studies of equine infectious anemia virus (EIAV) have indicated alternative cellular pathways and c

242 vaccines to equine infectious anemia virus (EIAV) have revealed a broad spectrum of efficacy ranging

243 Equine infectious anemia virus (EIAV) infection of horses is characterized by recurring

244 Equine infectious anemia virus (EIAV) infection of horses is characterized by well-defin

245 (N-MLV) and equine infectious anemia virus (EIAV) infection, promotion of higher-order association r

246 e lentivirus equine infectious anemia virus (EIAV) into cells requires a low-pH step.

247 Equine infectious anemia virus (EIAV) is a lentivirus that causes persistent infection i

248 Equine infectious anemia virus (EIAV) is a lentivirus with in vivo cell tropism primaril

249 L domain of equine infectious anemia virus (EIAV) is apparently unique in its reported ability to in

250 Equine infectious anemia virus (EIAV) is unique among enveloped viruses studied to date

251 (HIV-1) and equine infectious anemia virus (EIAV) L domain-derived peptides.

252 us (HIV) and equine infectious anemia virus (EIAV) lentiviral vectors in a variety of human cell type

253 Using the equine infectious anemia virus (EIAV) lentivirus model system, we previously demonstrate

254 myristylated equine infectious anemia virus (EIAV) MA and its interaction with PIP2-C4 primarily usin

255 nfected with equine infectious anemia virus (EIAV) neutralized homologous virus and several envelope

256 We examined equine infectious anemia virus (EIAV) particles and found that approximately 2% of the p

257 us (HIV) and equine infectious anemia virus (EIAV) particles.

258 e strains of equine infectious anemia virus (EIAV) prevent superinfection of previously infected cell

259 us (MVV) and equine infectious anemia virus (EIAV) readily interacted with LEDGF.

260 sting of the equine infectious anemia virus (EIAV) regulatory gene rev.

261 Equine infectious anemia virus (EIAV) Rev is an essential regulatory protein that facili

262 9 protein of equine infectious anemia virus (EIAV) revealed a progressive loss in replication phenoty

263 variants of equine infectious anemia virus (EIAV) that differed in sensitivity to broadly neutralizi

264 Vmac239) and equine infectious anemia virus (EIAV) the most dependent and human immunodeficiency viru

265 e lentivirus equine infectious anemia virus (EIAV) to investigate the cellular restrictions for lenti

266 ruses except equine infectious anemia virus (EIAV) use the small accessory protein Vif to counteract

267 9 protein of equine infectious anemia virus (EIAV) utilizes a unique YPDL motif as a late assembly do

268 e attenuated equine infectious anemia virus (EIAV) vaccine (EIAV(D9)) capable of protecting 100% of h

269 protein from equine infectious anemia virus (EIAV), a lentivirus sharing the same cone-shaped capsid

270 DL) motif in equine infectious anemia virus (EIAV), and a related sequence in HIV-1, bind the endosom

271 (HIV-1) and equine infectious anemia virus (EIAV), and inhibits the accumulation of viral reverse tr

272 vaccine for equine infectious anemia virus (EIAV), based on mutation of the viral S2 accessory gene,

273 ct N-MLV and equine infectious anemia virus (EIAV), but not HIV-1, HIV-2, SIVmac or SIVagm, whilst AG

274 s, including equine infectious anemia virus (EIAV), exclusively infect cells of the monocyte-macropha

275 virus (BIV), equine infectious anemia virus (EIAV), feline immunodeficiency virus (FIV), and Rous sar

276 lentivirus, equine infectious anemia virus (EIAV), occurs in most infected horses and involves MHC c

277 virus (FIV), equine infectious anemia virus (EIAV), or N-tropic murine leukemia virus (MLV) postentry

278 Equine infectious anemia virus (EIAV), uniquely among lentiviruses, does not encode a vi

279 Using equine infectious anemia virus (EIAV), we now demonstrate differential effects of cellul

280 tarGen is an equine infectious anemia virus (EIAV)-based lentiviral vector that expresses the photore

281 viral vector equine infectious anemia virus (EIAV).

282 receptor for equine infectious anemia virus (EIAV).

283 (HIV-1), and equine infectious anemia virus (EIAV).

284 g protein of equine infectious anemia virus (EIAV).

285 AV2)/GDNF or equine infectious anemia virus (EIAV)/GDNF into the caudate.

286 eshifting in equine anemia infectious virus (EIAV) by using full-length provirus replication and Gag/

287 e 1 [HIV-1], equine infectious anemia virus [EIAV]) and unrestricted (NB-tropic murine leukemia virus

288 terminal repeats (LTRs) and produce viruses (EIAV(19) and EIAV(17), respectively) of dramatically dif

289 er hand, virion production was enhanced when EIAV-infected cells were incubated briefly (2 h) with th

290 First, virion production was reduced when EIAV-infected cells were treated with phallacidin, a cel

291 , HIV-1 RT made closely spaced cuts, whereas EIAV RT made only a single cut.

292 To define further the mechanisms by which EIAV adapts vesicle trafficking machinery to facilitate

293 perinfection and explored the means by which EIAV(vMA-1c) overcomes this restriction.

294 not impaired by proteasome inhibitors, while EIAV/PTAP and EIAV/PPPY release is strongly disrupted by

295 s to define viral parameters associated with EIAV-induced cell killing and begin to explore the mecha

296 t prior infection of equine fibroblasts with EIAV did not alter the ability of vMA-1c to infect and k

297 studies demonstrated that immunization with EIAV(UK)deltaS2 elicited mature virus-specific immune re

298 e surface of cells chronically infected with EIAV, suggesting that wild-type EIAV interferes with sup

299 d immunodeficient (SCID) foals infected with EIAV.

300 Comparison between the wild-type (wt) EIAV-CA and a variant lacking the beta-hairpin structure