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 1 restriction, we find that MLV glycoGag and EIAV S2 proteins, which, like Nef, antagonize SERINC-med

32 , specifically, HIV-1 Nef, MLV glycoGag, and EIAV S2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 low-pH constraint implicates endocytosis in EIAV entry.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 vealed additive suppression of YPDL-mediated EIAV budding.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 101 fragment potently impairs the budding of EIAV when it is rendered PTAP or PPPY dependent; (iii) b

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

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

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

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

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

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

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

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

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

119 ernal vesicles inhibited productive entry of EIAV.

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

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

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

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

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

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

126 both eA3F1 and eA3F2 are weak inhibitors of EIAV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 ine fibroblasts compared to other strains of EIAV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 for the EIAV slippery sequence in supporting EIAV replication.

168 omoted transfers with higher efficiency than EIAV RT.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 -(409-715) was sufficient for binding to the EIAV YPDL motif; (ii) overexpression of AIP1/Alix or AP-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 19/wenv17 of equine infectious anemia virus (EIAV) differ in env and long terminal repeats (LTRs) and

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

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

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

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

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

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

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

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

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

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 2 protein of equine infectious anemia virus (EIAV), and the Nef protein of human immunodeficiency vir

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

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

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

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

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

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

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

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

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

282 viral vector equine infectious anemia virus (EIAV).

283 receptor for equine infectious anemia virus (EIAV).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

300 d immunodeficient (SCID) foals infected with EIAV.

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