ライフサイエンスコーパス: FeLV

1 FeLV subgroup A (FeLV-A) is transmitted in natural infec

2 FeLV-945 is a representative isolate of the natural feli

3 FeLV-945 was previously identified as a natural isolate

4 FeLV-945, the predominant isolate associated with non-T-

5 FeLV-A receptor specificity was maintained when changes

6 FeLV-B evolves from FeLV-A in the infected cat through a

7 FeLV-B SUs can functionally substitute for FeLIX in medi

8 FeLV-B was subject to G-->A hypermutation with a predomi

9 FeLV-Bs have been shown to infect cells using the Pit1 r

10 FeLV-T is the first example of a naturally occurring typ

11 Subgroup A FeLV (FeLV-A) is the virus that is transmitted from cat

12 ated the virus to be an ecotropic subgroup A FeLV with 98% nucleotide sequence homology to another Fe

13 horizontally transmissible FeLV subgroup A (FeLV-A) but was found to differ from a prototype to a la

14 FeLV subgroup A (FeLV-A) is transmitted in natural infections, and FeLV s

15 ransmitted feline leukemia virus subgroup A (FeLV-A) often produce mutants (termed FeLV-C) that bind

16 acid change, the resulting viruses acquired FeLV-T receptor specificity.

17 ably, we find that Fr-MLV RBD also activates FeLV-T infection of cells expressing the Fr-MLV receptor

18 ovirus entry and the interrelationship among FeLV variants that evolve in vivo.

19 Since the TM genes of FeLV-945 and FeLV-A/61E are nearly identical but the SU genes differ

20 rface (SU) envelope proteins from FeLV-A and FeLV-B, and testing their infectivity, we have defined g

21 ubgroup conversion from FeLV-A to FeLV-A and FeLV-B, as determined by the interference assay, appeare

22 ap the determinants for cofactor binding and FeLV-T infection.

23 Pit1-mediated cellular infection by GALV and FeLV-B.

24 A) is transmitted in natural infections, and FeLV subgroups B, C, and T can evolve directly from FeLV

25 er study suggested that the VRA of A-MLV and FeLV-B functionally interact with the presumptive extrac

26 ombinant containing the U3 region of another FeLV that lacks repetitive URE sequences, none of which

27 98% nucleotide sequence homology to another FeLV-A clone (F6A/61E), which had also been fully sequen

28 Following immunization, anti-FeLV antibodies were not detected in any kitten.

29 nate the possibility of coinoculation of any FeLV-B which may be present in the inoculum prepared by

30 As FeLV-C impairs the in vivo differentiation of burst-form

31 In some cases, such as FeLV-T, a nonclassical receptor that includes both a tra

32 er simple retroviruses, including subgroup B FeLV (FeLV-B), and FeLIX is a secreted cellular protein

33 roteins of feline leukemia virus subgroup B (FeLV-B) and amphotropic murine leukemia virus (A-MLV) ar

34 fact that feline leukemia virus subgroup B (FeLV-B) and amphotropic murine leukemia virus (A-MLV) ha

35 (GALV) and feline leukemia virus subgroup B (FeLV-B) can use the same receptor, Pit1, to infect human

36 strains of feline leukemia virus subgroup B (FeLV-B), we compared the binding and infectivity pattern

37 n (RBD) of feline leukemia virus subgroup B (FeLV-B).

38 ction, and an additional interaction between FeLV-B VRB and Pit1 loop 2 is essential.

39 at there may be a direct interaction between FeLV-T and the Pit1 receptor.

40 sequences may influence interactions between FeLV-B SU and the human Pit2 receptor.

41 eks p.i., with all tumor DNAs harboring both FeLV-A and rFeLV proviruses.

42 In contrast, substitution of both FeLV-945 LTR and SU into FeLV-A/61E resulted in multicen

43 Moreover, these cells specifically bound FeLV-A-pseudotyped virus particles, indicating that the

44 ke mediated by feTHTR1 was indeed blocked by FeLV-A infection, and in feline fibroblasts that natural

45 the targeted destruction of erythroblasts by FeLV-C may derive from their greater sensitivity to this

46 required for cofactor-dependent infection by FeLV-T.

47 whether they also could mediate infection by FeLV-T.

48 ses, RD114 and feline leukemia virus type C (FeLV-C), were significantly higher than the level of gib

49 Feline leukemia virus-C (FeLV-C) causes red cell aplasia in cats, likely through

50 ins and pseudotype virions carrying chimeric FeLV-B/A-MLV envelopes, we show that FeLV-B and A-MLV VR

51 High levels of circulating FeLV-specific effector CTLs appeared before virus neutra

52 ecular clone, F6A, or a new molecular clone, FeLV-A, Rickard strain (FRA).

53 the first report of a replication-competent FeLV vector with high-level and stable expression of a t

54 the single-enhancer, triplication-containing FeLV LTR, typical of non-T-cell, non-B-cell lymphomas in

55 these results suggest that fusion-defective FeLV-T and GALV are restricted to homologous RBD rescue

56 ir ability to act as receptors for different FeLV-Bs.

57 to arise via recombination between ecotropic FeLV-A and endogenous FeLV (enFeLV) env elements, the in

58 nucleotide of the env gene in the ecotropic FeLV-A Rickard (FRA) provirus.

59 atterns of retrovirus vectors bearing either FeLV-B-90Z or FeLV-B-GA envelopes.

60 ays, we engineered mutations found in either FeLV-A/T or FeLV-T, individually and in combination, int

61 cient transduction of human HSCs with either FeLV-C- or RD114-pseudotyped retroviral particles may im

62 tion between ecotropic FeLV-A and endogenous FeLV (enFeLV) env elements, the in vivo studies were con

63 ptor-binding domains derived from endogenous FeLV could render cells permissive for FeLV-T.

64 d cellular protein expressed from endogenous FeLV-related sequences (enFeLV).

65 ly, this arginine is not found in endogenous FeLV sequences or in recombinant viruses recovered from

66 parts, neither nearly full-length endogenous FeLV molecular clones (CFE-6 and CFE-16) nor their isola

67 hus suggest that the inability of endogenous FeLV LTRs in gene transactivation is not due to cell lin

68 nt study, we demonstrate that the endogenous FeLV LTRs do not generate LTR-specific RNA transcripts i

69 d simply by overexpression of the endogenous FeLV-C receptor homologue.

70 of N-terminal substitution of the endogenous FeLV-derived env sequences were detected at 8 weeks p.i.

71 nsactivational potential of these endogenous FeLV LTR sequences.

72 ity to undergo recombination with endogenous FeLV (enFeLV), leading to a high frequency of transition

73 ated recombinogenic activity with endogenous FeLV sequences in feline cells to produce polytropic rec

74 is derived by recombination with endogenous FeLV-like sequences, and its product can functionally su

75 Since endogenous FeLVs may affect the infectiousness or pathogenicity of

76 a feline leukemia virus retroviral Envelope (FeLV Env) protein for productive infection of feline AH9

77 re, infection of AH927 cells by an exogenous FeLV subgroup A virus did not induce production of such

78 oduction of an RNA transcript from exogenous FeLV LTRs correlates with their transactivational activi

79 ort, we show that the U3 region of exogenous FeLV LTRs can induce transcription from collagenase IV (

80 Unlike their exogenous FeLV counterparts, neither nearly full-length endogenous

81 like sequences that are related to exogenous FeLV LTRs.

82 infectiousness or pathogenicity of exogenous FeLVs, genomic variation in enFeLVs represents a candida

83 ity are strongly induced in cells expressing FeLV LTRs and that LTR-specific RNA transcripts are gene

84 derived cofactors can efficiently facilitate FeLV-T infection only of cells expressing Pit1, not of c

85 Subgroup A FeLV (FeLV-A) is the virus that is transmitted from cat to cat

86 ple retroviruses, including subgroup B FeLV (FeLV-B), and FeLIX is a secreted cellular protein expres

87 Since subgroup B polytropic FeLVs (FeLV-B) are known to arise via recombination between eco

88 The major determinant for FeLV-C-induced anemia has been mapped to a small region

89 enous FeLV could render cells permissive for FeLV-T.

90 The cell surface entry receptor for FeLV-A is a putative thiamine transporter (THTR1).

91 ceptor was also functional as a receptor for FeLV-A, albeit with reduced efficiency compared to the f

92 identification of the cellular receptor for FeLV-A, which is the most transmissible form of FeLV.

93 feTHTR2 does not function as a receptor for FeLV-A.

94 that the cDNA encodes a binding receptor for FeLV-A.

95 rotein that also functions as a receptor for FeLV-B.

96 cloned a putative cell surface receptor for FeLV-C (FLVCR) by using a human T-lymphocyte cDNA librar

97 The results suggest an important role for FeLV-specific CTLs in retroviral immunity and demonstrat

98 tion of FeLV-945 envelope gene sequences for FeLV-A/61E sequences conferred a small but statistically

99 that cofactor binding is not sufficient for FeLV-T infection and suggest that there may be a direct

100 ne Pit2 protein are likely to be targets for FeLV-B infection in the cat.

101 vo experiments: (i) subgroup conversion from FeLV-A to FeLV-A and FeLV-B, as determined by the interf

102 bgroups B, C, and T can evolve directly from FeLV-A by mutation and/or recombination with endogenous

103 feline leukemia viruses (FeLV-T) evolve from FeLV-A in infected animals and demonstrate host cell spe

104 FeLV-B evolves from FeLV-A in the infected cat through acquisition of cellul

105 chimeric surface (SU) envelope proteins from FeLV-A and FeLV-B, and testing their infectivity, we hav

106 ction may directly or indirectly result from FeLV-C binding to its receptor.

107 e for how FeLV-B species evolve in vivo from FeLV-A and present a new experimental approach for effic

108 ding frames are reminiscent of a functioning FeLV genome, and the 5' and 3' long terminal repeat sequ

109 hese results provide direct evidence for how FeLV-B species evolve in vivo from FeLV-A and present a

110 10 and 16 weeks postinoculation (p.i.); (ii) FeLV-B-like recombinants (rFeLVs), however, could be det

111 In FeLV infections, as in other retroviral infections, it i

112 nfected mice failed to detect any changes in FeLV U3 sequences other than that in the URE.

113 The mutational changes in FeLV-945 were shown to confer significant functional dif

114 tion, we studied the longitudinal changes in FeLV-specific cytotoxic T lymphocytes (CTLs) in a group

115 more detailed studies of the early events in FeLV transmission and may provide insights into FeLV pat

116 uncation in the env gene occurred de novo in FeLV lymphomagenesis and that such a product, tenv could

117 gin, the role that Pit1 and Pit2 may play in FeLV-B replication in the cat is unclear.

118 LTR) of this virus, like the LTRs present in FeLV proviruses from other cats with AML, contains an un

119 hat raising the plasma levels of thiamine in FeLV-infected cats may ameliorate the pathogenic effects

120 infection by these immunodeficiency-inducing FeLV-T variants.

121 vel T-cell cytopathic and syncytium-inducing FeLV in the host.

122 ced into the same cell type, as well as into FeLV-C-resistant rat (NRK 52E) cells, to verify its role

123 V transmission and may provide insights into FeLV pathogenesis.

124 nto a retroviral vector, was introduced into FeLV-C-resistant murine (NIH 3T3) cells.

125 Substitution of the FeLV-945 LTR into FeLV-A/61E resulted in a significantly more rapid diseas

126 Substitution of the FeLV-945 LTR into FeLV-A/61E resulted in pathogenesis indistinguishable fr

127 ubstitution of both FeLV-945 LTR and SU into FeLV-A/61E resulted in multicentric lymphoma of non-T-ce

128 orizontally transmissible prototype isolate, FeLV-A/61E.

129 Moreover, the U3 sequences of LC-FeLV were found to have about half as much transcription

130 rs to be specific to exogenous, leukemogenic FeLVs.

131 nctionally substitute for FeLIX in mediating FeLV-T infection.

132 nfected mice, those infected with the F-MuLV/FeLV recombinants were able to generate and replicate mi

133 feline leukemia virus (FeLV), which we named FeLV-A (Rickard) or FRA, was characterized with respect

134 es manifested striking similarity to natural FeLV-B isolates, within the mid-SU region of the env seq

135 These Env proteins used an unidentified non-FeLV receptor for entry.

136 e unit can direct entry via the nonclassical FeLV-T receptor pathway.

137 Endogenous, nonleukemogenic FeLV LTRs, therefore, do not transactivate cellular gene

138 is, although incompletely, in the absence of FeLV-945 LTR.

139 on interference, confirmed the assignment of FeLV-945 to subgroup A.

140 receptor, although in all cases, binding of FeLV-B SU to human Pit2 was weak.

141 ptor binding domain; however, in the case of FeLV-B-90Z, the C terminus also contributes to the recog

142 an explanation for the two major classes of FeLV-B that have been observed in vivo.

143 The vaccine consisting of FeLV DNA with the IL-12 and IL-18 genes conferred signif

144 t FeLIX is likely the primary determinant of FeLV-T tropism.

145 absence of other unique sequence elements of FeLV-945 to determine the disease spectrum.

146 relatively avirulent, transmissible form of FeLV, 61E.

147 V-A, which is the most transmissible form of FeLV.

148 in which the LTR and envelope (env) gene of FeLV-945, or the LTR only, was substituted for homologou

149 nes and the other expressing the env gene of FeLV-A/Glasgow-1.

150 Since the TM genes of FeLV-945 and FeLV-A/61E are nearly identical but the SU

151 Further, the impact of FeLV-945 env on the disease outcome was dependent on the

152 lenged by the intraperitoneal inoculation of FeLV-A/Glasgow-1 and were then monitored for a further 1

153 Libraries of FeLV Env proteins with random amino acid substitutions i

154 ences upstream of the enhancer in the LTR of FeLV may favor the activation of this promoter in myeloi

155 The LTR of FeLV-945 is unusual in that it contains only a single co

156 udy was undertaken to identify mechanisms of FeLV pathogenesis that might become evident by comparing

157 disease in a natural cohort, is a member of FeLV subgroup A but differs in sequence from the FeLV-A

158 otype to a larger extent than the members of FeLV-A differ among themselves.

159 blood CD34+ cells with equivalent numbers of FeLV-C and GALV or RD114 and GALV-pseudotyped retrovirus

160 meric envelope proteins encoding portions of FeLV-B could also enter cells by using a related recepto

161 The LTR enhancer sequences of FeLV contain identical binding sites for some of the tra

162 We determined the structure of FeLV-B RBD, which has FeLIX activity, to a 2.5-A resolut

163 There are four subgroups of FeLV, A, B, C, and T, each of which has a distinct recep

164 The substitution of FeLV-945 envelope gene sequences for FeLV-A/61E sequence

165 Thus, substitution of FeLV-945 U3 sequences into the M-MuLV long terminal repe

166 Substitution of FeLV-A/61E SU with that of FeLV-945 altered the clinical

167 mal human cell types are fully supportive of FeLV replication, innate resistance of blood cells could

168 murine leukemia virus (F-MuLV) with that of FeLV clone 33.

169 Substitution of FeLV-A/61E SU with that of FeLV-945 altered the clinical presentation and resulted

170 emia virus (Mo-MuLV) was replaced by that of FeLV-945, a provirus of unique long terminal repeat (LTR

171 pathogenesis indistinguishable from that of FeLV-A/61E, namely, thymic lymphoma of T-cell origin.

172 rminal repeat and envelope gene for those of FeLV-A/61E altered the disease spectrum entirely, from a

173 determining viral replication and tropism of FeLV-81T.

174 These findings thus suggest that the LTRs of FeLVs can independently activate transcription of specif

175 esents a candidate for genetic influences on FeLV leukemogenesis in cats.

176 rovirus vectors bearing either FeLV-B-90Z or FeLV-B-GA envelopes.

177 eas incubation with soluble RBDs from MLV or FeLV-B does not.

178 neered mutations found in either FeLV-A/T or FeLV-T, individually and in combination, into the backbo

179 t render these cells permissive to any other FeLV subgroup.

180 this virus was also novel compared to other FeLVs, including both the parental virus 61E and the imm

181 eins was greater than that found in parental FeLV isolates.

182 Since subgroup B polytropic FeLVs (FeLV-B) are known to arise via recombination betw

183 -acid changes all occur outside of predicted FeLV receptor-binding domains.

184 sent in the inoculum prepared by propagating FeLV-A in feline cell cultures.

185 nistered plasmid DNA of either the prototype FeLV, subgroup A molecular clone, F6A, or a new molecula

186 functional differences compared to prototype FeLV-A viruses.

187 ffers in sequence from the FeLV-A prototype, FeLV-A/61E, in the surface glycoprotein (SU) and long te

188 line cells to produce polytropic recombinant FeLV subgroup B-like viruses which also contained the IR

189 s the outcomes of infection with recombinant FeLVs in which the LTR and envelope (env) gene of FeLV-9

190 MLV and GALV RBDs are not able to render FeLV-T infectious.

191 tical but the SU genes differ significantly, FeLV-945 SU is implicated in the outcome.

192 loys Pit1 as a receptor but requires soluble FeLV RBD for entry.

193 Some FeLV-Bs infected cells expressing feline Pit2 and feline

194 Furthermore, the finding that some FeLV-Bs can use both Pit1 and Pit2 may explain previous

195 ive selection for the generation of specific FeLV-B recombinants, offering an explanation for the two

196 The specific FeLV-Bs described here, which can enter cells using eith

197 Specifically, FeLV-B SUs could efficiently mediate infection of cells

198 retrovirus feline leukemia virus subgroup T (FeLV-T) requires FeLIX, a cellular coreceptor that is en

199 oup A (FeLV-A) often produce mutants (termed FeLV-C) that bind to a distinct cell surface receptor an

200 tly of the presence of the N- and C-terminal FeLV-T receptor determinants.

201 ells expressing the Fr-MLV receptor and that FeLV-B RBD is a competitive inhibitor of infection under

202 The findings demonstrate that FeLV-945 SU alters pathogenesis, although incompletely,

203 arrow from recipient sheep demonstrated that FeLV-C- or RD114-pseudotyped vectors were present at sig

204 Evidence demonstrates that FeLV-945 SU and LTR are required together to fully recap

205 We also found that FeLV-B gp70 residues F60 and P61 and A-MLV residues Y60

206 y was undertaken to test the hypothesis that FeLV-945 SU can act in the absence of other unique seque

207 Our studies imply that FeLV-B VRA residues F60 and P61 interact with the Pit1 E

208 Pit2 may explain previous observations that FeLV-B and GALV, which primarily uses Pit1, display nonr

209 We previously observed that FeLV-B/A-MLV envelope glycoprotein chimeras spliced betw

210 Our results show that FeLV-A infection can indeed disrupt thiamine uptake with

211 himeric FeLV-B/A-MLV envelopes, we show that FeLV-B and A-MLV VRA and VRB interact in a modular manne

212 These studies suggest that FeLV-T infection relies on the following property of mam

213 The FeLV-945 LTR was shown to contain unique repeat elements

214 The FeLV-945 SU gene was shown to encode mutational changes

215 The FeLV-945 surface glycoprotein (SU) is closely related to

216 The FeLV-B envelope gene is derived by recombination with en

217 In contrast, substitution of both the FeLV-945 LTR and env gene changed the disease outcome en

218 The receptors for all but the FeLV-A subgroup have been defined previously.

219 r/channel-type protein, as a receptor by the FeLV Env backbone suggests that multipass transmembrane

220 not all required for receptor binding by the FeLV-B SU cofactors used in this study.

221 RBD appear to influence how efficiently the FeLV-B surface unit can bind to feline Pit2 and promote

222 to cat, suggesting that cells expressing the FeLV-A receptor are important targets at the earliest st

223 nfection and binding to cells expressing the FeLV-A receptor or the FeLV-T receptors.

224 (M-MuLV) with homologous sequences from the FeLV-945 LTR.

225 subgroup A but differs in sequence from the FeLV-A prototype, FeLV-A/61E, in the surface glycoprotei

226 These findings identify the FeLV-945 LTR and SU gene as determinants of disease.

227 These results implicated the FeLV-945 SU as a determinant of pathogenic spectrum.

228 In particular, genetic variations in the FeLV long terminal repeat (LTR) and SU gene have been li

229 2) by the LTR is an intermediate step in the FeLV LTR-mediated induction of AP-1 activity.

230 T-cell killing by cytopathic variants in the FeLV model.

231 d by three intramuscular inoculations of the FeLV DNA vaccine alone or in combination with plasmids e

232 hly related to the N-terminal portion of the FeLV envelope protein, which includes the receptor-bindi

233 protein that is similar to a portion of the FeLV envelope protein.

234 Of the FeLV, murine leukemia virus, and gibbon ape leukemia vir

235 Substitution of the FeLV-945 LTR into FeLV-A/61E resulted in a significantly

236 Substitution of the FeLV-945 LTR into FeLV-A/61E resulted in pathogenesis in

237 A comparison of the FeLV-B and Fr-MLV RBD structures illustrates how recepto

238 ion 73 within variable region A (VRA) of the FeLV-B envelope surface unit (SU) is necessary for viral

239 cells expressing the FeLV-A receptor or the FeLV-T receptors.

240 The results showed that the FeLV-945 LTR determined the kinetics of disease.

241 f cellular sequences that are related to the FeLV envelope gene.

242 lded D17-specific Env proteins that used the FeLV-C receptor.

243 l envelope proteins determined entry via the FeLV-A receptor independently of the presence of the N-

244 f the viral surface unit (SU), because these FeLV-B sequences are acquired by recombination with enFe

245 ents: (i) subgroup conversion from FeLV-A to FeLV-A and FeLV-B, as determined by the interference ass

246 ilar sequence hallmarks and were assigned to FeLV subgroup A.

247 Although the majority of cats exposed to FeLV develop a transient infection and recover, a propor

248 dies in cats that recovered from exposure to FeLV.

249 of naive cats following oronasal exposure to FeLV.

250 FeLIX is nearly identical to FeLV-B envelope sequences that encode the N-terminal hal

251 primary and established human cell lines to FeLV-B, the most likely zoonotic variant.

252 uences from a feline cell line permissive to FeLV-A into a murine cell line that was not permissive.

253 FeLV-C but no change in susceptibilities to FeLV-B and other retroviruses.

254 This feline cDNA conferred susceptibility to FeLV-A when reintroduced into nonpermissive cells, but i

255 y cells caused substantial susceptibility to FeLV-C but no change in susceptibilities to FeLV-B and o

256 The gene conferring susceptibility to FeLV-C was isolated and reintroduced into the same cell

257 elated to natural horizontally transmissible FeLV subgroup A (FeLV-A) but was found to differ from a

258 cats infected with a prototype transmissible FeLV clone, 61E.

259 el with the most prevalent human cell-tropic FeLV variant, FeLV-B.

260 Moreover, substitution of the unique FeLV-945 long terminal repeat and envelope gene for thos

261 ase potential and specificity of this unique FeLV LTR, we replaced the U3 region of the LTR of the er

262 the results obtained by Lauring et al. using FeLV-T, a virus that employs Pit1 as a receptor but requ

263 st prevalent human cell-tropic FeLV variant, FeLV-B.

264 molecularly cloned a feline leukemia virus (FeLV) (clone 33) from a domestic cat with acute myeloid

265 IV)] and oncoviruses [feline leukemia virus (FeLV) and human T cell leukemia virus (HTLV)] that diffe

266 ducing, T cell-tropic feline leukemia virus (FeLV) has evolved such that it cannot infect cells unles

267 Studies of feline leukemia virus (FeLV) have illustrated the importance of the genotype of

268 The outcome of feline leukemia virus (FeLV) infection in nature is variable, including maligna

269 ant in the control of feline leukemia virus (FeLV) infection led us to test a DNA vaccine administere

270 Feline leukemia virus (FeLV) is a common naturally occurring gammaretrovirus of

271 Feline leukemia virus (FeLV) is a horizontally transmitted virus that causes a

272 Feline leukemia virus (FeLV) is a naturally transmitted gammaretrovirus that in

273 Feline leukemia virus (FeLV) is an important pathogen of domestic cats.

274 r clone of subgroup A feline leukemia virus (FeLV) is considered to be highly infectious but weakly p

275 Feline leukemia virus (FeLV) is still a major cause of morbidity and mortality

276 ope (Env) proteins of feline leukemia virus (FeLV) subgroups A and C.

277 ifferent subgroups of feline leukemia virus (FeLV) use different host cell receptors for entry.

278 solate of the natural feline leukemia virus (FeLV) variant predominant in non-T-cell malignant, proli

279 ant for T-cell-tropic feline leukemia virus (FeLV) variants, the best studied of which is the immunod

280 njection of ecotropic feline leukemia virus (FeLV), subgroup A, plasmid DNA.

281 groups A, B, and C of feline leukemia virus (FeLV), use a multiple-membrane-spanning transport protei

282 new provirus clone of feline leukemia virus (FeLV), which we named FeLV-A (Rickard) or FRA, was chara

283 oteins, tagged with a feline leukemia virus (FeLV)-derived epitope tag, which are efficiently incorpo

284 plified the exogenous feline leukemia virus (FeLV)-related env gene species from lymphosarcomas induc

285 s assessed by detection of infectious virus, FeLV p27 capsid antigen, and proviral DNA in the blood.

286 bone of the transmissible form of the virus, FeLV-A.

287 Subgroup B feline leukemia viruses (FeLV-Bs) use the gibbon ape leukemia virus receptor, Pit

288 lasts to subgroup C feline leukemia viruses (FeLV-C) was eliminated simply by overexpression of the e

289 thic, T-cell-tropic feline leukemia viruses (FeLV-T) evolve from FeLV-A in infected animals and demon

290 thic, T-cell-tropic feline leukemia viruses (FeLV-T).

291 lymphoma induced by feline leukemia viruses (FeLVs) are the commonest forms of illness in domestic ca

292 eat (LTR) region of feline leukemia viruses (FeLVs) can enhance expression of certain cellular genes

293 etroviruses such as feline leukemia viruses (FeLVs) occurs worldwide, but the basis of human resistan

294 uman cells in vitro Feline leukemia viruses (FeLVs) rank high on this list, but neither domestic nor

295 Here, we have addressed whether FeLV-A infection might disrupt thiamine uptake into cell

296 Thus, while FeLV-Bs that are able to use feline Pit2 can evolve by r

297 es recovered from feline cells infected with FeLV-A.

298 lls are uniquely resistant to infection with FeLV-B due to the activity of cellular enzymes that muta

299 n protection against zoonotic infection with FeLV.IMPORTANCE Domestic exposure to gammaretroviruses s

300 es demonstrated that retrovirus vectors with FeLV-C and RD114 pseudotypes were present at 1.5 to 1.6