ライフサイエンスコーパス: FeLV

1 FeLV proviral and antigen levels were also measured in 6

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

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

4 FeLV-945 was previously identified as a natural isolate

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

6 FeLV-A is the primary virus from which other subgroups h

7 FeLV-A receptor specificity was maintained when changes

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

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

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

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

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

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

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

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

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

17 revalent FeLV among cats is FeLV subgroup A (FeLV-A), and specific binding of FeLV-A Env to its viral

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

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

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

21 restingly, the same mutation was found in an FeLV isolate from naturally occurring thymic lymphoma an

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

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

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

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

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

27 between domestic cat cell susceptibility and FeLV long terminal repeat (LTR) copy number, similar to

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

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

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

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

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

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

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

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

39 ame lethal mutation in the env genes of both FeLV and murine ERV provides a common mechanism shared b

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

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

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

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

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

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

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

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

48 LV than domestic cat cells, and domestic cat FeLV restriction was highly related to enFeLV-LTR copy n

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

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

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

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

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

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

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

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

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

58 ed a negative correlation between endogenous FeLV (enFeLV) copy number and exogenous FeLV (exFeLV) in

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

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

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

62 shows that puma cells, which lack endogenous FeLV, produce more virus more rapidly than domestic cat

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

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

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

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

67 nsactivational potential of these endogenous FeLV LTR sequences.

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

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

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

71 Since endogenous FeLVs may affect the infectiousness or pathogenicity of

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

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

74 nous FeLV (enFeLV) copy number and exogenous FeLV (exFeLV) infection outcomes in domestic cats.

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

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

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

78 like sequences that are related to exogenous FeLV LTRs.

79 elements negatively correlate with exogenous FeLV replication.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 Terminal tissues from FeLV-infected Florida panthers and domestic cats had sim

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

104 ers, but Florida panther tissues have higher FeLV antigen loads.

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

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

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

108 he endemic domestic cat host, differences in FeLV susceptibility among species has not been evaluated

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

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

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

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

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

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

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

116 V transmission and may provide insights into FeLV pathogenesis.

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

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

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

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

121 The most prevalent FeLV among cats is FeLV subgroup A (FeLV-A), and specific binding of FeLV-A

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

123 rs to be specific to exogenous, leukemogenic FeLVs.

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

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

126 y number, similar to observations in natural FeLV infections.

127 TG35-2-phenotypic provirus from a naturally FeLV-infected cat, from which the FeLV Env (TG35-2) gene

128 Recently, we identified a new FeLV Env (TG35-2) gene from a pseudotyped virus that doe

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

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

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

132 A novel FeLV variant arose from a subtle mutation of FeLV-A Env,

133 orter, is a potential receptor for the novel FeLV variant.

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

135 Mutation analysis of FeLV Env demonstrated that amino acid substitutions with

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

137 subgroup A (FeLV-A), and specific binding of FeLV-A Env to its viral receptor, thiamine transporter f

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

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

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

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

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

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

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

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

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

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

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

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

150 provide a tool for further investigation of FeLV infectious disease.IMPORTANCE Feline leukemia virus

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

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

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

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

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

156 FeLV variant arose from a subtle mutation of FeLV-A Env, which altered the specific interaction of th

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

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

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

160 Five subgroups of FeLV, A to D and T, each with distinct receptor usages,

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

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

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

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

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

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

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

168 rus in hematopoietic cell lines with that of FeLV-A 61E by measuring the viral RNA copy numbers.

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

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

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

172 In infected cats, novel variants of FeLV with altered receptor specificity for viral entry h

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

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

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

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

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

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

179 d not render these cells permissive to other FeLV subgroups or feline endogenous retrovirus.

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

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

182 The most prevalent FeLV among cats is FeLV subgroup A (FeLV-A), and specifi

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

184 functional differences compared to prototype FeLV-A viruses.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 naturally FeLV-infected cat, from which the FeLV Env (TG35-2) gene was previously isolated, and comp

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

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

240 termined for each individual and compared to FeLV viral outcomes.

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

242 dies in cats that recovered from exposure to FeLV.

243 of naive cats following oronasal exposure to FeLV.

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

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

246 amples lacking enFeLV are more permissive to FeLV infection than domestic cat samples, suggesting tha

247 that puma fibroblasts are more permissive to FeLV than domestic cat cells, and domestic cat FeLV rest

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

249 , suggesting that this effect is specific to FeLV-LTR elements.

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

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

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

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

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

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

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

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

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

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

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

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

262 ver events.IMPORTANCE Feline leukemia virus (FeLV) can infect a variety of felid species.

263 While feline leukemia virus (FeLV) has been shown to infect felid species other than

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

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

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

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

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

269 us disease.IMPORTANCE Feline leukemia virus (FeLV) is a member of the genus Gammaretrovirus, which ca

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

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

272 Feline leukemia virus (FeLV) is horizontally transmitted among cats and causes

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

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

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

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

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

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

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

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

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

282 generate recombinant feline leukemia virus (FeLV).

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

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

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

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

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

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

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

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

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

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

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

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

295 (Felis catus) and pumas (Puma concolor) with FeLV and quantitated proviral and viral antigen loads.

296 eplication does not, however, correlate with FeLV env copy number, suggesting that this effect is spe

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