ライフサイエンスコーパス: ALV

1 ALV display should enable an improvement in the diversit

2 ALV plus RBV may represent an effective IFN-free treatme

3 ALV pol sequences were first identified in particle-asso

4 ALV RNA sequences from both the gag and env regions were

5 ALV-B and pH-dependent Semliki Forest virus (SFV) entere

6 ALVs were apparently eliminated indirectly when tumor-sp

7 -PCR revealed 61,600, 348,000, and 1,665,000 ALV-E RNA copies per dose of Stamaril, YF-FIOCRUZ, and Y

8 ified the following motif: G[ILV]NCX(20,100)[ALV]X(2)[ILV]GGCCX(3)PX(2)I, which we propose to be a si

9 of reciprocal chimeras between EU-8 and LR-9 ALVs.

10 ate that evolutionary pressure on subgroup A ALV [ALV(A)] entry exerted by the presence of a competit

11 main of the TVA receptor for ALV subgroup A (ALV-A), fused via a proline-rich linker peptide to a 110

12 eceptor for avian leukosis virus subgroup A (ALV/A), we provide direct evidence that K6a(+) cells are

13 the requirements for avian leukosis virus A (ALV-A) infection were examined.

14 s escape population contained three abundant ALV(A) variant viruses, all with mutations in the surfac

15 earance of proviral c-myc integrations after ALV infection of lymphoma-susceptible birds, and to dete

16 s, the model predicted 71% and 79% SVR after ALV 400 mg with RBV 400 mg twice-daily for 24 and 36 wee

17 Alisporivir (ALV) is a cyclophilin inhibitor with pan-genotypic activ

18 with the envelope protein of subgroup B ALV (ALV-B) in the presence of three different lysosomotropic

19 ors for the noncytopathic subgroup E of ALV (ALV-E): TVB(T), a turkey subgroup E-specific ALV recepto

20 hat evolutionary pressure on subgroup A ALV [ALV(A)] entry exerted by the presence of a competitive i

21 None of the samples were seropositive by an ALV-E-based Western blot assay or had detectable EAV or

22 tion of a truncated myb gene product from an ALV-myb readthrough RNA.

23 another type of ligand incorporated into an ALV receptor-containing bridge protein can also function

24 -2, and efficiently mediated the entry of an ALV-A vector into cells.

25 tumors by intraductal injection of RCAS (an ALV/A-derived vector) carrying the gene encoding the pol

26 usly to cell surface EGF receptors and to an ALV-A surface envelope-Ig fusion protein.

27 e potency of nonpathogenic ALV-E, MDV-2, and ALV-E plus MDV-2 in boosting the incidence of LL-like ly

28 G were challenged separately with ALV(A) and ALV(C).

29 cal receptor interference pattern: ALV-B and ALV-D can interfere with infection by all three viral su

30 s B and D of avian leukosis virus (ALV-B and ALV-D), as a tumor necrosis factor receptor-related deat

31 serves as a cellular receptor for ALV-B and ALV-D.

32 infection, but not to infection by ALV-B and ALV-D.

33 Thus, ALV-B and ALV-E interact in fundamentally different ways with this

34 These data demonstrate that ALV-B and ALV-E use functional death receptors to enter cells, and

35 e type 1 receptor, is specific for ALV-B and ALV-E.

36 ues mediating the binding between chNHE1 and ALV-J gp85.

37 The results show the absence of EAV and ALV integrants in DNA prepared from MVVE-inoculated huma

38 hese possibilities, we have analyzed EAV and ALV particles in a measles virus vaccine equivalent (MVV

39 efective particles or infection with EAV and ALV pseudotypes bearing measles virus envelopes.

40 ntial consequences of integration of EAV and ALV sequences in human DNA, which may result from nonpro

41 regulatory factors of miRNA and lncRNA, and ALV gene expression.

42 Another ALV was found in stocks of RSV and called Rous-associate

43 ern blot analysis of virus pellets with anti-ALV RT antiserum detected three distinct RT proteins in

44 To better characterize vaccine-associated ALV-E, we examined the endogenous ALV proviruses (ev loc

45 yped with the envelope protein of subgroup B ALV (ALV-B) in the presence of three different lysosomot

46 killing by avian leukosis virus subgroup B (ALV-B) in cultures has been extensively studied, but the

47 We believe ALV display provides an extension to antibody display on

48 t for the nonreciprocal interference between ALV subgroups B, D, and E.

49 of TVB(S1) explains the NRI pattern between ALV-B and -E: subgroup B viruses establish receptor inte

50 SRP1 and Spt16 are able to individually bind ALV IN, but only the FACT complex effectively stimulates

51 sidues 28 to 39 both could effectively block ALV-J infection.

52 genes delivered by retroviral vectors, block ALV(A) infection of cultured chicken cells ( approximate

53 hNHE1 residues 28 to 39, effectively blocked ALV-J infection.

54 In contrast, both ALV-E and EAV particle-associated RNA were detected at e

55 The data from this study suggested that both ALV-E and MDV-2 play an important role in enhancement of

56 infection by all three viral subgroups, but ALV-E only interferes with infection by subgroup E virus

57 protein to the cognate TVB receptors and by ALV-B infection of a chicken embryo fibroblast cell line

58 ree subgroups, whereas those pre-infected by ALV-E are resistant only to superinfection by other subg

59 ins were much more resistant to infection by ALV(A) ( approximately 200-fold) than were control cells

60 va-mIgG significantly inhibited infection by ALV(A) (95 and 100% respectively) but had no measurable

61 ese cells highly susceptible to infection by ALV-A vectors.

62 to ALV-E infection, but not to infection by ALV-B and ALV-D.

63 on, which has been linked to cell killing by ALV-B, plays no crucial role in cell death induction.

64 ransduction of TVB-expressing lymphocytes by ALV vectors bearing a subgroup B envelope.

65 hat ALV-B-mediated apoptosis is triggered by ALV-B Env-TVB(S3) interactions.

66 Here we characterize ALV-J strain PDRC-59831, a newly studied U.S. isolate of

67 was not seen in previous work characterizing ALV-J-induced myeloid leukosis.

68 ale mated with inbred WL females, the cloned ALV receptor gene cosegregated with two markers linked t

69 uced in a virus-free system by cocultivating ALV-B Env-expressing cells with TVB(S3)-expressing cells

70 anscriptase (TERT) gene promoter is a common ALV integration target.

71 Replication-competent ALV-based retroviral vectors with subgroup B or C env we

72 In contrast, ALV integrates more randomly throughout the genome, whic

73 eceptor type that is specific for cytopathic ALV may also have important implications for understandi

74 emonstrate that CAR1 is the subgroup B and D ALV susceptibility gene located at tvb(s3).

75 ignated CAR1, specific for subgroups B and D ALV was cloned, and it was proposed that this gene was t

76 activated caspase-dependent apoptosis during ALV-B infection.

77 within the complex networks utilized during ALV response.

78 a chicken receptor for subgroups B, D, and E ALV.

79 a cellular receptor specific for subgroup E ALV.

80 Two individual ALV subgroup E (ALV-E) field strains, designated AF227 and AF229, were i

81 t data do not support transmission of either ALV or EAV to recipients of the U.S.-made vaccine and pr

82 r with the envelope (Env) proteins of either ALV-B or ALV-E.

83 (RFS) line, of chickens lacks all endogenous ALV and is fully susceptible to all subgroups of ALV, in

84 associated ALV-E, we examined the endogenous ALV proviruses (ev loci) present in a White Leghorn CEF

85 r breeder flocks in the absence of exogenous ALV infection.

86 imic avian leukosis but is free of exogenous ALV infection; inoculation of the nonpathogenic ALV-E or

87 long terminal repeat sequences of exogenous ALV subgroups A to D in any of the vaccines.

88 Second, it represents the first ALV-based system that allows gene transfer and expressio

89 Although TVB is essential for ALV-B-mediated cell death, binding of the ALV-B envelope

90 sis factor receptor family, is essential for ALV-B-mediated cell death.

91 t in TVB(S1) for ALV-E infection but not for ALV-B infection.

92 ger type 1 (chNHE1) as a binding protein for ALV-J.

93 extracellular domain of the TVA receptor for ALV subgroup A (ALV-A), fused via a proline-rich linker

94 lope glycoproteins and Tva, the receptor for ALV(A), that result in receptor interference.

95 tein, that serves as a cellular receptor for ALV-B and ALV-D.

96 ecrosis factor receptor-related receptor for ALV-B, -D, and -E.

97 determine whether the cellular receptor for ALV-E is a CAR1-like protein, a cDNA library was made fr

98 a disulfide bond requirement in TVB(S1) for ALV-E infection but not for ALV-B infection.

99 The antiviral effect was specific for ALV(A), which is consistent with a receptor interference

100 ignated the type 1 receptor, is specific for ALV-B and ALV-E.

101 r form, the type 2 receptor, is specific for ALV-B.

102 new insights into the control strategies for ALV-J infection.

103 n B cells, as this cell type is targeted for ALV tumor induction following integration of LTR sequenc

104 V provirus that was known to render its host ALV resistant.

105 Understanding how ALV integration is regulated could facilitate the develo

106 primer within the virion is much greater in ALV than in MuLV.

107 ly with ALV-J gp85; ECL3 is also involved in ALV-J gp85 binding.

108 sceptible to all subgroups of ALV, including ALV-E.

109 ation of established mouse tumors, including ALVs.

110 Two individual ALV subgroup E (ALV-E) field strains, designated AF227 a

111 Both ev-18 and ev-19 can express infectious ALV-E, while ev-1, ev-3, and ev-6 are defective.

112 chicken cells gave no evidence of infectious ALV, which is consistent with the phenotypes of the ev l

113 ction, confirming the presence of infectious ALV-E.

114 ility of the soluble Tva proteins to inhibit ALV(A) entry into susceptible cells.

115 s are sufficient to mediate viral entry into ALV-J nonpermissive cells.

116 Avian leukosis virus subgroup J (ALV-J) is a simple retrovirus that can cause hemangiomas

117 Avian leukosis virus subgroup J (ALV-J) is an important concern for the poultry industry.

118 or XSR, of avian leukosis virus subgroup J (ALV-J), a member of avian retrovirus, encodes a novel mi

119 hat, like HA, the conformation of the mature ALV-A envelope glycoprotein is metastable and that infec

120 s critical for receptor function and mediate ALV-J entry.IMPORTANCE chNHE1 is a cellular receptor of

121 ding of ALV-J gp85 and efficiently mediating ALV-J cell entry.

122 binding and entry assays to map the minimal ALV-J gp85-binding domain of chNHE1.

123 y was designed to test the impact of two new ALV-E isolates, recently derived from commercial broiler

124 various levels of defective or nondefective ALV-E sequences.

125 chNHE1 residues converted the nonfunctional ALV-J receptor huNHE1 to a functional one.

126 tal evidence on the potency of nonpathogenic ALV-E, MDV-2, and ALV-E plus MDV-2 in boosting the incid

127 e; and inoculation of both the nonpathogenic ALV-E and SB-1 escalates it to much higher levels.

128 infection; inoculation of the nonpathogenic ALV-E or MDV-2 (SB-1) boosts the incidence of the diseas

129 es an additional constraint on activation of ALV-A fusion that proceeds by a mechanism comparable to

130 PCR analysis of ALV and EAV proviral sequences in peripheral blood monon

131 nal domain responsible for chNHE1 binding of ALV-J gp85 and efficiently mediating ALV-J cell entry.

132 inimal domain required for chNHE1 binding of ALV-J gp85.

133 ocarbamate enhanced the cytopathogenicity of ALV-B.

134 egulated could facilitate the development of ALV-based vectors for use in human gene therapy.

135 of treatment duration and different doses of ALV plus RBV on sustained virologic response (SVR).

136 treated for 6 weeks with different doses of ALV with or without ribavirin (RBV).

137 eceptors for the noncytopathic subgroup E of ALV (ALV-E): TVB(T), a turkey subgroup E-specific ALV re

138 says were developed to examine expression of ALV-E particles (EV) in CEF supernatants.

139 id leukosis induction map to the env gene of ALV-J.

140 treatment did not overcome the inhibition of ALV-B entry by lysosomotropic agents.

141 PDRC-59831, a newly studied U.S. isolate of ALV-J.

142 nclude that the U.S. and English isolates of ALV-J derive from a common ancestor and are not the resu

143 hip between the U.S. and English isolates of ALV-J.

144 licles, although they show similar levels of ALV infection and integration as lymphoma-susceptible st

145 ients treated with 1,000, 800, and 600 mg of ALV once-daily, respectively.

146 ing to ALV-E SU and permitting entry only of ALV-E, have unambiguously identified this protein as a c

147 , as a principal cellular binding partner of ALV integrase (IN).

148 most of the genome, the envelope protein of ALV-J (EnvJ) shares low homology with the others.

149 .IMPORTANCE chNHE1 is a cellular receptor of ALV-J, a retrovirus that causes infections in chickens a

150 Release of ALV-like virus particles from uninoculated CEF was also

151 Replication of ALV-J depends on a functional cellular receptor, the chi

152 or available to mediate subsequent rounds of ALV-B entry.

153 thus expanding the flexibility and scope of ALV-mediated gene delivery.

154 chECL1, suggesting that the binding site of ALV-J gp85 on chNHE1 is probably located on the apex of

155 ions for understanding how some subgroups of ALV cause cell death.

156 and is fully susceptible to all subgroups of ALV, including ALV-E.

157 This 'bystander' elimination of ALVs required stromal cells expressing major histocompat

158 d IFN-gamma receptors for the elimination of ALVs.

159 Therefore, bystander killing of ALVs may result from IFN-gamma and TNF acting on tumor s

160 espectively) but had no measurable effect on ALV(C) infection.

161 c fowl produce piRNAs targeting ALV from one ALV provirus that was known to render its host ALV resis

162 rence (NRI): cells preinfected with ALV-B or ALV-D are resistant to superinfection by viruses of all

163 activated upon binding of a soluble ALV-B or ALV-E surface envelope-immunoglobulin fusion protein to

164 e envelope (Env) proteins of either ALV-B or ALV-E.

165 Western blot assay or had detectable EAV or ALV-E RNA sequences by RT-PCR.

166 the interaction of TVB(S1) with ALV-B Env or ALV-E Env.

167 Despite significant homology with the other ALV subgroups across most of the genome, the envelope pr

168 In contrast with the other ALV subgroups, ALV-J predominantly induces myeloid leuko

169 cellular receptor for the highly pathogenic ALV-J.

170 nonreciprocal receptor interference pattern: ALV-B and ALV-D can interfere with infection by all thre

171 hat the absence of primer at the PBS in pol- ALV is due to the deficiency of the primer species withi

172 teraction plays an essential role in priming ALV Env for subsequent low pH triggering.

173 to a murine version of EGFRvIII and promotes ALV-A entry selectively into cells that express this cel

174 in infected cells, the FACT complex promotes ALV integration activity, with proviral integration freq

175 block the entry of wild-type and pseudotyped ALV-B in two different cell lines, strongly suggesting t

176 and low RBV levels in patients that received ALV plus RBV.

177 ic resistance is instead mediated by reduced ALV LTR enhancer-driven transcription in the target lymp

178 infection with AF227, AF229, and a reference ALV-E strain, RAV60, in RFS chickens.

179 he FACT complex directly binds and regulates ALV integration efficiency in vitro and in infected cell

180 LR-9, a related ALV with differences from EU-8 in the gag and pol genes,

181 cant levels of a soluble form of the Tvb(S3) ALV receptor in a binding assay.

182 This indicates that, in contrast to SFV, ALV-B is unable to fuse at the cellular surface, even at

183 is also activated upon binding of a soluble ALV-B or ALV-E surface envelope-immunoglobulin fusion pr

184 roups, we asked whether binding of a soluble ALV-E surface envelope protein (SU) to its receptor can

185 interference was also observed when soluble ALV surface (SU)-immunoglobulin fusion proteins were bou

186 ffects associated with infection by specific ALV subgroups, we asked whether binding of a soluble ALV

187 ALV-E): TVB(T), a turkey subgroup E-specific ALV receptor, and TVB(S1), a chicken receptor for subgro

188 only the FACT complex effectively stimulates ALV integration activity in vitro Likewise, in infected

189 In contrast with the other ALV subgroups, ALV-J predominantly induces myeloid leukosis in meat-typ

190 uent low-pH step are critical for successful ALV-B infection.

191 Domestic fowl produce piRNAs targeting ALV from one ALV provirus that was known to render its h

192 and the DeltaW38 homozygous chickens tested ALV-J-resistant, in contrast to DeltaW38 heterozygotes a

193 These data demonstrate that ALV-B and ALV-E use functional death receptors to enter

194 Here, we report the unexpected finding that ALV entry depends on a critical low pH step that was ove

195 These studies indicate that ALV receptor-ligand bridge proteins may be generally use

196 Taken together, our results indicated that ALV-B-mediated apoptosis is triggered by ALV-B Env-TVB(S

197 Here we report that ALV-E SU-receptor interactions can induce apoptosis in q

198 the 4 RNA expression datasets revealed that ALV infection is detected by pattern-recognition recepto

199 These data suggest that ALV can package its RNA as monomers that subsequently di

200 The data suggest that ALV integrations in the TERT promoter region drive the o

201 These data suggest that ALV-J induces oncogenesis by insertional mutagenesis, an

202 fferent cell lines, strongly suggesting that ALV-B requires a low-pH step for entry.

203 se slow uptake rates support the theory that ALV-B utilizes endocytic pathways to enter cells.

204 The ALV(A) mutants efficiently infected cells expressing the

205 determinants of the interaction between the ALV(A) glycoproteins and the Tva receptor.

206 d expressed in line 0 chicken embryos by the ALV(B)-based vector RCASBP(B).

207 Instead, we show that signaling by the ALV-B receptor, TVB(S3), a member of the tumor necrosis

208 mammalian transgenic system that employs the ALV receptor TVB, thus expanding the flexibility and sco

209 l determinants of chNHE1 responsible for the ALV-J receptor activity, a series of chimeric receptors

210 oviruses and demonstrates the utility of the ALV experimental system in characterizing the mechanism(

211 s in the normally extreme specificity of the ALV(A) glycoproteins for Tva may represent an evolutiona

212 elope glycoproteins and soluble forms of the ALV(A) receptor Tva were analyzed both in vitro and in v

213 competitive inhibitor, a soluble form of the ALV(A) Tva receptor linked to a mouse immunoglobulin G t

214 or ALV-B-mediated cell death, binding of the ALV-B envelope protein to its cognate receptor TVB activ

215 contribute to a better understanding of the ALV-J infection mechanism and also provide new insights

216 ne indicates that this complex regulates the ALV life cycle at the level of integration.

217 These data led to the suggestion that the ALV-J env gene might have arisen by multiple recombinati

218 t that both ev classes may contribute to the ALV present in vaccines.

219 only the parental cancer cells but also the ALVs.

220 igen-positive parental cancer cells, but the ALVs escaped, grew and killed the host.

221 Therefore, ALV-A infection is dependent on the synergistic effects

222 The role of these ALV-E field isolates in development of and the potential

223 Thus, ALV-B and ALV-E interact in fundamentally different ways

224 T activity could be blocked by antibodies to ALV RT.

225 EF CAR1-related protein, specific binding to ALV-E SU and permitting entry only of ALV-E, have unambi

226 zacytidine-induced and noninduced CEF led to ALV infection, confirming the presence of infectious ALV

227 usceptibility to ALV-E infection, but not to ALV-B infection, when expressed in transfected human 293

228 The resistance to ALV-J was examined both in vitro and in vivo, and the De

229 Line 6(3) strain chickens are resistant to ALV tumorigenesis, largely failing to develop Myc-transf

230 To characterize the response to ALV challenge, we developed a novel methodology that com

231 This regulation is shown to be specific to ALV, as disruption of the FACT complex did not inhibit e

232 identified that conferred susceptibility to ALV-E infection, but not to ALV-B infection, when expres

233 mmalian cells can be rendered susceptible to ALV-A infection by attaching a soluble form of TVA to th

234 fibroblasts (TEFs), which are susceptible to ALV-E infection, but not to infection by ALV-B and ALV-D

235 We studied two ALV PR(-) mutants: one containing a large (>1.9-kb) inve

236 ved biological differences between these two ALV subgroups.

237 ed a subgroup E sequence, an endogenous-type ALV.

238 We showed that extensively nicked wild-type ALV genomic RNAs melt cooperatively.

239 interference patterns from that of wild-type ALV(A), indicating that the mutant glycoproteins are pos

240 gle-chain Fv antibody was optimized by using ALV display, improving affinity >2,000-fold, from microm

241 that, at least for the wild-type and variant ALV(A)s tested, the receptor binding affinity was direct

242 ectly eliminate these antigen loss variants (ALVs) in a model system when the parental cancer cells e

243 The escape of antigen-loss variants (ALVs) is a major obstacle to T cell-based immunotherapy

244 alyzed pol- mutants of avian leukosis virus (ALV) and murine leukemia virus (MuLV) for the presence o

245 The avian leukosis virus (ALV) entry mechanism is controversial, with evidence for

246 s with the recombinant avian leukosis virus (ALV) EU-8 induces a high incidence of rapid-onset B-cell

247 Avian leukosis virus (ALV) has been used as a model system to understand the m

248 Avian leukosis virus (ALV) has endogenized prior to chicken domestication, rem

249 ce for the presence of avian leukosis virus (ALV) in both CEF supernatants and vaccines.

250 Avian leukosis virus (ALV) induces bursal lymphoma in chickens after proviral

251 Avian leukosis virus (ALV) induces bursal lymphoma in tumor-susceptible chicke

252 Avian leukosis virus (ALV) induces tumors by integrating its proviral DNA into

253 highly susceptible to avian leukosis virus (ALV) induction of bursal lymphoma, involving proviral in

254 Avian leukosis virus (ALV) infection induces bursal lymphomas in chickens afte

255 ediate alpharetroviral avian leukosis virus (ALV) integration are unknown.

256 Avian leukosis virus (ALV) is detrimental to poultry health and causes substan

257 The avian leukosis virus (ALV) long terminal repeat (LTR) contains a compact trans

258 s study, we identified avian leukosis virus (ALV) proviral integration sites in rapid-onset B cell ly

259 ic mice expressing the avian leukosis virus (ALV) receptor TVB, fused to monomeric red fluorescent pr

260 proteins comprised of avian leukosis virus (ALV) receptors fused to epidermal growth factor (EGF) ca

261 found that endogenous avian leukosis virus (ALV) retroviral insertions were not mobilized during in

262 A new subgroup of avian leukosis virus (ALV) that includes a unique env gene, designated J, was

263 An avian leukosis virus (ALV) was found in some chicken embryos and named resista

264 A new subgroup of avian leukosis virus (ALV), designated subgroup J, was identified recently.

265 eukaryotic retrovirus, avian leukosis virus (ALV), offers a robust, eukaryotic version of bacteriopha

266 Avian leukosis virus (ALV), previously shown to be noninfectious for humans, w

267 al vector based on the avian leukosis virus (ALV), we inserted into the chicken genome a transgene en

268 al integration site in avian leukosis virus (ALV)-induced B-cell lymphomas originally identified by i

269 010, sporadic cases of avian leukosis virus (ALV)-like bursal lymphoma, also known as spontaneous lym

270 mily or to the avian sarcoma-leukosis virus (ALV)-related subgroup E endogenous virus loci.

271 c subgroups B and D of avian leukosis virus (ALV-B and ALV-D), as a tumor necrosis factor receptor-re

272 AV) and the endogenous avian leukosis virus (ALV-E), which originate from the chicken embryonic fibro

273 Subgroup J avian leukosis virus (ALV-J) is a recently identified avian oncogenic retrovir

274 ptor of the subgroup J avian leukosis virus (ALV-J).

275 The avian leukosis-sarcoma virus (ALV) group of retroviruses provides a useful experimenta

276 between the subgroup A avian leukosis virus [ALV(A)] envelope glycoproteins and soluble forms of the

277 ons between subgroup A avian leukosis virus [ALV(A)] envelope glycoproteins and Tva, the receptor for

278 subgroup B, D, and E avian leukosis viruses (ALV) encoded by the s1 allele of the chicken tvb locus.

279 subgroup B, D, and E avian leukosis viruses (ALV) is determined by specific alleles of the chicken tv

280 eptor for subgroup A avian leukosis viruses (ALV-A) can mediate viral entry when expressed as a trans

281 eptor for subgroup A avian leukosis viruses (ALV-A), fused to the MR1 single-chain antibody that bind

282 ubgroups B, D, and E avian leukosis viruses (ALV-B, -D, and -E) share the same chicken receptor, TVB(

283 ubgroup E endogenous avian leukosis viruses (ALV-E) and endogenous avian viruses (EAV).

284 the past several years, ALV J type viruses (ALV-J) have been isolated from broiler breeder flocks in

285 wild-type and mutant avian leukosis viruses (ALVs) in an attempt to (i) better understand the site(s)

286 ic subgroup E of the avian leukosis viruses (ALVs).

287 eterozygotes and wild-type birds, which were ALV-J-susceptible.

288 red predominantly in uninfected cells, while ALV-B-infected cells were protected against cell death.

289 week of treatment, which was associated with ALV monotherapy, high body weight, and low RBV levels in

290 le roles in myeloid leukosis associated with ALV-J.

291 Clonal expansion of cells with ALV integrations driving overexpression of the TERT anti

292 functional ECL that interacts directly with ALV-J gp85; ECL3 is also involved in ALV-J gp85 binding.

293 Free (SPF) layer chickens were infected with ALV-J or maintained as non-injected controls.

294 The absence of evidence of infection with ALV-E or EAV in 43 YF vaccine recipients suggests low ri

295 r interference (NRI): cells preinfected with ALV-B or ALV-D are resistant to superinfection by viruse

296 aracterizing the interaction of TVB(S1) with ALV-B Env or ALV-E Env.

297 (B)stva-mIgG were challenged separately with ALV(A) and ALV(C).

298 o selectively target retroviral vectors with ALV envelope proteins to cells expressing EGF receptors.

299 lly identified by infection of chickens with ALVs of two different subgroups.

300 In the past several years, ALV J type viruses (ALV-J) have been isolated from broil