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 to a viral Env fusion protein, comprising an ALV-B surface Env protein and the Fc region of an immuno

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

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

25 -2, and efficiently mediated the entry of an ALV-A vector into cells.

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

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

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 ceptor related to the receptor for ALV-B and ALV-D.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 protein, demonstrating that this cytopathic ALV receptor can mediate cell death.

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

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

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

78 within the complex networks utilized during ALV response.

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

80 a cellular receptor specific for subgroup E ALV.

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

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

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

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

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

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

89 nsformation different from that proposed for ALV.

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

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

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

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

94 ellular receptor related to the receptor for ALV-B and ALV-D.

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

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

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

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

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

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

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

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

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

104 Understanding how ALV integration is regulated could facilitate the develo

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

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

107 tially occupied by primer in MuLV but not in ALV.

108 ation of established mouse tumors, including ALVs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 ocarbamate enhanced the cytopathogenicity of ALV-B.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 cellular receptor for the highly pathogenic ALV-J.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 ot required for B-cell transformation by the ALV/RSV family of viruses or that nonacute transforming

198 eric animals produced animals that carry the ALV provirus as a transgene.

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

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

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

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

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

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

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

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

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

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

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

210 only the parental cancer cells but also the ALVs.

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

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

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

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

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

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

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

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

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

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

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

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

223 Chicken embryo fibroblasts susceptible to ALV-B infection and transfected quail QT6 cells expressi

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

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

226 ved biological differences between these two ALV subgroups.

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

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

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

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

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

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

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

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

235 er elements within the avian leukosis virus (ALV) and Rous sarcoma virus (RSV) LTR enhancers in a pat

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

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

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

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

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

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

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

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

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

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

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

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

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

249 ons of the RSV and the avian leukosis virus (ALV) LTRs.

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

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

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

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

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

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

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

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

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

259 An avian leukosis virus (ALV)-based retroviral vector system was used for the eff

260 ts have indicated that avian leukosis virus (ALV)-E may utilize a cellular receptor related to the re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

279 oups B and D avian leukosis-sarcoma viruses (ALVs).

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

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

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

283 ly by infecting susceptible blastocysts with ALV-based retroviral vectors.

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

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

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

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

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

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

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

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

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

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