ライフサイエンスコーパス: MLV

1 MLV Gag is recruited to virological synapses through the

2 MLV glycoGag is an alternative version of the structural

3 MLV integration is known to prefer regions in or near tr

4 MLV matrix-mediated membrane targeting is required for G

5 MLV Nsp1beta had no effect on KPNA1; however, a mutant w

6 MLV released from cells carrying N-acyl-modified sialic

7 MLV vaccines are widely used to control PRRS; however, t

8 MLV-laden macrophages then form long-lived synaptic cont

9 MLV-laden uropods also mediate contacts between MLV-infe

10 MLVs with ecotropic host ranges show the greatest variab

11 d is a critical determinant for the Siglec-1/MLV interaction.

12 d sequence in the nonneurovirulent Friend 57 MLV.

13 otein by v-Abl is a critical component in Ab-MLV transformation.

14 of full-length SHIP significantly reduces Ab-MLV pre-B-cell transformation.

15 (hA3G), unlike mA3, is fully active against MLVs.

16 Although MLV Gag is sufficient for selective incorporation to occ

17 Although MLV integration sites are significantly enriched at TSS,

18 fficient transfection similar to amphotropic MLV vectors.

19 infection by ecotropic, but not amphotropic, MLV reporters.

20 Moreover, LP-BM5, an MLV strain that has been demonstrated to induce immune a

21 is communication between the bilayers in an MLV when they undergo the gel-fluid transition; this com

22 etween the transitions in the bilayers of an MLV is responsible for their apparent higher cooperativi

23 o not support an association between CFS and MLV-related viruses, including XMRV, and the off-label u

24 nding sites analyzed using ChIP-Seq data and MLV-integration sites revealed significant positive corr

25 PB and MLV highly correlated with Cohesin, Mediator and ESC-spe

26 PB and MLV preferred highly expressed genes, whereas Tol2 and S

27 tion of EEs was MLV>/=20 mm with RT3DTEE and MLV>/=16 mm with 2DTEE.

28 attenuation of virulent PRRSV in RVRp13 and MLV quickly reverted to wild-type sequences during the p

29 he parental virus of RVRp13 and RVRp22), and MLV.

30 ated histones, BET protein-binding sites and MLV-integration sites.

31 ence comparison with the RVRp13, VR2332, and MLV genomes.

32 vaccines are an unlikely source of XMRV and MLV exposure in humans and are consistent with the mount

33 We found no evidence of XMRV and MLV in eight live attenuated human vaccines further supp

34 possible source of introduction of XMRV and MLV into human populations.

35 uman vaccines using generic PCR for XMRV and MLV sequences.

36 ed and unspliced RNA transcripts of XMRV and MLV, resulting in their nuclear retention or degradation

37 Viruses bearing MLV IN C-terminal truncations can provide new avenues to

38 rformed to determine the association between MLV and EEs.

39 Finally, uropods mediated contact between MLV-infected B cells and uninfected T cells to form viro

40 -laden uropods also mediate contacts between MLV-infected B cells and uninfected T cells to form viro

41 ns of Brd4 ET residues essential for binding MLV IN also impair interaction of Brd4 with a number of

42 n different house mouse subspecies, but both MLV types are found in the classical strains of laborato

43 trans-infection, primarily of surface-bound MLV particles, efficiently occurred.

44 l, MLV Env is packaged almost exclusively by MLV particles, thus preventing incorporation into HIV pa

45 y in the enhancement of HIV-1 infectivity by MLV glycoGag.

46 ntly be drawn into contact zones mediated by MLV Env and receptor, a finding that is consistent with

47 V particles are produced from the same cell, MLV Env is packaged almost exclusively by MLV particles,

48 In human EC cells, MLV integration occurs normally, but no viral gene expre

49 LV PIC, we developed a replication-competent MLV in which the integrase protein was tagged with a FLA

50 was observed within 30 days in concentrated MLVs phase, while 16.0+/-0.3% of rutin was still encapsu

51 We generated a concordant MLV IN CCD structural model using SWISS-MODEL, MMM-tree

52 CasBrE Env possesses 6/8 consensus MLV glycosylation sites (gs) but is missing gs3 and gs5

53 al echocardiography (RT3DTEE) in determining MLV and its accuracy in identifying the risk for EEs com

54 esidues within MA are critical for directing MLV Gag to virological synapses.

55 ltimerization of Gag are sufficient to drive MLV Gag to the uropod.

56 Each P-MLV has an E-MLV backbone with P- or X-ERV replacements that together

57 se Y chromosome.envvariations define three E-MLV subtypes, one of which carries duplications of vario

58 ich region ofenv Outside theenvregion, all E-MLVs are related to different nonecotropic MLVs.

59 The viral receptor for ecotropic MLV (eMLV), a classical model for retrovirus infection m

60 s suggest a novel role for GRB2 in ecotropic MLV entry and infection by facilitating mCAT-1 trafficki

61 eous emergence of fully infectious ecotropic MLV in B6 mice with a range of distinct immune deficienc

62 pic replacements in the progenitor ecotropic MLV genome are more extensive than previously appreciate

63 rCasE) or nonneurovirulent (Fr57E) ecotropic MLVs influenced their viability and/or differentiation.

64 emonstrated their significance for effective MLV integration at transcription start sites.

65 ction of HIV-1 or murine leukemia virus Env (MLV-Env)-pseudotyped HIV-1 particles was enhanced in IFN

66 For murine leukemia virus envelope (MLV Env) glycoprotein, incorporation into foreign viral

67 For murine leukemia virus envelope (MLV Env) glycoprotein, incorporation into foreign viral

68 These exogenous MLVs derive from endogenous retroviruses (ERVs) that wer

69 ukemia virus (GaLV) Env or with a chimeric F-MLV Env with a GaLV cytoplasmic tail domain (CTD).

70 ing Friend murine leukemia virus envelope (F-MLV Env) are actively recruited to HIV-1 assembly sites

71 A series of F-MLV Env mutants that added or deleted one, two, or three

72 erefore more likely to explain the loss of F-MLV infectivity incurred by mutations in key ISD residue

73 , in fact, result in a substantial loss of F-MLV infectivity, independently of host immunity, challen

74 cells impaired the infectivity of both the F-MLV double mutant and the wild-type F-MLV strain, sugges

75 contribution of the hydrophobicity of the F-MLV Env membrane-spanning domain (MSD) to its incorporat

76 Indeed, the F-MLV mutant retained infectivity when it was produced by

77 bly, a loss of infectivity incurred by the F-MLV mutant with the E14R and A20F double ISD mutation wa

78 the F-MLV double mutant and the wild-type F-MLV strain, suggesting a finely tuned relationship betwe

79 Unlike F-MLV Env (+1L and +2L), HIV-1 Env (+1L and +2L) infectivi

80 ins, such as Friend murine leukemia virus (F-MLV) Env, but not with the related gibbon ape leukemia v

81 otein of the Friend murine leukemia virus (F-MLV) ISD has been reported to abolish its immunosuppress

82 To explore the role of sialic acid for MLV trans-infection at a submolecular level, we analyzed

83 demonstrated that the viral determinants for MLV Gag to localize to the uropod in polarized B cells a

84 The results provide insights for MLV integration target site selection and also explain t

85 s still able to outcompete HIV particles for MLV Env.

86 elucidate the importance of BET proteins for MLV integration efficiency and targeting and provide a r

87 Basic residues in MA that are required for MLV Gag recruitment to virological synapses between HEK2

88 nsors, IFI203, DDX41, and cGAS, required for MLV nucleic acid recognition.

89 e enhancer regions are the major targets for MLV integration; this means that MLV preferentially inte

90 Conversely, cell-free MLV and VSV virion yields and VSV spread to distal cells

91 s of lentiviral (HIV-1) and gammaretroviral (MLV) fluorescent complexes in the nuclei of infected cel

92 Despite extensive studies, how MLV achieves this difficult task has remained a mystery.

93 We still do not understand how MLV resists mA3-induced G-to-A mutation.

94 However, MLV Env preferentially assembles with MLV virions.

95 roteins with modified histone sites impaired MLV but not HIV-1 integration in infected cells.

96 Despite the fact that mA3 in MLV particles does not induce detectable deaminations up

97 f-width approximately 1.5 degrees C) than in MLVs ( approximately 0.1 degrees C).

98 ced the complete genomes of seven infectious MLVs isolated from geographically separated Eurasian and

99 Our study provides a novel insight into MLV nuclear export.

100 In solution, the isolated MLV IN CTD adopts an SH3 domain fold flanked by a C-term

101 o a distinctive, largely Y-chromosome-linked MLV ERV subtype.

102 e of the Moloney murine leukemia virus IN (M-MLV) C-terminal domain (CTD) and a structural homology m

103 In the context of a fully active minimal M-MLV glycoGag construct, truncations of the cytoplasmic d

104 Furthermore, the cytoplasmic domain of M-MLV glycoGag was fully sufficient to transfer the activi

105 e ecotropic Moloney murine leukemia virus (M-MLV), the Nef-like effect is mediated by the glycosylate

106 a bimodal mechanism for BET protein-mediated MLV integration into select chromatin locations.

107 induction was required to reveal the anti-Mo-MLV activity of tetherin in vivo.

108 B lymphoma Mo-MLV insertion region 1 (Bmi1) is a Polycomb Group (PcG)

109 b complex proto-oncogene BMI1 [B lymphoma Mo-MLV insertion region 1 homolog (mouse)] is essential for

110 Surprisingly, Mo-MLV replication and disease progression was not signific

111 is finding was explained by the fact that Mo-MLV infection did not induce detectable tetherin express

112 nant phosphorylated viral protein of Moloney MLV and is required for virus viability.

113 s chromatin binding in the wild-type Moloney MLV p12 protein.

114 riction of N-tropic murine leukemia virus (N-MLV) and equine infectious anemia virus (EIAV) infection

115 y selected N-tropic murine leukemia virus (N-MLV) mutants escaping from rhesus macaque TRIM5alpha (rh

116 ibition of N-tropic murine leukemia virus (N-MLV).

117 whether their infection by the neurovirulent MLV FrCasE contributed to neurodegeneration by affecting

118 E-MLVs are related to different nonecotropic MLVs.

119 that both neurovirulent and nonneurovirulent MLVs interfere with oligodendrocyte differentiation.

120 r RNAs are rarely exported from the nucleus, MLV actively exports unspliced viral RNAs to the cytopla

121 ne leukemia virus (MLV) system consisting of MLV-integrase fused to enhanced green fluorescent protei

122 nstrates L-domain activity in the context of MLV replication to direct virus release and infectious v

123 romatin is highlighted by the development of MLV-based vectors for human gene-therapy.

124 Surprisingly, the matrix domain of MLV Gag is not required for this selectivity, since MLV

125 the first time that the cytosolic domain of MLV glycoGag contains all the information needed to enha

126 ide comprising the ET binding motif (EBM) of MLV IN can disrupt the cognate interaction of Brd4 with

127 The block to MLV expression of MLV genomes is relieved upon cellular differentiation.

128 the glycolipid and glycoprotein fractions of MLV producer cells.

129 ain without blocking active incorporation of MLV Env into HIV virions.

130 NSD3, LANA of herpesvirus, and integrase of MLV, which involves formation of an intermolecular amphi

131 lylated ganglioside-dependent interaction of MLV particles with Siglec-1.

132 inhibit OL differentiation, irrespective of MLV neurovirulence.

133 ion may be attributed in part to the lack of MLV enhancer function in human EC cells.

134 we provide evidence showing that the lack of MLV gene expression may be attributed in part to the lac

135 The uropod localization of MLV Gag was dependent on plasma membrane (PM) associatio

136 RT3DTEE measurement of MLV was obtained with Advanced QLAB Quantification Softw

137 we have studied the RNA export mechanism of MLV and found that (i) the genome contains a sequence wh

138 lly replace the main phosphorylated motif of MLV p12 and can rescue the viral titer of a strain with

139 4) as the main cellular binding partners of MLV integrase (IN) and demonstrated their significance f

140 rd2, -3, -4) as cellular-binding partners of MLV integrase.

141 ions affects the global targeting profile of MLV vectors.

142 The major structural protein of MLV particles, Gag, frequently co-localized with Siglec-

143 matrix domain, contribute to recruitment of MLV Env into retroviral particles.

144 al synapses that mediates the recruitment of MLV Gag via the basic cluster of MA and Gag multimerizat

145 w that the C-terminal tail peptide region of MLV IN is important for the interaction with BET protein

146 al domain of BRD4 and the C-terminal tail of MLV IN.

147 ncing (NGS) to test hundreds of thousands of MLV Env mutants for the ability to be enriched in viral

148 is study, we tested hundreds of thousands of MLV Env mutants for the ability to be enriched in viral

149 ranscriptional silencing and upregulation of MLV gene expression.

150 e been serious concerns regarding the use of MLV as a vaccine virus due to the rapid reversion to vir

151 cantly increased the adjuvanting capacity of MLVs and OVA-encapsulating dehydration-rehydration vesic

152 y encapsulated (<10%) but highly adsorbed on MLVs surface (>60%) whatever MLVs composition.

153 We found no evidence of XMRV or other MLVs in these blood samples.

154 IN target capture complex together with our MLV domain structures, residues within the CCD alpha2 he

155 Analysis of 16 P-MLV genomes identified two segments consistently replace

156 While all 31 P-MLV ERVs map to the 95% of the laboratory mouse genome d

157 P-MLV-infected M. m. domesticus, no C57BL P-MLV ERVs were found in wild M. m. domesticus.

158 Each P-MLV has an E-MLV backbone with P- or X-ERV replacements

159 f the laboratory mouse genome derived from P-MLV-infected M. m. domesticus, no C57BL P-MLV ERVs were

160 naturally occurring, sometimes pathogenic P-MLV recombinants defines the limits and extent of inters

161 Thus, P-MLV ERVs show more insertional polymorphism than X-MLVs,

162 Although P-MLVs are deemed to be the proximal agents of disease ind

163 tropic mouse leukemia viruses (E-, X-, and P-MLVs) exist in mice as infectious viruses and endogenous

164 ytropic mouse leukemia viruses (X-MLVs and P-MLVs, respectively) have different host ranges but use t

165 few biologically characterized infectious P-MLVs have been sequenced for comparative analysis.

166 nomes of 16 naturally occurring infectious P-MLVs, 12 of which were typed for pathogenic potential.

167 The long terminal repeats of lymphomagenic P-MLVs are differentially altered by recombinations, dupli

168 viruses (ERVs) to produce polytropic MLVs (P-MLVs).

169 us retroviruses (ERVs) to produce polytropic MLVs (P-MLVs).

170 fused to enhanced green fluorescent protein (MLV-IN-EGFP).

171 ith modified live virus (MLV) (Ingelvac PRRS MLV).

172 Compared with Ingelvac PRRS((R)) MLV strain, A2MC2-P90 elicits higher virus neutralizing

173 y a direct binding assay using a recombinant MLV envelope protein receptor binding domain (RBD).

174 JQ-1 treatment or RNA interference, reduced MLV-integration frequencies at transcription start sites

175 us were negative for XMRV and highly related MLV sequences.

176 cells transduced with a clinically relevant MLV-based vector.

177 Glyco-Gag in the virion also rendered MLV resistant to other cytosolic sensors of viral revers

178 retroviral TRIM1 and TRIM62 proteins rescued MLV release.

179 general strategy for TRIM5alpha to restrict MLV but that significantly different specific interactio

180 The RT3DTEE MLV was larger than the 2DTEE value with a mean differen

181 ting and provide a route to developing safer MLV-based vectors for human gene therapy.

182 can wild mice and three previously sequenced MLVs to describe their relationships and identify their

183 We analyzed the genomes of seven MLVs isolated from Eurasian and American wild mice and t

184 is not required for this selectivity, since MLV Gag containing the matrix domain from HIV is still a

185 Six MLVs show close relationships to a small xenotropic ERV

186 r C-terminal fragments effectively stimulate MLV IN strand transfer activities in vitro.

187 related with PB but not with MLV, suggesting MLV prefers smaller promoter-enhancer loops, whereas PB

188 cellular proteins responsible for targeting MLV integration.

189 t variable regions in the PRRSV genome, than MLV.

190 higher genetic and phenotypic stability than MLV, and nine unique mutations were identified in the RV

191 Here, we demonstrate that MLV Gag localizes to the uropod in polarized B cells and

192 Our results indicate that MLV accumulates at the uropod of primary lymphocytes to

193 targets for MLV integration; this means that MLV preferentially integrates in regions that are favora

194 Together, our data reveal that MLV recruits RNAs from a novel host cell surveillance pa

195 We also show that MLV infection of neural progenitor cells (NPCs) in cultu

196 These results suggest that MLV infection is not directly cytotoxic to OPCs but rath

197 Our results suggest that MLV, not unlike HIV, accumulates at the uropod of primar

198 The MLV infection of primary B-cells was markedly more effic

199 images were also evaluated to determine the MLV.

200 the phase transitions of the bilayers in the MLV and, consequently, in an apparent increase in the co

201 racterized the structure and function of the MLV CAH.

202 1 infectivity is a conserved property of the MLV glycoGag cytoplasmic domain and involves AP-2-mediat

203 nriched at TSS, only a small fraction of the MLV integration sites (<15%) occur in this region.

204 sm controlling the differential roles of the MLV p12 protein in early and late replication.

205 requirements for retrograde transport of the MLV preintegration complex.

206 elated with transcriptional silencing of the MLV promoter through the deposition of repressive histon

207 We provide experimental evidence that the MLV CAH belongs to a group of charged, E(R/K)-rich, sing

208 nal and deletion analyses suggested that the MLV CAH forms a helical conformation, no structural or b

209 and APOBEC3 KO mice, we demonstrate that the MLV glycosylated Gag protein (glyco-Gag) enhances viral

210 of TRIM5alpha from different species to the MLV capsid core.

211 findings add HEMV as a second member to the MLV subgroup that uses mSMIT1 to gain entry into cells.

212 revents APOBEC3 packaging in the virion, the MLV glyco-Gag protein uses a unique mechanism to counter

213 ET) proteins Brd2, 3 and 4 interact with the MLV IN protein primarily through the BET protein ET doma

214 ify cellular proteins that interact with the MLV PIC, we developed a replication-competent MLV in whi

215 lator DCTN2/p50/dynamitin interacts with the MLV preintegration complex early in infection, suggestin

216 All three MLV subgroups are linked to leukemogenesis, which involv

217 velope (env) sequence variation define three MLV host range subgroups in laboratory mice: ecotropic,

218 nant Brd4(1-720) binds with high affinity to MLV integrase and stimulates correct concerted integrati

219 The block to MLV expression of MLV genomes is relieved upon cellular

220 repeat (LTR) U3 and could be transferred to MLV.

221 is associated with gene therapy trials using MLV vectors.

222 shown that the maximum length of vegetation (MLV)>/=10 mm is a predictor of embolic events (EEs) in p

223 vesicles (LUVs) and multilamellar vesicles (MLVs) are very different.

224 pid-based onion-type multilamellar vesicles (MLVs).

225 ison with the larger multilamellar vesicles (MLVs).

226 nera: HTLV-1, HIV-1, murine leukaemia virus (MLV), avian sarcoma leucosis virus (ASLV) and prototype

227 1, as well as that of murine leukemia virus (MLV) and Ebola virus (EBOV); knockdown of TIM-3 in diffe

228 We demonstrate that murine leukemia virus (MLV) and human immunodeficiency virus (HIV) are first ca

229 troviruses, including murine leukemia virus (MLV) and xenotropic murine leukemia virus (XMRV), named

230 Remarkably, although Moloney leukemia virus (MLV) assembles in the cytoplasm, precursors to specific

231 (Env) from the CasBrE murine leukemia virus (MLV) can cause acute spongiform neurodegeneration analog

232 Murine leukemia virus (MLV) can efficiently spread in tissue cultures by polari

233 identified to inhibit murine leukemia virus (MLV) demonstrated an ability to induce NF-kappaB/AP-1.

234 gamma-Retroviral murine leukemia virus (MLV) DNA integration into the host genome is favored at

235 cent additions to the murine leukemia virus (MLV) ecotropic subgroup: Mus cervicolor isolate M813 and

236 The glycoprotein murine leukemia virus (MLV) Env can readily form pseudotyped particles with man

237 ic constructs between murine leukemia virus (MLV) Gag and HBV Core to determine if the potential HBV

238 The p12 protein of murine leukemia virus (MLV) Gag is associated with the preintegration complex (

239 Here, we show that murine leukemia virus (MLV) has a unique means of counteracting APOBEC3 and oth

240 Murine leukemia virus (MLV) has been studied as one of the classic models of re

241 ) transposons and the murine leukemia virus (MLV) in mouse embryonic stem cells (ESCs).

242 rom the C terminus of murine leukemia virus (MLV) IN.

243 rt alterations to the murine leukemia virus (MLV) integrase (IN) protein that successfully result in

244 lecular mechanisms of murine leukemia virus (MLV) integration into host chromatin is highlighted by t

245 ntegration complex of murine leukemia virus (MLV) interacts with the dynein complex and that regulato

246 Murine leukemia virus (MLV) p12, encoded within Gag, binds the viral preintegra

247 sive manner, captures murine leukemia virus (MLV) particles and mediates their transfer to proliferat

248 triction of HIV-1 and murine leukemia virus (MLV) particles containing various proportions of restric

249 s (EIAV), or N-tropic murine leukemia virus (MLV) postentry and supported late HIV-1 life cycle steps

250 lycoGag) protein of a murine leukemia virus (MLV) similarly enhance the infectiousness of HIV-1 parti

251 a fluorescent Moloney murine leukemia virus (MLV) system consisting of MLV-integrase fused to enhance

252 Using a murine leukemia virus (MLV) variant with an unstable capsid that induces a stro

253 tonic inactivation of Murine Leukemia Virus (MLV) via 805 nm femtosecond pulses through gold nanorods

254 mmaretrovirus Moloney murine leukemia virus (MLV) was unaffected.

255 ses such as HIV-1 and murine leukemia virus (MLV), active receptor recruitment and trafficking occur

256 ficiency virus (SIV), murine leukemia virus (MLV), and the retrotransposon MusD.

257 retroviruses, such as murine leukemia virus (MLV), is unique.

258 retroviruses, such as murine leukemia virus (MLV), the identities of the cellular proteins involved i

259 We developed a Moloney mouse leukemia virus (MLV)-based retroviral replicating vector (RRV), Toca 511

260 nal repeats (LTRs) of murine leukemia virus (MLV)-based vectors and the vector-specific integration s

261 hes utilize HIV-1- or murine leukemia virus (MLV)-based vectors, which preferentially integrate near

262 s type 1 (HIV-1)- and murine leukemia virus (MLV)-derived viral vectors, respectively, than cells exp

263 iated viral target in murine leukemia virus (MLV)-induced neurodegeneration.

264 ciation of xenotropic murine leukemia virus (MLV)-related virus (XMRV) in prostate cancer and chronic

265 eplication of Moloney murine leukemia virus (MLV).

266 re natural targets of murine leukemia virus (MLV).

267 -PMV) but not Moloney murine leukemia virus (MLV).

268 ages in comparison with modified live virus (MLV) (Ingelvac PRRS MLV).

269 t strain, Ingelvac PRRS modified live virus (MLV), did not.

270 urrent commercial PRRSV modified live-virus (MLV) vaccines and other candidate vaccines.

271 h lacks endogenous murine leukaemia viruses (MLVs) able to replicate in murine cells.

272 Certain murine leukemia viruses (MLVs) are capable of inducing fatal progressive spongifo

273 Mouse leukemia viruses (MLVs) are found in the common inbred strains of laborato

274 Many murine leukemia viruses (MLVs) are partially resistant to restriction by mouse AP

275 aboratory mice carry mouse leukemia viruses (MLVs) of three host range groups which were acquired fro

276 mogenesis, ecotropic mouse leukemia viruses (MLVs) recombine with nonecotropic endogenous retroviruse

277 best cut-off value for prediction of EEs was MLV>/=20 mm with RT3DTEE and MLV>/=16 mm with 2DTEE.

278 hly adsorbed on MLVs surface (>60%) whatever MLVs composition.

279 When MLV and HIV particles are produced from the same cell, M

280 in was still encapsulated after 30 days when MLVs were diluted in water.

281 nsplanted transgenic NPCs showed that, while MLVs did not affect cellular engraftment or survival, th

282 wever, MLV Env preferentially assembles with MLV virions.

283 n sera and tissues than pigs challenged with MLV or RVRp13 at the first passage, and the attenuated r

284 amatically increased in pigs challenged with MLV or RVRp13 during the second passage.

285 omplementary high-affinity interactions with MLV IN and mononucleosomes (MNs).

286 F sites were correlated with PB but not with MLV, suggesting MLV prefers smaller promoter-enhancer lo

287 The 12 X-MLV ERVs predate the origins of laboratory mice; they we

288 ovel M. m. castaneus allele, originated in X-MLV-infected Asian mice.

289 restrictive XPR1 receptors, including the X-MLV-restricting laboratory mouse Xpr1(n) and a novel M.

290 XMRV and xenotropic murine leukemia virus (X-MLV) infection, suggesting that the xenografted human tu

291 and/or Southeast Asia, which is also where X-MLV-infected house mice evolved.

292 lytropic, and xenotropic MLVs (E-, P-, and X-MLVs, respectively).

293 Vs show more insertional polymorphism than X-MLVs, and these differences in ERV acquisition and fixat

294 avian species differ in susceptibility to X-MLVs, and 2 replacement mutations in the virus-resistant

295 pic and polytropic mouse leukemia viruses (X-MLVs and P-MLVs, respectively) have different host range

296 Xenotropic mouse leukemia viruses (X-MLVs) are broadly infectious for mammals except most of

297 mice: ecotropic, polytropic, and xenotropic MLVs (E-, P-, and X-MLVs, respectively).

298 onserved even among ecotropic and xenotropic MLVs, it was also fully sufficient for the rescue of nef

299 ich performed assays designed to detect XMRV/MLV nucleic acid, virus replication, and antibody.

300 riants and for the individual full-length XP-MLV ERVs found in the sequenced C57BL mouse genome.

301 he subspecies origins of laboratory mouse XP-MLV ERVs and their coevolutionary trajectory with their