ライフサイエンスコーパス: MLV

1 MLV also encodes a protein, glycoGag, that increases cap

2 MLV Gag is recruited to virological synapses through the

3 MLV glycoGag is a transmembrane version of the structura

4 MLV glycoGag is an alternative version of the structural

5 MLV glycoGag not only enhances MLV replication and disea

6 MLV incompatibility appeared to be caused by lack of inc

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

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

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

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

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

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

13 MLVs with ecotropic host ranges show the greatest variab

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

15 d sequence in the nonneurovirulent Friend 57 MLV.

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

17 Although MLV Gag is sufficient for selective incorporation to occ

18 Although MLV integration sites are significantly enriched at TSS,

19 Although MLV is considered a simple retrovirus compared to lentiv

20 fficient transfection similar to amphotropic MLV vectors.

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

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

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

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

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

34 rformed to determine the association between MLV and EEs.

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

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

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

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

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

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

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

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

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

44 her truncating the CT or by using a chimeric MLV Gag protein containing the HIV-1 MA without fully re

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

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

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

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

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

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

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

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

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

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

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

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

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

58 MLV glycoGag not only enhances MLV replication and disease progression but also increas

59 on.IMPORTANCE MLV glycoGag not only enhances MLV replication but also increases HIV-1 infectivity sim

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 However, MLV Env preferentially assembles with MLV virions.

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

88 which promotes viral replication.IMPORTANCE MLV glycoGag not only enhances MLV replication but also

89 enting its packaging into virions.IMPORTANCE MLV has existed in mice for at least a million years, in

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

91 embrane Env protein by the viral protease in MLV Env-pseudotyped HIV-1 particles bearing the MA mutat

92 be caused in part by fusogenic repression in MLV particles through an unknown mechanism.

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

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

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

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

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

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

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

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

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

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

103 B lymphoma Mo-MLV insertion region 1 (BMI1) has been reported to be an

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

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

106 d wild-type (WT) mice with Friend or Moloney MLV P50-deficient viruses, we found that APOBEC3 restric

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

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

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

110 etroviral proteins, specifically, HIV-1 Nef, MLV glycoGag, and EIAV S2.

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

112 E-MLVs are related to different nonecotropic MLVs.

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

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

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

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

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

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

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

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

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

122 the glycolipid and glycoprotein fractions of MLV producer cells.

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

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

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

126 inhibit OL differentiation, irrespective of MLV neurovirulence.

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

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

129 vaccines overcome some of the limitations of MLV with no risk of virulence reversion and emergence of

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

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

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

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

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

135 ions affects the global targeting profile of MLV vectors.

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

137 NC5 to antagonism by the glycoGag protein of MLV, suggesting that its virologic role is Nef specific.

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

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

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

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

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

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

144 ranscriptional silencing and upregulation of MLV gene expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 ALYREF plays an important role in regulating MLV replication.

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

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

170 retroviral TRIM1 and TRIM62 proteins rescued MLV release.

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

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

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

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

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

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

177 Six MLVs show close relationships to a small xenotropic ERV

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

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

180 cellular proteins responsible for targeting MLV integration.

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

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

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

184 potentiating TIM-1 restriction, we find that MLV glycoGag and EIAV S2 proteins, which, like Nef, anta

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

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

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

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

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

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

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

192 The MLV particle incompatibility appeared to be caused in pa

193 images were also evaluated to determine the MLV.

194 However, the MLV particle incompatibility was more nuanced.

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

196 racterized the structure and function of the MLV CAH.

197 1 infectivity is a conserved property of the MLV glycoGag cytoplasmic domain and involves AP-2-mediat

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

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

200 requirements for retrograde transport of the MLV preintegration complex.

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

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

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

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

205 Here, we show that the MLV P50 protein, produced from an alternatively spliced

206 located in multiple clusters throughout the MLV genome.

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

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

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

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

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

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

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

214 Thus, MLV encodes a protein, P50, that overcomes APOBEC3 restr

215 Thus, MLV has evolved multiple means of preventing APOBEC3 fro

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

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

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

219 stigated how glycoGag antagonizes Ser5 using MLV glycoMA and murine Ser5 proteins.

220 is associated with gene therapy trials using MLV vectors.

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

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

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

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

225 1, as well as that of murine leukemia virus (MLV) and Ebola virus (EBOV); knockdown of TIM-3 in diffe

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

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

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

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

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

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

232 It is not known if murine leukemia virus (MLV) encodes a Vif-like protein.

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

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

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

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

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

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

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

240 1 replication but not murine leukemia virus (MLV) infection and that miR-128 modulation of HIV-1 repl

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

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

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

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

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

246 in is compatible with murine leukemia virus (MLV) particles but incompatible with human immunodeficie

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

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

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

250 g the cleavage of the murine leukemia virus (MLV) transmembrane Env protein by the viral protease in

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

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

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

254 of pseudotyped HIV-1, murine leukemia virus (MLV), and vesicular stomatitis virus (VSV) particles.

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

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

257 (glycoGag) protein of murine leukemia virus (MLV), the S2 protein of equine infectious anemia virus (

258 n a model retrovirus, murine leukemia virus (MLV), using mass spectrometry and sequencing.

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 eplication of Moloney murine leukemia virus (MLV).

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

266 troviruses, including 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 Modified live virus (MLV) vaccines used in the field can persist and provide

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

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

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 compatible with HIV-1 particles but not with MLV particles.

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

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

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

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

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

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