ライフサイエンスコーパス: ERV

1 ERV promoters drive tissue-specific and lineage-specific

2 ERV proteins may trigger lupus through structural and fu

3 ERV reactivation is accompanied by an epigenetic shift f

4 ERVs are commonly found in two forms, the full-length pr

5 ERVs are epigenetically silenced during development, yet

6 ERVs are provirus insertions in germline cells that are

7 ERVs belong to a diverse group of mobile genetic element

8 ERVs can proliferate within the genome of their host unt

9 Starting with nearly 90,000 ERVs from 60 vertebrate host genomes, we construct phylo

10 tif in its cytoplasmic domain (YXXPhi: Y(156)ERV).

11 We report the existence of 51,197 ERV-derived promoter sequences that initiate transcripti

12 ion-defective human endogenous retrovirus 9 (ERV-9) and thousands of copies of its solitary long term

13 We show that the two most active ERV families, IAP and MusD/ETn, are major targets and ar

14 enome-wide study of the most recently active ERVs in the human and mouse genome.

15 Although one-year mortality after ERV is still high (54%), most survivors have good functi

16 gnificantly improved one-year survival after ERV compared with IMS.

17 le of Rif1 in the epigenetic defense against ERV activation.

18 nd performing simple correlations across all ERV lineages, we show that when ERVs lose the env gene t

19 s of L1 activity and massive expansion of an ERV family--occur in the same group of mammals.

20 subsequent revascularization (25%), or to an ERV group (n = 152), which mandated revascularization wi

21 ugus, to systematically identify and analyze ERVs in this species.

22 ce of different ERV lineages, so we analyzed ERV loci recovered from 38 mammal genomes by in silico s

23 on and interaction properties of the p24 and ERV-29 cargo adaptors, as well as their role in cellulas

24 rus (ERV) genes accompanies the response and ERV overexpression activates the response.

25 the formal potentials of the thioredoxin and ERV disulfides.

26 sulfide intermediate between thioredoxin and ERV domains was highlighted by rapid reaction studies in

27 pported clade in retroviral phylogenies, and ERVs that group with these genera have been termed class

28 g to germline integration and inheritance as ERVs, genetic parasites whose remnants today constitute

29 ion and increased chromatin accessibility at ERV regions and their neighboring genes.

30 Importantly, H3K9me3 is reduced at ERVs upon H3.3 deletion, resulting in derepression and d

31 we characterized a family of class II avian ERVs, "TgERV-F," that acquired a mammalian gammaretrovir

32 ity have revealed novel interactions between ERVs and their hosts, with the potential to cause or con

33 properties of individual ERE isolates (both ERVs and sLTRs) were then characterized in the following

34 BLT-1 in healthy subject neutrophils and by ERV-1 in diabetes.

35 ified p53 binding sites are accounted for by ERV copies with a p53 site.

36 rly 5% of the genome assembly is occupied by ERV-derived sequences, a quantity comparable to findings

37 pt that some of the gene products encoded by ERVs and other endogenous viral elements may offer to th

38 t-transcriptionally silence coding-competent ERVs, while 18 nt tRFs specifically interfere with rever

39 tern of retroviral evolution and contrasting ERV diversity with known retroviral diversity, our study

40 ion of dedicated host mechanisms controlling ERV activity have revealed novel interactions between ER

41 For patients with AMI complicated by CS, ERV resulted in improved 1-year survival.

42 termined the relative abundance of different ERV lineages, so we analyzed ERV loci recovered from 38

43 or arise by recombination between different ERVs.

44 Here we discuss ERV contributions to host genome structure and function,

45 oxin domain (Trx) and an FAD-binding-domain (ERV) toward the C-terminus.

46 le elements, endogenous retroviral elements (ERVs) containing long terminal repeats (LTRs), are silen

47 g in vitro and polymorphic ERVs, older fixed ERVs) allowed us to disentangle integration vs. fixation

48 tRNA primer binding site (PBS) essential for ERV reverse transcription.

49 sues, suggesting that tissues permissive for ERV activity gain access to an otherwise silenced source

50 eloped a pipeline to screen full genomes for ERVs, and using this pipeline, we have located over 800

51 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter

52 hat metabolizes DNA reverse-transcribed from ERV.

53 Functional ERV-1 was determined by phosphorylation of the signaling

54 al BLT-1, low levels of minimally functional ERV-1, and inversed coexpression when compared to neutro

55 ansgenic zebrafish harboring the beta-globin ERV-9 LTR coupled to the GFP gene, the LTR enhancer was

56 lobin gene locus showed that the beta-globin ERV-9 LTR enhancer initiated RNA synthesis from the LTR

57 s and the estimation of parameters governing ERV proliferation.

58 otal of 1,509 of approximately 319,000 human ERV LTR regions have a near-perfect p53 DNA binding site

59 The HRES-1 human ERV encodes a 28-kD nuclear autoantigen and a 24-kD smal

60 The most recently acquired human ERV is HERVK(HML-2), which repeatedly infected the prima

61 low gene density and elevated rates of human ERV integration in males for chromosome Y and segmental

62 ies for individual genes indicate that human ERV p53 sites are likely part of the p53 transcriptional

63 top codons during the evolution of the human ERV family HERV-K(HML2).

64 LTR, although members of one group of human ERVs (HERVs), HERV-K, were recently active with members

65 Unlike most other human ERVs, HERVK retained multiple copies of intact open read

66 The youngest human ERVs (HERVs) belong to the HERV-K(HML-2) subgroup and we

67 Gammaretrovirus genus and associated class I ERVs.

68 We sought to identify ERV progenitors, recombinational hot spots, and segments

69 ant H3.3 is enriched at class I and class II ERVs, notably those of the early transposon (ETn)/MusD f

70 with these genera have been termed class II ERVs.

71 Overall, our results implicate ERV enhancer co-option as a mechanism underlying the ext

72 rphism than X-MLVs, and these differences in ERV acquisition and fixation are linked to subspecies-sp

73 nts younger than 75 years (51.6% survival in ERV group vs 33.3% in IMS group).

74 t, accumulated mostly outside TUs, including ERVs related to ASLV.

75 onstrate that ZFP809 is required to initiate ERV silencing during embryonic development but becomes l

76 arly placental morphogenesis, because intact ERV envelope genes were found to be expressed in the syn

77 A polymorphic, intronic ERV at Slc15a2 triggers up to 49-fold increases in prema

78 pproximately 5% of other genes when intronic ERV polymorphisms are present.

79 en merged to the Repbase collection of known ERV/long terminal repeat (LTR) elements to annotate the

80 uence related to the gag gene of the MuERV-L ERV family.

81 f the methodology used here to analyze large ERV datasets and improve understanding of retroviral evo

82 lternatively, it is possible that this large ERV expansion set the stage for L1 extinction.

83 process became available when a full-length ERV isolated from koalas (KoRV) was shown to have integr

84 ave located over 800 endogenous epsilon-like ERV fragments in primate genomes.

85 ls and birds were screened, and epsilon-like ERV fragments were found in all primate and tree shrew g

86 However, epsilon-like ERVs have been identified in very few mammals.

87 ver 800 fragments of endogenous epsilon-like ERVs in the genomes of all major groups of primates, inc

88 y few mammals are known to have epsilon-like ERVs; however, we have identified over 800 fragments of

89 oxin domains to a catalytically more limited ERV domain has produced an efficient catalyst for the di

90 al history of a specific retrovirus lineage (ERV-Fc) that disseminated widely between ~33 and ~15 mil

91 All three major ERV classes include recently integrated proviruses, sugg

92 By mining ERVs from 65 host genomes sampled across vertebrate dive

93 distinctive, largely Y-chromosome-linked MLV ERV subtype.

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

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

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

97 The 12 X-MLV ERVs predate the origins of laboratory mice; they were a

98 ubspecies origins of laboratory mouse XP-MLV ERVs and their coevolutionary trajectory with their XPR1

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

100 A slowdown in most ERV groups is observed but we suggest that HERV-K activi

101 While most ERVs are relics of ancient integration events, "young" p

102 MV-ERV correctly displayed echistatin on the outer surface

103 MV-ERV grew to 10(6) plaque-forming units/mL, slightly lowe

104 ial cells on matrigels and unlike MV-Edm, MV-ERV infected newly formed blood vessels in chorioallanto

105 In animal models, MV-ERV but not the control MV-Edm caused the regression of

106 fection clearly show the potential use of MV-ERV in gene therapy for targeting tumor-associated vascu

107 specificity, potency, and feasibility of MV-ERV infection clearly show the potential use of MV-ERV i

108 as named measles virus echistatin vector (MV-ERV).

109 Notably, ERV activation in immunodeficient mice is prevented in h

110 ccount for the variable patterns of observed ERV genetic diversity.

111 he mechanistic level, Rif1 directly occupies ERVs and is required for repressive histone mark H3K9me3

112 ty-three percent of 1-year survivors (85% of ERV group and 80% of IMS group) were in New York Heart A

113 lecular mimicry, whereas the accumulation of ERV-derived nucleic acids stimulates interferon and anti

114 sessed by echocardiography, and a benefit of ERV is noted regardless of baseline LVEF or MR.

115 nt greater appreciation of the complexity of ERV biology and the identification of dedicated host mec

116 hes an important role for H3.3 in control of ERV retrotransposition in embryonic stem cells.

117 transcribed from many of the 4000 copies of ERV-9 LTR retrotransposons acted by a similar cis mechan

118 obal knockdown or locus-specific deletion of ERV-9 lncRNAs in human erythroblasts carrying approximat

119 m recent studies cataloging the diversity of ERV LTRs acting as important transcriptional regulatory

120 TNF-alpha or LPS increased the expression of ERV-1 by healthy and diabetic neutrophils.

121 formation decreases rapidly as a function of ERV age and that an age dependent model of solo-LTR form

122 The impact of ERV propagation on the evolution of gene regulation rema

123 counteracted LPS and TNF-alpha induction of ERV-1 overexpression and endogenous diabetic overexpress

124 Trex1 deficiency or blocked integration of ERV-encoded DNA also promotes lupus in murine models.

125 nt a model that unifies current knowledge of ERV biology into a single evolutionary framework.

126 Basal levels of ERV and viral defense gene expression significantly corr

127 A solitary long terminal repeat (LTR) of ERV-9 human endogenous retrovirus is located upstream of

128 The solitary LTRs of ERV-9 human endogenous retrovirus are middle repetitive

129 The solitary long terminal repeats (LTRs) of ERV-9 endogenous retrovirus contain the U3, R, and U5 re

130 The majority of ERV clades that we recover do not contain known retrovir

131 To dissect the functional mechanism of ERV-9 lncRNAs, we performed genome-wide RNA and ChIRP an

132 Here we show that an LTR retrotransposon of ERV-9 human endogenous retrovirus located 40-70 kb upstr

133 transcribed from the LTR retrotransposons of ERV-9 human endogenous retrovirus activated transcriptio

134 that intronic RNAs arising from U3 sLTRs of ERV-9 were expressed as both sense (S) and antisense (AS

135 Activation of ERVs is attributed to demethylation of chromatin and DNA

136 ethylation and transcriptional activation of ERVs, including CpG-rich IAP (intracisternal A particle)

137 Studying six categories of ERVs we quantitatively recapitulate patterns of insertio

138 g that the envelope of a particular class of ERVs of sheep, endogenous Jaagsiekte sheep retroviruses

139 te proviruses from the three main classes of ERVs, which were further resolved into 13 major families

140 reciated role for immunity in the control of ERVs and provide a potential mechanistic link between im

141 Here we study the control of ERVs in the commonly used C57BL/6 (B6) mouse strain, whi

142 has greatly contributed to the discovery of ERVs.

143 model explaining the uneven distribution of ERVs along the genome.

144 tion, we examine whether the distribution of ERVs can be explained by host factors predicted to influ

145 By characterizing the distribution of ERVs, we show that no major vertebrate lineage has escap

146 e diversity, we uncover a great diversity of ERVs, indicating that retroviral sequences are much more

147 cale consistent with a substantial effect of ERVs on the function and evolution of the human genome.

148 entified a novel and highly active family of ERVs (mysTR).

149 ls essential for integration and fixation of ERVs.

150 scape influences integration and fixation of ERVs.

151 solo-LTR formation describes the history of ERVs more accurately than the commonly used exponential

152 an unexpectedly strong functional impact of ERVs in disrupting gene transcription at a distance and

153 The investigation of ERVs of different evolutionary ages (young in vitro and

154 In this review, the involvement of ERVs in cancer initiation and progression is discussed,

155 The majority of ERVs cluster alongside exogenous retroviruses into two m

156 The minority of ERVs present within TUs were mainly in the antisense ori

157 ranslocation (TET) enzymes at LTR regions of ERVs, because vitamin C acts as a cofactor for TET prote

158 d sumoylation modifiers in the repression of ERVs.

159 any previously uncharacterized repressors of ERVs, and defined an essential role of Rif1 in the epige

160 KRAB-ZFP) family, initiates the silencing of ERVs in a sequence-specific manner via recruitment of he

161 e modification-based epigenetic silencing of ERVs.

162 Transcription of ERVs is derepressed in both sexes in nuage-mutant mice,

163 The findings suggest that, during oogenesis, ERV-9 LTR enhancers in the human genome could activate t

164 the infectivity of KoRV, like that of other ERVs, is substantially lower than that of GALV.

165 different substitution patterns for X- and P-ERVs.

166 Expression of particular ERVs is associated with several positive physiological f

167 genetic associations between the polymorphic ERV in cis and disrupted transcript levels.

168 Polymorphic ERVs occur relatively infrequently in gene introns and a

169 tionary ages (young in vitro and polymorphic ERVs, older fixed ERVs) allowed us to disentangle integr

170 contributions from xenotropic and polytropic ERVs differentially alter the regions responsible for re

171 ir relationships and identify their possible ERV progenitors.

172 peculate how this interaction could preserve ERV/host chimeric gene products affecting female fertili

173 opment, yet the cellular factors recognizing ERVs in a sequence-specific manner remain elusive.

174 LTR sequences derived from distantly related ERVs have been exapted as regulatory sequences for many

175 selection and ectopic recombination removing ERVs from the genome.

176 Importantly, Rif1 represses ERVs in human ESCs as well, and the evolutionally-conser

177 tic signal from large endogenous retrovirus (ERV) datasets by collapsing information to facilitate br

178 Endogenous retrovirus (ERV) elements have been shown to contribute promoter seq

179 Endogenous retrovirus (ERV) families are derived from their exogenous counterpa

180 on of hypermethylated endogenous retrovirus (ERV) genes accompanies the response and ERV overexpressi

181 e mapped thousands of endogenous retrovirus (ERV) germline integrants in highly divergent, previously

182 port that LTR class I endogenous retrovirus (ERV) retroelements impact considerably the transcription

183 uses up-regulation of endogenous retrovirus (ERV) RNAs in antigen-specific mouse B cells.

184 nce gene is a coopted endogenous retrovirus (ERV) sequence related to the gag gene of the MuERV-L ERV

185 ments (LINEs) and the endogenous retrovirus (ERV) superfamily.

186 biallelic and include endogenous retrovirus (ERV) targets, the rest show monoallelic binding based ei

187 ctionally transcribed endogenous retrovirus (ERV) transcripts, increased cytosolic dsRNA, and activat

188 etrotransposons, or endogenous retroviruses (ERV), account for most novel insertions and are expresse

189 on and silencing of endogenous retroviruses (ERV).

190 Endogenous retroviruses (ERVs) are abundant in mammalian genomes and contain sequ

191 Endogenous retroviruses (ERVs) are fixed and abundant in the genomes of vertebrat

192 Endogenous retroviruses (ERVs) are proposed as a molecular link between the human

193 Endogenous retroviruses (ERVs) are remnants of ancient retroviral infections, and

194 Endogenous retroviruses (ERVs) are the remnants of ancient retroviral infections

195 Endogenous retroviruses (ERVs) are vertically transmitted intragenomic elements d

196 Endogenous retroviruses (ERVs) are widespread in vertebrate genomes and have been

197 Endogenous retroviruses (ERVs) comprise 6-8% of the human genome.

198 Endogenous retroviruses (ERVs) constitute a substantial portion of mammalian geno

199 Endogenous retroviruses (ERVs) differ from typical retroviruses in being inherite

200 Endogenous retroviruses (ERVs) have contributed to more than 8% of the human geno

201 Repression of endogenous retroviruses (ERVs) in mammals involves several epigenetic mechanisms.

202 ectious viruses and endogenous retroviruses (ERVs) inserted into mouse chromosomes.

203 Endogenous retroviruses (ERVs) occupy extensive regions of the human genome.

204 Endogenous retroviruses (ERVs) of these 2 gammaretrovirus subtypes are largely se

205 highly enriched for endogenous retroviruses (ERVs) on a genome-wide level.

206 viruses have become endogenous retroviruses (ERVs) on several occasions, integrating into germ line c

207 Endogenous retroviruses (ERVs) represent ancestral sequences of modern retrovirus

208 Endogenous retroviruses (ERVs) represent genomic fossils of past retroviral infec

209 Endogenous retroviruses (ERVs) result from germ line infections by exogenous retr

210 ting in the form of endogenous retroviruses (ERVs) that account for nearly one-tenth of the mouse and

211 us MLVs derive from endogenous retroviruses (ERVs) that were acquired by the wild mouse progenitors o

212 e with nonecotropic endogenous retroviruses (ERVs) to produce polytropic MLVs (P-MLVs).

213 The life cycle of endogenous retroviruses (ERVs), also called long terminal repeat (LTR) retrotrans

214 al tracts, and also endogenous retroviruses (ERVs), comprising a substantial fraction of the mammalia

215 elements, including endogenous retroviruses (ERVs), constitute a large fraction of the mammalian geno

216 eds of thousands of endogenous retroviruses (ERVs), derived from ancient retroviral infections.

217 siderable number of endogenous retroviruses (ERVs), relics of ancestral infectious retroviruses, whos

218 Endogenous retroviruses (ERVs), the majority of which exist as degraded remnants

219 Endogenous retroviruses (ERVs), the remnants of retroviral infections in the germ

220 ividual families of endogenous retroviruses (ERVs), they have remained active throughout the mammalia

221 ng the germ line as endogenous retroviruses (ERVs), where they lose their infectivity over time but c

222 omes are made up of endogenous retroviruses (ERVs).

223 nous proviruses and endogenous retroviruses (ERVs).

224 ribution of chicken endogenous retroviruses (ERVs).

225 enome is made up of endogenous retroviruses (ERVs).

226 omic approach using endogenous retroviruses (ERVs).

227 them with endogenous germ line retroviruses (ERVs) acquired early in house mouse evolution.

228 REs (a total of 111 endogenous retroviruses [ERVs] and 488 solo long terminal repeats [sLTRs]) within

229 andomization to the early revascularization (ERV) or initial medical stabilization (IMS) arms of the

230 patients in the emergency revascularization (ERV) group and by clinical selection in 100 of 150 (67%)

231 treatment with emergency revascularization (ERV) versus initial medical stabilization (IMS).

232 the embryonic axin gene show that a solitary ERV-9 LTR has been stably integrated in the respective l

233 The solitary ERV-9 long terminal repeat (LTR) located upstream of the

234 Some ERV lineages proliferate by infecting germline cells, as

235 isease, there is mounting evidence that some ERVs have become integral components of normal host deve

236 rrying a single copy of the primate-specific ERV-9 LTR in the 100 kb human beta-globin gene locus.

237 in other tissues shows that species-specific ERV enhancer activity is generally restricted to hypomet

238 mouse viruses derive directly from specific ERVs or arise by recombination between different ERVs.

239 f innate immunity, and that lineage-specific ERVs have dispersed numerous IFN-inducible enhancers ind

240 To systematically study ERV repression, we carried out an RNAi screen in mouse e

241 introduce a phylogenetic framework to study ERV insertion and solo-LTR formation.

242 ay highly elevated levels of ZFP809-targeted ERVs in somatic tissues.

243 markedly less likely to form solo-LTRs than ERVs from other families.

244 We found that ERV-9 lncRNAs acted in cis to stabilize assembly of the

245 We also show that ERV abundance follows the Pareto principle or 20/80 rule

246 These findings suggest that ERV and two innate sensing pathways that detect them are

247 It also reinforced the concept that ERVs are causative agents of many cancers, a notion that

248 We found that ERVs have shaped the evolution of a transcriptional netw

249 We found that ERVs integrate in late-replicating AT-rich regions with

250 This work supports the hypothesis that ERVs play fundamental roles in placental morphogenesis a

251 Further analysis indicated that ERVs in humans, mice, and rats showed similar distributi

252 Circumstantial evidence suggests that ERVs play a role in mammalian reproduction, particularly

253 The ERV patients have a lower rate of deterioration than IMS

254 The ERV-9 LTR contains multiple CCAAT and GATA motifs and co

255 The ERV-9 LTRs are conserved during primate evolution, but t

256 Alternatively, the ERV-9 LTR enhancers, in initiating RNA syntheses into th

257 e space, and a larger protein containing the ERV/ALR domain, quiescin-sulfhydryl oxidase (QSOX).

258 tegration targeting, probably determined the ERV distribution.

259 A survival benefit for the ERV strategy was observed at all levels of LVEF and MR.

260 contrast, the proximal CXXC disulfide in the ERV (essential for respiration and vegetative growth) do

261 -year survival was 46.7% for patients in the ERV group compared with 33.6% in the IMS group (absolute

262 In the ERV group, the hazard ratio for death per diseased vesse

263 ults demonstrate the unique potential of the ERV fossil record for studying the processes of viral sp

264 The parent of origin of the ERV is associated with variable expression of nontermina

265 mic distances up to >12.5 kb upstream of the ERV, both in cis and between alleles.

266 As acted in cis to stabilize assembly of the ERV-9 LTR enhancer complex and facilitate long-range LTR

267 ts carrying approximately 4000 copies of the ERV-9 LTRs and in transgenic mouse erythroblasts carryin

268 A total of 114 of the ERV-derived transcription start sites can be demonstrate

269 The FAD prosthetic group of the ERV/ALR family of sulfhydryl oxidases is housed at the m

270 the redox properties between members of the ERV/ALR family of sulfhydryl oxidases provides insights

271 The results suggest that the ERV-9 LTR-initiated transcription process may modulate t

272 ed sulfhydryl oxidases and is related to the ERV/ALR family of sulfhydryl oxidases.

273 cluding the beta-globin gene locus where the ERV-9 LTR is juxtaposed to the locus control region (bet

274 The ERVs, in contrast, accumulated mostly outside TUs, inclu

275 These ERV families are primate-specific and transposed activel

276 CRISPR-Cas9 deletion of a subset of these ERV elements in the human genome impaired expression of

277 One of these ERV families, RLTR13D5, contributes hundreds of mouse-sp

278 bryos and embryonic stem cells (ESCs), these ERVs remain silenced when Np95 is deleted alone or in co

279 Transcription of these ERVs is, however, tightly regulated by dedicated epigene

280 histone modifications) in +/-32 kb of these ERVs' integration sites and in control regions, and anal

281 In human tissues, ERV-9 LTR enhancer was active also in oocytes and stem/p

282 and occurs upstream of ESET, linking H3.3 to ERV-associated H3K9me3.

283 leukotriene B4 (BLT-1) on neutrophils and to ERV-1/ChemR23 on monocyte/macrophages.

284 he IMS group compared with those assigned to ERV.

285 Assignment to ERV was the only independent predictor of outcome at one

286 ferases and facilitates their recruitment to ERV regions.

287 l genomes identified segmental homologies to ERVs of different host range subgroups.

288 e that recruitment of DAXX, H3.3 and KAP1 to ERVs is co-dependent and occurs upstream of ESET, linkin

289 ibution of de novo ASLV integration sites to ERVs indicated that purifying selection against gene dis

290 es direct recruitment of Chaf1a and Sumo2 to ERVs.

291 While aberrant or uncontrolled ERV expression has been perceived as a potential cause o

292 el of recovery for shock patients undergoing ERV is similar to that of historical controls not in car

293 provide a useful framework for understanding ERV evolution, enabling the testing of evolutionary hypo

294 lutionary side effects, it is useful to view ERVs as fossil representatives of retroviruses extant at

295 s across all ERV lineages, we show that when ERVs lose the env gene their proliferation within that g

296 nfections and certain cancers, coincide with ERV expression, suggesting that transcriptional reawaken

297 s and a range of pathologies associated with ERVs, including cancer.

298 imeric transcripts that are initiated within ERV long terminal repeat (LTR) sequences and read-throug

299 ach P-MLV has an E-MLV backbone with P- or X-ERV replacements that together cover 100% of the recombi

300 ow close relationships to a small xenotropic ERV subgroup largely confined to the inbred mouse Y chro