ライフサイエンスコーパス: ERV

1 ERV activation was accompanied by significant hippocampu

2 ERV reactivation in Tlr7 (-/-) mice was comparable in th

3 ERV reactivation is accompanied by an epigenetic shift f

4 ERV RNA and Xist A-repeat bind the RRM domains of Spen i

5 ERV-DC sequence diversity was present across wild and do

6 ERV-DC14 was detected at a high frequency in European wi

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

8 ERVs are epigenetically silenced during development, yet

9 ERVs are molecular remnants of ancient retroviruses and

10 ERVs are provirus insertions in germline cells that are

11 ERVs make up 8 to 10% of human and mouse genomes and ran

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

13 the antiretroviral soluble factor Refrex-1 (ERV-DC7 and ERV-DC16), or can generate recombinant felin

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

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

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

17 eveal that hA3G can potently restrict active ERV in vivo and suggest that expansion of the APOBEC3 lo

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

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

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

21 Insertion of an ERV into an A-repeat deficient Xist rescues binding of X

22 ngly, deletion or epigenetic silencing of an ERV-derived enhancer suppresses cell growth by inducing

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

24 nces, including major satellite, LINE-1, and ERV.

25 d four loci: ERV-DC6, ERV-DC7, ERV-DC14, and ERV-DC16.

26 plication competent (ERV-DC10, ERV-DC18, and ERV-DC14), produce the antiretroviral soluble factor Ref

27 roviral soluble factor Refrex-1 (ERV-DC7 and ERV-DC16), or can generate recombinant feline leukemia v

28 monstrate preferential gene derepression and ERV reactivation in AML with chromosomal deletions, prov

29 ssibility, active histone modifications, and ERV RNA transcription.

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

31 However, it is unknown how broadly RBPs and ERV transcripts directly interact to provide a posttrans

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

33 the formal potentials of the thioredoxin and ERV disulfides.

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

35 on of expression between individual RBPs and ERVs from single-cell or bulk RNA-sequencing data.

36 nous retrovirus (ERV) transcription and anti-ERV antibody reactivity are implicated in lupus pathogen

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

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

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

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

41 fic phenotypes through the interplay between ERVs and their hosts.

42 ovides a unique model for understanding both ERV fate and cat domestication.

43 tation to demonstrate that RBM4 indeed bound ERV transcripts at CGG consensus elements.

44 ted in an elevated transcript level of bound ERVs of the HERV-K and -H families, as well as increased

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

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

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

48 genous retroviruses (ERVs) of domestic cats (ERV-DCs) are one of the youngest feline ERV groups in do

49 n wildcats, unlike the replication-competent ERV-DC14 that is commonly present in domestic cats.

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

51 us); some members are replication competent (ERV-DC10, ERV-DC18, and ERV-DC14), produce the antiretro

52 In conclusion, ERVs have evolved species-specific phenotypes through th

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

54 d demonstrate a role for RBM4 in controlling ERV expression.

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

56 members are replication competent (ERV-DC10, ERV-DC18, and ERV-DC14), produce the antiretroviral solu

57 silvestris) and detected four loci: ERV-DC6, ERV-DC7, ERV-DC14, and ERV-DC16.

58 s) and detected four loci: ERV-DC6, ERV-DC7, ERV-DC14, and ERV-DC16.

59 This Review describes ERV origins, their diversity and their relationships to

60 or arise by recombination between different ERVs.

61 Overproduction of non-ecotropic ERV (NEERV) envelope glycoprotein gp70 and resultant nep

62 revents aberrant expression of ERV elements (ERVs) has been functionally co-opted via a stress-induce

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

64 Of note, independently evolved ERVs are associated with the expression of human-specifi

65 ats (ERV-DCs) are one of the youngest feline ERV groups in domestic cats (Felis silvestris catus); so

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

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

68 e we studied 2 independent murine models for ERV activation: muMT strain (lacking B cells and antibod

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

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

71 retroviruses and discusses the potential for ERVs to reveal virus-host interactions on evolutionary t

72 regulatory elements, that have evolved from ERVs.

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

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

75 T mice and ICVI-STZ mice induced hippocampal ERV activation, as shown by increased gene and protein e

76 1 was present in European wildcats; however, ERV-DC16, but not ERV-DC7, was unfixed in European wildc

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

78 acking, since no replication-competent human ERV have been identified.

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

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

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

82 Gammaretrovirus genus and associated class I ERVs.

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

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

85 y sequestration of induced immunostimulatory ERV dsRNAs.

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

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

88 nsposable element (TE) insertions, including ERVs, in the human genome.

89 Increased ERV expression in lupus patients inversely correlated wi

90 Intriguingly, HIV-1-induced ERVs harboring transcription start sites are primarily f

91 pobec3 (-/-) Tlr7 (-/-) mice, and infectious ERV virions could not be amplified through coculture wit

92 ergence of replication-competent, infectious ERV in Tlr7 (-/-) mice.

93 V loci can recombine and generate infectious ERV.

94 in mice prevents the emergence of infectious ERV from endogenous loci.

95 transgene abrogated emergence of infectious ERV in the Tlr7 (-/-) background.

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

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

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

99 Here, we investigated ERV-DC in European wildcats (Felis silvestris silvestris

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

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

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

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

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

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

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

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

108 lvestris silvestris) and detected four loci: ERV-DC6, ERV-DC7, ERV-DC14, and ERV-DC16.

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

110 s, suggesting that loss of KRAB-ZFP-mediated ERV control may contribute to human lupus pathogenesis.

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

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

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

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

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

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

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

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

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

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

121 urally occurring thymic lymphoma and a mouse ERV, suggesting a common mechanism of virus inactivation

122 imultaneous epigenetic silencing of multiple ERVs, we demonstrate that ERV deregulation directly alte

123 ion in the env genes of both FeLV and murine ERV provides a common mechanism shared by endogenous and

124 No ERV RNA was detected in the plasma of hA3G(+) Apobec3 (-

125 uropean wildcats; however, ERV-DC16, but not ERV-DC7, was unfixed in European wildcats.

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

127 ifferent cat lineages and generated numerous ERVs in the host genome, some of which remain replicatio

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

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

130 of ERV activation, provided confirmation of ERV impact.

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

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

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

134 Mutation and subsequent disruption of ERV loci is therefore an indispensable component of the

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

136 hat normally prevents aberrant expression of ERV elements (ERVs) has been functionally co-opted via a

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

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

139 diomyocytes in vitro to discover hundreds of ERV transcripts from the primate-specific MER41 family,

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

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

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

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

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

145 mline genes, demonstrating the prevalence of ERV-driven mechanisms in mammals.

146 ed to provide for the continued restraint of ERV in the human genome.IMPORTANCE Although APOBEC3 prot

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

148 nes protein (STING), 2 downstream sensors of ERV activation, provided confirmation of ERV impact.

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

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

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

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

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

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

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

156 has greatly contributed to the discovery of ERVs.

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

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

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

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

161 ls essential for integration and fixation of ERVs.

162 scape influences integration and fixation of ERVs.

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

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

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

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

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

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

169 d sumoylation modifiers in the repression of ERVs.

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

171 ve decline; however, in mammals, the role of ERVs in learning and memory remains unclear.

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

173 e modification-based epigenetic silencing of ERVs.

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

175 sibility that a genome-wide transposition of ERVs rewired germline gene expression in a species-speci

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

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

178 Polymorphic ERVs occur relatively infrequently in gene introns and a

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

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

181 ir relationships and identify their possible ERV progenitors.

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

183 nts inversely correlated with three putative ERV-suppressing KRAB-ZFPs, suggesting that loss of KRAB-

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

185 ematically identified RBPs that may regulate ERV function and demonstrate a role for RBM4 in controll

186 candidates for an RBP negatively regulating ERV expression was RNA-binding motif protein 4 (RBM4).

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

188 selection and ectopic recombination removing ERVs from the genome.

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

190 activates a subset of endogenous retroviral (ERV) elements in mouse embryonic stem cells, with gain o

191 ds to derepression of endogenous retroviral (ERV) elements, unmasking this cellular source of "self"

192 ation results from an endogenous retroviral (ERV) insertion upstream of the Ptf1a gene resulting in i

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

194 Here we identify six endogenous retrovirus (ERV) families with AML-associated enhancer chromatin sig

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

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

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

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

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

200 Elevated endogenous retrovirus (ERV) transcription and anti-ERV antibody reactivity are

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

202 ficantly derepressing endogenous retrovirus (ERV)3-1, with promoter demethylation, enhanced chromatin

203 Endogenous retroviruses (ERV) are found throughout vertebrate genomes, and failur

204 the restriction of endogenous retroviruses (ERV) have been limited to in vitro studies.

205 Among them, endogenous retroviruses (ERV) represent sequences that closely resemble the provi

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

207 on and silencing of endogenous retroviruses (ERV).

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

209 Although endogenous retroviruses (ERVs) are known to harbor cis-regulatory elements, their

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

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

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

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

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

215 Here, we show that endogenous retroviruses (ERVs) influence species-specific germline transcriptomes

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

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

218 Endogenous retroviruses (ERVs) of domestic cats (ERV-DCs) are one of the youngest

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

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

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

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

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

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

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

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

227 In the case of endogenous retroviruses (ERVs), a TE subclass, experimental interrogation is cons

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

229 R retrotransposons, endogenous retroviruses (ERVs), and exogenous retroviruses.

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

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

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

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

234 al elements, termed endogenous retroviruses (ERVs), that comprise ~8% of the human genome.

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

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

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

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

239 omic approach using endogenous retroviruses (ERVs).

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

241 nous proviruses and endogenous retroviruses (ERVs).

242 sequences known as endogenous retroviruses (ERVs).

243 ome is derived from endogenous retroviruses (ERVs).

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

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

246 lized to a small interval adjacent to the Sd ERV insertion overlapping a known Ptf1a enhancer region,

247 Here, we detected several ERV-DC loci in Felis silvestris silvestris Notably, a sp

248 tivity and precision for detecting simulated ERV and other TE insertions derived from real polymorphi

249 Some ERV lineages proliferate by infecting germline cells, as

250 Some ERVs have been shown to be transcribed under physiologic

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

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

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

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

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

256 to-meiosis transition in male mice, specific ERVs function as active enhancers to drive germline gene

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

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

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

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

261 Overall, our results demonstrate that ERV activation is associated with cognitive impairment i

262 encing of multiple ERVs, we demonstrate that ERV deregulation directly alters the expression of adjac

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

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

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

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

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

268 Together, we propose that ERVs fine-tune species-specific transcriptomes in the ma

269 This work reveals that ERVs are a previously unappreciated source of AML enhanc

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

271 ecific single nucleotide polymorphism in the ERV-DC14 env gene, which results in a replication-defect

272 n, resulting in an E148K substitution in the ERV-DC14 envelope (Env).

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

274 d mouse, and indicate that the effect of the ERV insertion on Ptf1a expression may be mediated by inc

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

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

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

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

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

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

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

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

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

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

285 Spen binds directly to ERV RNAs that show structural similarity to the A-repeat

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 es direct recruitment of Chaf1a and Sumo2 to ERVs.

290 for Toll-like receptor 7 (TLR7), transcribed ERV loci can recombine and generate infectious ERV.

291 The existence of two ERV-DC14 phenotypes provides a unique model for understa

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

293 t the full spectrum of polymorphic (unfixed) ERVs using whole-genome sequencing (WGS) data.

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

295 dogenous and exogenous retroviruses by which ERVs can be inactivated after endogenization.

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 seases have been found to be associated with ERVs.

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