ライフサイエンスコーパス: HERV

1 HERV (-H, -K, and -L family)-specific T cell responses w

2 HERV DNA sequences in the human genome represent the rem

3 HERV-E expression in ccRCC linearly correlated with HIF-

4 HERV-K (HML-2) RNA was found in plasma fractions of HIV-

5 HERV-K deoxyuridine triphosphate nucleotidohydrolase ind

6 HERV-K ENV imparts an endocytic entry pathway that requi

7 HERV-K envelope and deoxyuridine triphosphate nucleotido

8 HERV-K expression strongly correlated with TDP-43, a mul

9 HERV-K pol transcripts were increased in patients with A

10 HERV-K(HML-2)-specific CD8+ T cells obtained from HIV-1-

11 HERV-K18 env transcripts were not significantly differen

12 HERV-K18 env transcripts, HHV-6 viral copy number, and H

13 HERVs are silenced in most normal tissues, up-regulated

14 ngth RNA of the env gene of the type 1 and 2 HERV-K (HML-2) viruses collected from the plasma of seve

15 ind CD8(+) T cell populations recognizing 29 HERV-derived peptides representing 18 different HERV loc

16 nsistent with the proposed mode of action, a HERV-K(HML-2)-specific CD8+ T cell clone exhibited compr

17 on status at all sites reported to contain a HERV-K provirus.

18 hree-dimensional topological structure for a HERV molecule-and find that the RcRE resembles the HIV-1

19 hat allow us to obtain detailed and accurate HERV-K HML-2 expression profiles.

20 Only the more recently acquired HERVs, such as the HERV-K (HML-2) group, maintain coding

21 ype K (HERV-K), the youngest and most active HERV, has been associated with various cancers and neuro

22 transcripts, proteins, and antibody against HERV-K are detected in cancers, auto-immune, and neurode

23 13 years) were tested for responses against HERV peptides in gamma interferon (IFN-gamma) enzyme imm

24 Also, HERV-K18 env transcripts did not correlate with HHV-6 vi

25 This work also demonstrates that although HERV-K (HML-2) proviruses in the human genome are highly

26 For this purpose, we constructed an HERV-K dUTPase wild-type sequence, as well as specific m

27 Nuclear export of both HIV-1 and HERV-K mRNAs is dependent on the interaction between a s

28 localization and coassembly of HIV-1 Gag and HERV-K Gag also required nucleocapsid (NC).

29 -reactivity between homologous HIV-1-Pol and HERV-K(HML-2)-Pol determinants, raising the possibility

30 ntromeric markers (alpha-satellite units and HERV-K copies) were observed in neoplastic samples as co

31 possibility that homology between HIV-1 and HERVs plays a role in shaping, and perhaps enhancing, th

32 etermine which of the 91 currently annotated HERV-K (HML-2) proviruses are regulated by Tat.

33 -like particles that were recognized by anti-HERV-K (HML-2) antibodies.

34 se findings suggest a possible role for anti-HERV immunity in the control of chronic HIV-1 infection

35 is article, we demonstrate that a human anti-HERV-K (HML-2) transmembrane protein Ab binds specifical

36 ith early HIV-1 infection have stronger anti-HERV T cell responses than uninfected controls.

37 In addition, the magnitude of the anti-HERV T cell response was inversely correlated with HIV-1

38 rating a library of 1169 potential antigenic HERV-derived peptides predicted for presentation by 4 HL

39 to identify closely related elements such as HERV-K from short read sequence data.

40 echanism by which human retroviruses such as HERV-K might contribute to TDP-43-mediated propagation o

41 cine that targets conserved antigens such as HERV.

42 ) coimmunoprecipitation of virion-associated HERV-K(CON) Gag with HIV-1 Gag, and (iii) rescue of a la

43 Further, because HERV-K is insertionally polymorphic, the genome burden o

44 n marked contrast to other betaretroviruses, HERV-K ENV imparts broad species tropism in cultured cel

45 ral therapy (HAART) had stronger and broader HERV-specific T cell responses than HAART-suppressed pat

46 l cells (PAEC) to apoptosis was increased by HERV-K deoxyuridine triphosphate nucleotidohydrolase in

47 V) in which the glycoprotein was replaced by HERV-K ENV.

48 transporter-1 (MCT-1) as a receptor used by HERV-T for attachment and infection.

49 ric analyses of an HLA-B51-restricted CD8(+) HERV response in one HIV-1-infected individual revealed

50 Five common HERV-K dUTPase variants were found to be highly associat

51 Here, we provide comprehensive HERV-K HML-2 expression profiles specific for productive

52 on targeting using a reconstituted consensus HERV-K (designated HERV-K(Con)).

53 eplication and that certain highly conserved HERV-derived proteins may serve as promising therapeutic

54 ediate the nuclear export of RcRE-containing HERV-K mRNAs, which contributes to elevated production o

55 In contrast, HERV-K (HML-2) RNA sequences found in the blood of breas

56 and (iii) rescue of a late-domain-defective HERV-K(CON) Gag by wild-type (WT) HIV-1 Gag.

57 Myristylation-deficient HERV-K(CON) Gag localized to nuclei, suggesting cryptic

58 Gag failed to rescue myristylation-deficient HERV-K(CON) Gag to the plasma membrane.

59 Here we describe HERV-H LTR-associating protein 2 (HHLA2) as a member of

60 a reconstituted consensus HERV-K (designated HERV-K(Con)).

61 , there are conflicting reports on detecting HERV RNA in non-cellular clinical samples such as plasma

62 V-derived peptides representing 18 different HERV loci, of which HERVH-5, HERVW-1, and HERVE-3 have m

63 imary lymphocytes express up to 32 different HERV-K envelopes, and that at least two of the most expr

64 A human endogenous retrovirus type E (HERV-E) was recently found to be selectively expressed i

65 ing a reference set of k-mers unique to each HERV-K locus and applies mixture model-based clustering

66 previously unreported HERV-K(HML2) elements (HERV-K is human endogenous retrovirus K).

67 Elevated HERV expression, mediated by HIV infection or other stre

68 of the HERV-K RcRE, contributing to elevated HERV-K expression in HIV-infected patients.

69 The youngest human ERVs (HERVs) belong to the HERV-K(HML-2) subgroup and were end

70 although members of one group of human ERVs (HERVs), HERV-K, were recently active with members that r

71 This apparently exapted HERV-T env could not support virion infection but could

72 control of HIV-1 infection and for exploring HERV-K(HML-2)-targeted HIV-1 vaccines and immunotherapeu

73 nd that one of the most abundantly expressed HERV-K envelopes not only makes a full-length protein bu

74 To identify the most expressed HERV-Ks in an unbiased manner, we analyzed their express

75 We focus on one family, HERV-K HML-2 (HK2) that has been most recently active ev

76 lpha can serve as transcriptional factor for HERV-E by binding with HIF response element (HRE) locali

77 d here, we characterize the requirements for HERV-K ENV to mediate infectious cell entry.

78 s population-specific sequence variation for HERV-K proviruses at several loci.

79 odern infectious HERV-K has yet to be found, HERV-K activation has been associated with cancers, auto

80 Four HERV-K loci on different chromosomes were analyzed in ba

81 Furthermore, HERV-K(CON) Gag was found to coassemble with HIV-1 Gag,

82 A close relative of gammaretroviruses, HERV-T, circulated in primates for 25 million years (MY)

83 Indeed, reverse transcription of genomic HERV-K RNA into the DNA form is able to occur in three d

84 All known genomic HERVs are inactive due to mutation, but we were able to

85 xpression of the endogenous retrovirus group HERV-K (HML-2) is seen in many human cancers, although t

86 son human endogenous retrovirus subfamily H (HERV-H) in creating topologically associating domains (T

87 members of one group of human ERVs (HERVs), HERV-K, were recently active with members that remain ne

88 ge of human endogenous retroviruses (HERVs), HERV-K(HML2), is upregulated in many cancers, some autoi

89 The results for all four loci showed higher HERV-K expression in the basal subtype, suggesting simil

90 The HML2 (HERV-K) group constitutes the most recently acquired fam

91 in myeloid malignancies, thereby implicating HERVs as potential targets for immunotherapeutic therapi

92 We fail to demonstrate a difference in HERV-K18 env transcripts, HHV-6 viral copy number, and H

93 ses a small and heterogeneous enhancement in HERV transcription without altering T cell recognition.

94 V-1 Tat protein caused a 13-fold increase in HERV-K (HML-2) gag RNA transcripts in Jurkat T cells and

95 e LTR was found to be hypomethylated only in HERV-E-expressing ccRCC while other tumors and normal ti

96 region on the mRNA (RRE in HIV-1 and RcRE in HERV-K).

97 small viral protein (Rev in HIV-1 and Rec in HERV-K) and a region on the mRNA (RRE in HIV-1 and RcRE

98 iously understood, and it may be relevant in HERV-K-associated human diseases.

99 veals the structural basis for the increased HERV-K expression observed in HIV-infected patients.

100 While a modern infectious HERV-K has yet to be found, HERV-K activation has been a

101 ghout the human genome, but as no infectious HERV-K virus has been detected to date, the mechanism by

102 Intriguingly, HERV-K Gag overexpression reduced not only HIV-1 release

103 ncytins, this protein, called suppressyn, is HERV-derived, placenta-specific and well-conserved over

104 rt that human endogenous retrovirus group K (HERV-K) (HML-2) proviruses are expressed at significantl

105 st that human endogenous retrovirus group K (HERV-K) provirus expression plays a role in the pathogen

106 mplicated the human endogenous retrovirus K (HERV-K) dUTPase located within the PSORS1 locus in the m

107 expression of human endogenous retrovirus K (HERV-K) in PAH versus control lungs (n=4).

108 encoded by a human endogenous retrovirus K (HERV-K) may be a candidate gene for the psoriasis suscep

109 V, as well as human endogenous retrovirus K (HERV-K)108--a betaretrovirus-like human endogenous retro

110 Human endogenous retrovirus-K (HERV-K) human mouse mammary tumor virus-like 2 (HML-2) i

111 n of the human endogenous retrovirus type K (HERV-K) (HML-2), we used next-generation sequencing to d

112 n of the human endogenous retrovirus type K (HERV-K) has been associated with various cancers and aut

113 The HERV type K (HERV-K) HML-2 (HK2) family contains proviruses that are

114 Human Endogenous Retrovirus type K (HERV-K) is the only HERV known to be insertionally polym

115 Human endogenous retrovirus type K (HERV-K) proviruses are scattered throughout the human ge

116 n of the Human Endogenous Retrovirus Type K (HERV-K), the youngest and most active HERV, has been ass

117 s of the human endogenous retrovirus type-K (HERV-K) (HML-2) family.

118 ription of the HML-2 lineage of HERV type K [HERV-K(HML-2)] and the expression of Gag and Env protein

119 tested for human endogenous retrovirus-K18 (HERV-K18) env transcripts using a TaqMan quantitative po

120 ot in more distantly related species lacking HERV-H elements.

121 Moreover, the ability of modern HERV-K viruses to proceed through reverse transcription

122 that canonical retroviruses package, modern HERV-K viruses can contain reverse-transcribed DNA (RT-D

123 Moreover, HERV-K18 Env incorporation into HIV-1 virions is depende

124 dy, we demonstrate that wild-type and mutant HERV-K dUTPase proteins induce the activation of NF-kapp

125 uman primary cells with wild-type and mutant HERV-K dUTPase proteins triggered the secretion of T(H)1

126 ls that seemingly lack K111, we discover new HERV-K (HML-2) members hidden in pericentromeres of seve

127 -1 infection activates expression of a novel HERV-K (HML-2) provirus, termed K111, present in multipl

128 RNA sequences from novel HERV-K (HML-2) proviruses were discovered, including K11

129 he prevalence of individual and co-occurring HERV-K proviruses; we provide a visualization tool to ea

130 The ability of HERV-H to create TAD boundaries depends on high transcri

131 nome, and we have detected the activation of HERV-K (HML-2) proviruses in the blood of patients with

132 Because activation of HERV-K and coexpression of this virus with HIV-1 have be

133 These properties reflect the activity of HERV-K and suggest the existence of additional unique lo

134 ur approach through single locus analysis of HERV expression in 13 ENCODE cell types.

135 We performed a cross-sectional analysis of HERV-specific T cell responses in 42 vertically HIV-1-in

136 Construction of a near-complete catalog of HERV-T fossils in primate genomes allowed us to estimate

137 necessary to discriminate the complexity of HERV-K expression.

138 This justifies the consideration of HERV-K(HML-2)-specific and cross-reactive T cell respons

139 diabetes have significantly fewer copies of HERV-K(C4) and that this effect is not solely due to lin

140 We conclude that the slower dynamics of HERV-H suggest a host role for the internal regions of t

141 Our results show elevation of HERV-K expression exclusively in the basal subtype of ID

142 n important role in activating expression of HERV-K (HML-2) in the setting of HIV-1 infection.

143 The expression of HERV-K (HML-2) is tightly regulated but becomes markedly

144 al repeat, suggesting that the expression of HERV-K (HML-2) RNA in these patients may involve sense a

145 The expression of HERV-K (HML-2), the family of HERVs that most recently e

146 families, as well as increased expression of HERV-K envelope protein.

147 anation for HIV-1 Rev-mediated expression of HERV-K in HIV-infected patients.

148 data indicated that increased expression of HERV-K is associated with decreased mutation of H-Ras (w

149 Expression of HERV-Ks has been linked to different pathological condit

150 In a fraction of HERV-K loci (Type 2 proviruses), nuclear export of the u

151 As in all retroviruses, a fraction of HERV-K transcripts is exported from the nucleus in unspl

152 nscript encoding the entire envelope gene of HERV-E as expressed selectively in ccRCC tumors, as dist

153 y, one of them, the envelope glycoprotein of HERV-K18, is incorporated into HIV-1 in an HIV matrix-sp

154 that a previously undetected, large group of HERV-K (HML-2) proviruses, which are descendants of the

155 ce more recently, such as the HML-2 group of HERV-K elements, still retain intact open reading frames

156 Furthermore, 3 weekly injections of HERV-K deoxyuridine triphosphate nucleotidohydrolase ind

157 f upstream genes, while de novo insertion of HERV-H elements can introduce new TAD boundaries.

158 ted in transcription of the HML-2 lineage of HERV type K [HERV-K(HML-2)] and the expression of Gag an

159 ing element that is conserved in the LTRs of HERV-K-10, -K-11, and -K-20, and validated the functiona

160 erating procedures for robust measurement of HERV RNA.

161 ndings provide insight into the mechanism of HERV-K expression and a structural explanation for HIV-1

162 ag was 3-fold reduced upon overexpression of HERV-K(CON) Gag.

163 We have identified a specific pattern of HERV-K expression in ALS, which may potentially define t

164 ted in part because population prevalence of HERV-K provirus at each polymorphic site is lacking and

165 -1 Gag, as demonstrated by (i) processing of HERV-K(CON) Gag by HIV-1 protease in virions, (ii) coimm

166 which contributes to elevated production of HERV-K proteins in HIV-infected patients.

167 uate the potential for T cell recognition of HERV elements in myeloid malignancies by mapping transcr

168 complexity of the genome-wide regulation of HERV-K (HML-2) expression by Tat.

169 provide structural insight for regulation of HERV-K expression.

170 We pinpointed RBM4 regulation of HERV-K to a CGG-containing element that is conserved in

171 nscription, as transcriptional repression of HERV-H elements prevents the formation of boundaries.

172 ed entry pathway and that the restriction of HERV-K to primate genomes reflects downstream stages of

173 have been conducted to determine the role of HERV-K dUTPase in psoriasis.

174 les such as plasma that suggest the study of HERV RNA can be daunting.

175 The study of HERV RNA for human translational studies should be perfo

176 covery and case-control association study of HERV-K dUTPase variants in 708 psoriasis cases and 349 h

177 f the NF-Y sites are in select subclasses of HERV LTR repeats.

178 ribed loci in the HML-2 and 3 subfamilies of HERV-K, with a specific pattern of expression including

179 n particular, RNA from the HML-2 subgroup of HERV-K proviruses has been reported to be highly express

180 i, suggesting cryptic nuclear trafficking of HERV-K Gag.

181 tem to investigate to what extent virions of HERV-Kcon, murine leukemia virus, and HIV-1 have the abi

182 expression of HERV-K (HML-2), the family of HERVs that most recently entered the genome, is tightly

183 ur study thus uncovers T cell recognition of HERVs in myeloid malignancies, thereby implicating HERVs

184 ect these resources will advance research on HERV-K contributions to human diseases.

185 ssays demonstrated that the effect of Tat on HERV-K (HML-2) expression occurred at the level of the t

186 enous Retrovirus type K (HERV-K) is the only HERV known to be insertionally polymorphic; not all indi

187 ith the also-upregulated expression of other HERV-K genes.

188 lination via its envelope protein pathogenic HERV-W (pHERV-W) ENV (formerly MS-associated retrovirus

189 However, attempts to link a polymorphic HERV-K with any disease have been frustrated in part bec

190 phic, the genome burden of known polymorphic HERV-K is variable in humans; this burden is lowest in E

191 is of a total of 36 nonreference polymorphic HERV-K proviruses, including 19 newly reported loci, wit

192 ulations with any combination of polymorphic HERV-K provirus.

193 s, which could recognize HLA-A*0201-positive HERV-E-expressing kidney tumor cells.

194 tained both immature and correctly processed HERV-K (HML-2) proteins and virus-like particles that we

195 tides predicted to be products of the CT-RCC HERV-E envelope transcript-stimulated CD8(+) T cells, wh

196 n endogenous retrovirus HERV-E (named CT-RCC HERV-E).

197 igher antibody responses against recombinant HERV-K dUTPase in psoriasis patients compared with contr

198 Taken together, we generated high-resolution HERV-K expression profiles specific for activated human

199 Moreover, using a resuscitated HERV-K virus construct, we show that both viruses with R

200 against stable human endogenous retroviral (HERV) antigens.

201 oblast-specific human endogenous retroviral (HERV) envelope proteins, called syncytins, and their wid

202 previously that human endogenous retroviral (HERV) mRNA transcripts and protein are found in cells of

203 tif searches in Human Endogenous Retroviral (HERV) RNA sequences.

204 d from the novel human endogenous retrovirus HERV-E (named CT-RCC HERV-E).

205 at upregulation of the endogenous retrovirus HERV-K could both initiate and sustain activation of the

206 ess the maturation of the extinct retrovirus HERV-K (HML-2).

207 acterization of Human Endogenous Retrovirus (HERV) expression within the transcriptomic landscape usi

208 nellovirus, and human endogenous retrovirus (HERV) reads.

209 ement (LINE) or human endogenous retrovirus (HERV) repeats as a cause of deletions, duplications, and

210 transduction of human endogenous retrovirus (HERV)-Kcon, a consensus of the HERV-K(HML-2) family, wer

211 Human endogenous retrovirus (HERV)-specific T cell responses in HIV-1-infected adults

212 Expression of a human endogenous retrovirus (HERV-K) was determined in autopsy brain tissue of patien

213 of an endogenized human-specific retrovirus (HERV-K, HML-2) from loci in chromosomes 12 and 19.

214 RNA of a type K human endogenous retrovirus, HERV-K (HML-2), at high titers in the plasma of HIV-1-in

215 most recently endogenized human retrovirus, HERV-K, can encode individual functional proteins.

216 Human endogenous retroviruses (HERV) form a substantial part of the human genome, but m

217 Human endogenous retroviruses (HERV) make up 8% of the human genome.

218 Though most human endogenous retroviruses (HERVs) are thought to be irrelevant to our biology notab

219 Human endogenous retroviruses (HERVs) are viruses that have colonized the germ line and

220 Human endogenous retroviruses (HERVs) make up 8% of the human genome.

221 ne lineage of human endogenous retroviruses (HERVs), HERV-K(HML2), is upregulated in many cancers, so

222 Human endogenous retroviruses (HERVs), which are remnants of ancestral retroviruses int

223 s composed of human endogenous retroviruses (HERVs), which are thought to be inactive remnants of anc

224 Human endogenous retroviruses (HERVs), which make up approximately 8% of the human geno

225 sociated with human endogenous retroviruses (HERVs).

226 Of all the endogenous retroviruses, HERV-K viruses are the most intact and biologically acti

227 While the youngest of these retroviruses, HERV-K(HML-2), termed HK2, is able to code for all viral

228 understand the structural basis for HIV Rev-HERV-K RcRE recognition.

229 Here, we show HERV-E expression is restricted to the clear cell subtyp

230 as higher T-cell responses against a single HERV-K dUTPase peptide (P<0.05).

231 A single HERV-T provirus in hominid genomes includes an env gene

232 fection, but our knowledge on which specific HERV-Ks are expressed in primary lymphocytes currently i

233 We applied this approach to study HERV-K expression in the presence or absence of producti

234 d HERVE-3 have more profound responses; such HERV-specific T cells are present in 17 of the 34 patien

235 s opposed to the other subtypes) and suggest HERV-K as a possible target for cancer vaccines or immun

236 These data support HERV-K dUTPase as a potential contributor to psoriasis p

237 retrovirus in the ninth intron of C4, termed HERV-K(C4), is a notable component.

238 in cells of HIV-1-infected patients and that HERV-K (HML-2)-specific T cells can eliminate HIV-1-infe

239 ring HIV-1 infection, it is conceivable that HERV-K could affect HIV-1 replication, either by competi

240 We conclude that HERV-K ENV dictates an evolutionarily conserved entry pa

241 We also demonstrate that HERV-H loci are markedly less likely to form solo-LTRs t

242 We demonstrate that HERV-K ENV undergoes a proteolytic processing step and t

243 Here, we provide evidence that HERV-K viruses currently found in the human genome are a

244 part a narrow species tropism, we found that HERV-K ENV mediates broad tropism encompassing cells fro

245 These data indicate that HERV-specific T cells may participate in controlling HIV

246 It is possible that HERV-Ks contribute to human disease because people diffe

247 Haplotype analysis revealed that HERV-K haplotypes containing the non-risk alleles for rs

248 We show that HERV-K(C4) is a novel marker of type 1 diabetes that acc

249 We show that HERV-K18 Env can be incorporated into HIV-1 but not simi

250 t ERV groups is observed but we suggest that HERV-K activity may have increased in humans since they

251 This study suggests that HERV-K (HML-2) is active in HIV-1-infected patients, and

252 The HERV type K (HERV-K) HML-2 (HK2) family contains proviru

253 The HERV-K (HML-2) family is the most recent group of these

254 he more recently acquired HERVs, such as the HERV-K (HML-2) group, maintain coding open reading frame

255 elope protein that prevents infection by the HERV-T virus and likely contributed to the extinction of

256 Our data support an independent role for the HERV-K dUTPase on psoriasis susceptibility, and suggest

257 In conclusion, this report identifies the HERV-K HML-2 loci whose expression profiles differ upon

258 es of protein and drug binding motifs in the HERV RNA ensemble that do not occur in minimum free ener

259 In HIV-1-infected individuals, the HERV-K (HML-2) viral RNA showed evidence of frequent rec

260 gy notable exceptions include members of the HERV-H family that are necessary for the correct functio

261 ipitation assays, mutational analysis of the HERV-K (HML-2) long terminal repeat, and treatments with

262 imary lymphocytes, and the expression of the HERV-K (HML-2) rec and np9 oncogenes was also markedly i

263 osylation sites, suggesting that some of the HERV-K (HML-2) viral RNAs have undergone reverse transcr

264 evated transcript level of bound ERVs of the HERV-K and -H families, as well as increased expression

265 After adjusting the association of the HERV-K dUTPase variants for the potential confounding ef

266 Expression of the HERV-K envelope gene (env) was highly significantly incr

267 to evaluate differences in expression of the HERV-K family in breast cancers of the various subtypes.

268 is able to mediate the nuclear export of the HERV-K RcRE, contributing to elevated HERV-K expression

269 s retrovirus (HERV)-Kcon, a consensus of the HERV-K(HML-2) family, were analyzed and found to reside

270 idence supporting the recent activity of the HERV-K(HML2) group, which has been implicated in human d

271 f HLA alleles associated with psoriasis, the HERV-K SNPs rs9264082 and rs3134774 remained significant

272 Here, we report the HERV-K expression profile of primary lymphocytes from 5

273 yotic cells allowed us to broadly survey the HERV-K ENV-dictated tropism.

274 he youngest human ERVs (HERVs) belong to the HERV-K(HML-2) subgroup and were endogenized within the p

275 The extent to which the HERV-K (HML-2) proviruses become activated and the natur

276 nalyses reveal enhanced transcription of the HERVs in patients; meanwhile DNA-demethylating therapy c

277 These HERV-specific T cell responses were inversely correlated

278 Deleting these HERV-H elements eliminates their corresponding TAD bound

279 e also show experimentally that two of these HERV-K env sequences (K18 and K102) retain their ability

280 nt T cell populations corresponding to these HERV and HIV-1 epitopes, ruling out cross-reactivity.

281 mmunity against antigenic components of this HERV-E.

282 We observe that three HERV-Ks (KII, K102, and K18) constitute over 90% of the

283 Thus, hsaHTenv may have contributed to HERV-T extinction, and could also potentially regulate c

284 test magnitude observed for the responses to HERV-L.

285 2, and K18) constitute over 90% of the total HERV-K expression in primary human lymphocytes of five d

286 ited to hPSCs, as these actively transcribed HERV-H elements and their corresponding TAD boundaries a

287 myeloid malignancies by mapping transcribed HERV genes and generating a library of 1169 potential an

288 RNA message reveals previously undiscovered HERV-K (HML-2) genomic sequences.

289 nificantly activates expression of 26 unique HERV-K (HML-2) proviruses, silences 12, and does not sig

290 verall, our results offer evidence of unique HERV-E envelope peptides presented on the surface of ccR

291 identifying six novel, previously unreported HERV-K(HML2) elements (HERV-K is human endogenous retrov

292 proviruses), nuclear export of the unspliced HERV-K mRNA appears to be mediated by a cis-acting signa

293 he interactions of the authentic upregulated HERV-K HML-2 elements and HIV-1.

294 fection or other stressors, can have various HERV-related biological consequences.

295 lls expressing Gag proteins of both viruses, HERV-K(CON) Gag colocalized with HIV-1 Gag at the plasma

296 We investigated 826 fixed and 1,065 in vitro HERV-Ks in human, and 1,624 fixed and 242 polymorphic ET

297 wed that human endogenous retrovirus type W (HERV-W) contributes significantly to brain damage.

298 ted that human endogenous retrovirus type W (HERV-W) negatively affects oligodendroglial precursor ce

299 Whether HERV-specific immunity exists in vertically HIV-1-infect

300 o further probe the endocytic route by which HERV-K infects cells.

301 dence that HIV-1 Gag heteromultimerizes with HERV-K Gag at the plasma membrane, presumably through NC

302 Notably, unlike WT HERV-K(CON) Gag, HIV-1 Gag failed to rescue myristylatio