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-K113 has full-length open reading frames for all vi

12 HERV-K18 env transcripts were not significantly differen

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

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

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

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

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

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

19 h humoral and cell-mediated immunity against HERV-K can be found in BC patients.

20 13 years) were tested for responses against HERV peptides in gamma interferon (IFN-gamma) enzyme imm

21 T-cell responses against HERV-K were also detected in peripheral blood mononuclea

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

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

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

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

26 in HERV-K proviruses in the human genome and HERV-K DNA generated during in vitro replication in the

27 xed in the modern human genome (HERV-K60 and HERV-KI) were subjected to hypermutation by a cytidine d

28 esponsible for hypermutation of HERV-K60 and HERV-KI.

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

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

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

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

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

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

35 g assays detected significant titers of anti-HERV-K env IgG in a large proportion of BC patients.

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 cine that targets conserved antigens such as HERV.

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

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

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

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

43 able of mutating and inhibiting infection by HERV-K(HML-2) in cell culture.

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

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

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

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

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

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

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

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

52 In contrast, HERV-K113 Gag supported only very low levels of particle

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

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

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

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

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

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

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

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

61 C45A3) and an endogenous retroviral element (HERV-K_22q11.23), a prostate-specific androgen-repressed

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

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

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

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

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

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

68 t de novo immune responses against expressed HERV elements is unclear.

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

70 re capable of lysing target cells expressing HERV-K env protein in BC patients but not in normal fema

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

72 We examined loci in one family, HERV-K(HML2), and found that the deletion rate decreased

73 ion targeting with the distribution of fixed HERV elements in the human genome.

74 ERV-K(Con) integration sites and older fixed HERV-Ks.

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

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

77 Nevertheless, as viral "fossils," HERVs may provide insights into ancient retrovirus-host

78 We also found HERV-K-specific CTLs that were capable of lysing target

79 We found HERV-K env protein expression in 88% of BC (n = 119) but

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

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

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

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

84 s that are fixed in the modern human genome (HERV-K60 and HERV-KI) were subjected to hypermutation by

85 In contrast, genomic HERV-K proviruses are found preferentially outside trans

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

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

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

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

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

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

92 addition, precise mapping of the defects in HERV-K proviruses as was done here identifies the key po

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

94 the spectrum of mutations that are found in HERV-K proviruses in the human genome and HERV-K DNA gen

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

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

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

98 Thus, including HERV-K109, at least two HERV-K proviruses in human genom

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

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

101 assess the possible existence of infectious HERV-K alleles within the human population.

102 rovide a new lease of life for research into HERVs and disease.

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

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

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

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

107 that RNA from human endogenous retrovirus K (HERV-K) (HML-2), a relatively recent entrant into the hu

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

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

110 Human endogenous retrovirus K (HERV-K) is the most intact retrovirus in the human genom

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

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

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

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

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

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

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

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

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

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

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

122 The main difficulty is that most HERVs investigated to date are present at the same locus

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

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

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

126 -1 infection activates expression of a novel HERV-K (HML-2) provirus, termed K111, present in multipl

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

128 us retroviruses (HERVs) by comparing de novo HERV integration targeting with the distribution of fixe

129 a distribution intermediate between de novo HERV-K(Con) integration sites and older fixed HERV-Ks.

130 sruptive to host mRNA synthesis, but de novo HERV-K(Con) integration within transcription units showe

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

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

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

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

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

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

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

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

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

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

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

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

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

147 In this study, we determined the extent of HERV-K env expression in human breast cancer (BC) and wh

148 The Gag of HERV-K101 allowed production of viral particles and infe

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

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

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

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

153 e deaminase responsible for hypermutation of HERV-K60 and HERV-KI.

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

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

156 erating procedures for robust measurement of HERV RNA.

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

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

159 The sequence of this portion of HERV-K CA showed similarities to that of human immunodef

160 electron microscopy, we show the presence of HERV-K (HML-2) virus-like particles in the plasma of lym

161 -1 Gag, as demonstrated by (i) processing of HERV-K(CON) Gag by HIV-1 protease in virions, (ii) coimm

162 The envelope (Env) protein of HERV-K18 encodes a superantigen that strongly stimulates

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

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

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

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

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

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

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

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

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

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

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

174 These findings indicate that accumulation of HERVs in the human germline is a two-step process: integ

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

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

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

178 er, a new class of insertionally polymorphic HERV-K family members, present in a minority of individu

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

180 We propose that insertionally polymorphic HERVs could be novel genetic risk factors and hence prov

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

182 es of Alu, L1 and SVA elements (and possibly HERV-K elements) remain actively mobile in the human gen

183 ontain both immature and correctly processed HERV-K (HML-2) Gag and envelope proteins.

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

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

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

187 f recombinational deletion for dating recent HERV integrations.

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

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

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

191 against stable human endogenous retroviral (HERV) antigens.

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

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

194 ssion of latent human endogenous retroviral (HERV) proteins.

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

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

197 e that elements of the endogenous retrovirus HERV-K (HML-2) can be found in the blood of modern-day h

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

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

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

201 be derived from human endogenous retrovirus (HERV) type E and were expressed in RCC cell lines and fr

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

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

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

205 Indeed, one endogenous retrovirus [HERV-K(HML-2)], which has replicated in humans for the p

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

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

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

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

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

211 cumulation of human endogenous retroviruses (HERVs) by comparing de novo HERV integration targeting w

212 Human endogenous retroviruses (HERVs) comprise approximately 8% of the human genome, bu

213 fate of most human endogenous retroviruses (HERVs) has been to undergo recombinational deletion.

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

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

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

217 Human endogenous retroviruses (HERVs) result from ancestral infection by infectious vir

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

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

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

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

222 sociated with human endogenous retroviruses (HERVs).

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

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

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

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

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

228 However, no single HERV-K provirus in the human genome today appears to be

229 in ETV1 fusions, including TMPRSS2, SLC45A3, HERV-K_22q11.23, C15ORF21, and HNRPA2B1.

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

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

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

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

234 t pronounced for certain members of the SVA, HERV, LINE-1P, AluY, and MaLR families.

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

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

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

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

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

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

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

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

243 We found that HERV-K(Con) integrated preferentially in transcription u

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

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

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

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

248 These data suggest that HERV-E is activated in RCC and that it encodes an overex

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 Phylogenetic analyses suggest that the HERV-P family may be divided into two distinct categorie

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

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

274 These HERV-specific T cell responses were inversely correlated

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

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

277 mmunity against antigenic components of this HERV-E.

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

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

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

281 2, and K18) constitute over 90% of the total HERV-K expression in primary human lymphocytes of five d

282 e investigated the abilities of Gag from two HERV-K proviruses to support production of virus-like pa

283 Thus, including HERV-K109, at least two HERV-K proviruses in human genome today have functional

284 We also present striking evidence that two HERV-K(HML-2) proviruses that are fixed in the modern hu

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

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

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

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

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

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

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

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

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

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

295 reading frames for all viral proteins, while HERV-K101 has a full-length gag open reading frame and i

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

297 during in vitro stimulation of BC PBMC with HERV-K antigen.

298 with autologous dendritic cells pulsed with HERV-K env SU antigens.

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

300 We also found that the youngest HERV-K elements in the human genome showed a distributio