ライフサイエンスコーパス: HHV-6

1 erosis, the neurotropic human herpesvirus 6 (HHV-6).

2 a cellular receptor for human herpesvirus 6 (HHV-6).

3 ction as a receptor for human herpesvirus 6 (HHV-6).

4 V), BK virus (BKV), and human herpesvirus 6 (HHV-6).

5 showing the nasal cavity is a reservoir for HHV-6.

6 vere pathological conditions associated with HHV-6.

7 HHV-6 and HHV-7 and by quantitative PCR for HHV-6.

8 nome copy numbers were highest for HSV-1 and HHV-6.

9 n T cells and then infected these cells with HHV-6.

10 life to define the pattern of acquisition of HHV-6.

11 ellular tropism and pathogenic mechanisms of HHV-6.

12 IHHV-6 group compared with the group without HHV-6 (71.4% vs. 31.4%; P = 0.04).

13 n with a well-defined time of acquisition of HHV-6, 93 percent had symptoms, and 38 percent were seen

14 Human herpesvirus 6 (HHV-6), a common resident virus of the human CNS, has be

15 ll autopsy samples consistently demonstrated HHV-6 active infection in the hippocampus.

16 HHV-6 active infection was defined as detection of viral

17 irus (HHV)-6 and monitored the recipient for HHV-6 after transplantation.

18 MDV and HHV-6, among other herpesviruses, harbor telomeric repea

19 ar dynamic range of 5 to 5 x 10(6) copies of HHV-6 and a sensitivity of five gene copies per reaction

20 svirus 6 (HHV-6) chromosomal integration had HHV-6 and beta-globin DNA quantified in various samples

21 Truncated CI-HHV-6 and extra-chromosomal circular molecules are likel

22 tion (PCR) and reverse-transcriptase PCR for HHV-6 and HHV-7 and by quantitative PCR for HHV-6.

23 We prospectively studied HHV-6 and HHV-7 at multiple sites in pregnant women to d

24 Treatment of HHV-6 and HHV-7 disease includes antiviral therapy and c

25 We found no cases of symptomatic HHV-6 and HHV-7 disease.

26 HHV-6 and HHV-7 DNAemia were not significantly associate

27 HHV-8) of the eight human herpesviruses; the HHV-6 and HHV-7 polymerases contain an alanine at this a

28 randomized to be monitored in real-time for HHV-6 and HHV-7 viremia by polymerase chain reaction at

29 d be demonstrated from routine monitoring of HHV-6 and HHV-7 viremia in graft or patient outcome afte

30 In the "monitoring" group, HHV-6 and HHV-7 viremia occurred in 23 of 64 patients (3

31 The potential utility of monitoring for HHV-6 and HHV-7 viremia remains unclear.

32 Over the course of the week, the DNAs of HHV-6 and HHV-7 were detected significantly more often (

33 re naturally infected with viral homologs of HHV-6 and HHV-7, which we provisionally named MneHV6 and

34 d may be affected by the interaction between HHV-6 and HHV-7.

35 ce of EBV in saliva but has little effect on HHV-6 and HHV-7.

36 infants had proven transplacentally acquired HHV-6 and mothers had documented ciHHV-6, and we sequenc

37 provide a window into the immune response to HHV-6 and provide a basis for tracking HHV-6 cellular im

38 The decreased T-cell responses to HHV-6 and the altered cytokine profile were consistent w

39 rom 6 infants with transplacentally acquired HHV-6 and with samples of their parents' hair.

40 assage of chromosomally integrated HHV-6 (CI-HHV-6) and from transplacental passage of maternal HHV-6

41 n, viral copy number of human herpesvirus-6 (HHV-6) and human herpesvirus-7 (HHV-7) were measured in

42 Human herpesvirus 6 (HHV-6) and oncogenic Marek's disease virus (MDV) have be

43 D46, which serves as a cellular receptor for HHV-6, and CD3 were downmodulated.

44 rrow suppression), and herpes simplex virus, HHV-6, and CMV in AIDS patients (accelerating the rate o

45 R assay demonstrated shedding of HHV-7, EBV, HHV-6, and CMV, listed by order of magnitude.

46 (GVHD), treatments, clinical signs, outcome, HHV-6, and other infections were collected for a histori

47 with transplacentally acquired HHV-6 had CI-HHV-6, and the mother's CI-HHV-6 variant was the same va

48 using polymerase chain reaction and assessed HHV-6 antibody reactivity in the cerebrospinal fluid of

49 polymerase chain reaction detection and anti-HHV-6 antibody response was also demonstrated.

50 e skin, because normal CD4(+) T cells gained HHV-6 antigen after in vitro coculture with highly virus

51 ergence of monomyeloid precursors expressing HHV-6 antigen in the circulation during this clinical co

52 uggest that monomyeloid precursors harboring HHV-6 are navigated by HMGB-1 released from damaged skin

53 Collectively, these results suggested HHV-6 as a possible pathogen in a subset of encephalitis

54 Plasma samples were tested for HHV-6 at baseline and twice weekly after transplantation

55 y integrated copy of human herpesvirus 6 (CI-HHV-6), but the consequences of integration for the viru

56 om 24 patients were found to be positive for HHV-6 by real-time PCR.

57 a physiologically relevant study model, that HHV-6 can severely affect the physiology of secondary ly

58 se to HHV-6 and provide a basis for tracking HHV-6 cellular immune responses.

59 n-10 (IL-10) were appropriate markers of the HHV-6 cellular response.

60 competent patients with human herpesvirus 6 (HHV-6) chromosomal integration had HHV-6 and beta-globin

61 germline passage of chromosomally integrated HHV-6 (CI-HHV-6) and from transplacental passage of mate

62 ide are carriers of chromosomally integrated HHV-6 (ciHHV-6), which is inherited as a genetic trait.

63 ine transmission of chromosomally integrated HHV-6 (ciHHV-6).

64 The majority of human herpesvirus 6 (HHV-6) congenital infections (86%) originate from germ l

65 ortance of iciHHV-6 loss from telomeres, the HHV-6 copy number should be assessed in tumours that ari

66 determine whether transplacentally acquired HHV-6 could derive from the transmission of reactivated

67 ue to the genetic transmission of integrated HHV-6 could have been misinterpreted as substantial acti

68 We aimed to determine whether CI-HHV-6 could replicate and cause transplacentally acquire

69 The HHV-6 detection rate in this population was therefore 1.

70 These data show that HHV-6 differentially influences the functions of naive T

71 seroconversion and/or a low concentration of HHV-6 DNA (<3.0 log(10) copies/ml) in a seronegative ser

72 ly in PBMCs from pregnant women (66.9%) than HHV-6 DNA (22.2%; P<.0001), but both were found at low r

73 FISH confirmed that HHV-6 DNA colocalized with telomeric regions of one alle

74 The mean HHV-6 DNA concentration (log(10) copies/milliliter) in b

75 HHV-6 DNA concentration (log(10) copies/ml) was measured

76 0) copies/milliliter) in blood was 7.0 (>/=1 HHV-6 DNA copies/leukocyte), and in serum it was 5.3 (>/

77 es/leukocyte), and in serum it was 5.3 (>/=1 HHV-6 DNA copies/lysed cell).

78 Although the frequency of HHV-6 DNA did not differ significantly by sample type, H

79 The mean concentration of CSF HHV-6 DNA in 9 children with primary infection (2.4 log(

80 Detection of HHV-6 DNA in cervical secretions is associated with HHV-

81 HHV-6 DNA in CSF and serum may not reflect the level of

82 NA in cervical secretions is associated with HHV-6 DNA in PBMC samples.

83 The prevalences of CSF HHV-6 DNA in primary infection and chromosomal integrati

84 omal integration is the most likely cause of HHV-6 DNA in the CSF of the immunocompetent.

85 sy specimens, we found that the frequency of HHV-6 DNA in the olfactory bulb/tract region was among t

86 The characteristically high HHV-6 DNA levels in chromosomal integration may confound

87 The mean HHV-6 DNA load (log(10) copies)/hair follicle was 4.2 (>

88 nd child, had unusually high copy numbers of HHV-6 DNA per milliliter of blood.

89 Pregnant women with HHV-6 DNA present in cervical swabs had a greater odds o

90 cervical swabs had a greater odds of having HHV-6 DNA present in the blood than did pregnant women w

91 44 NAWM samples, 7 (15.9%) were positive for HHV-6 DNA sequences, versus 37 (57.8%) of 64 MS plaques

92 HHV-6 DNA was detected in 10 (21.7%) of 46 samples from

93 HHV-6 DNA was detected in a total of 52 of 126 (41.3%) n

94 did not differ significantly by sample type, HHV-6 DNA was significantly more common in MS plaques, s

95 The children's saliva was tested weekly for HHV-6 DNA with the use of the polymerase chain reaction.

96 nd at low rates in cervical swabs (HHV-7 vs. HHV-6 DNA, 3.0% vs. 7.5%; P=.19).

97 HHV-6 DNA, variant type, and viral loads were determined

98 ce and concentration of human herpesvirus 6 (HHV-6) DNA in the cerebrospinal fluid (CSF) of the immun

99 The frequency of human herpesvirus 6 (HHV-6) DNA was assessed in autopsy material from multipl

100 group compared with the group with low-level HHV-6 DNAemia (71.4% vs. 37.1%; P = 0.12) and those with

101 71.4% vs. 37.1%; P = 0.12) and those without HHV-6 DNAemia (71.4% vs. 42.9%; P = 0.25), although thes

102 ence of HHV-6 DNAemia and factors related to HHV-6 DNAemia and death after allogeneic stem cell trans

103 We investigated the incidence of HHV-6 DNAemia and factors related to HHV-6 DNAemia and d

104 had low-level HHV-6 DNAemia, and 506 had no HHV-6 DNAemia before liver transplantation.

105 eriod, 44 patients (n=44/220, 20%) presented HHV-6 DNAemia in whole blood, including three integrated

106 HHV-6 DNAemia was not associated with death (P=0.151).

107 HHV-6 DNAemia was not significantly associated with cyto

108 HHV-6 DNAemia was not so frequent after allogeneic trans

109 The factors associated with HHV-6 DNAemia were as follows: cord blood transplantatio

110 Factors associated with HHV-6 DNAemia were similar to those for other infections

111 Seven had CIHHV-6, 35 had low-level HHV-6 DNAemia, and 506 had no HHV-6 DNAemia before liver

112 with those of patients with low-level or no HHV-6 DNAemia.

113 her incidence of CMV disease was observed in HHV-6 DNAemic patients.

114 Human herpesvirus 6 (HHV-6) employs the complement regulator CD46 (membrane c

115 Our results show that any diagnosis of HHV-6 encephalitis or other type of active central nervo

116 aluates publications on human herpesvirus 6 (HHV-6) encephalitis recognizing firstly that HHV-6A and

117 en aimed at identifying human herpesvirus 6 (HHV-6)-encoded proteins that modulate immune recognition

118 Like other known herpesviruses, HHV-6 encodes multiple glycoproteins, several of which h

119 Currently, the route of HHV-6 entry into the CNS is unknown.

120 wing primary infection, human herpesvirus 6 (HHV-6) establishes a persistent infection for life.

121 les exhibited significantly higher levels of HHV-6 expression compared with the normal control sample

122 ntial of HHV-7 is unclear, it can reactivate HHV-6 from latency and thus contributes to severe pathol

123 nd those previously shown to be critical for HHV-6 fusion (i.e. short consensus repeats 2 and 3).

124 d ciHHV-6, and we sequenced and compared the HHV-6 gB gene sequences for each pair.

125 HHV-6 gene transcription was detected in all tissue samp

126 In summary, we show that the CI-HHV-6 genome disrupts stability of the associated telome

127 c DNA and cDNA confirmed the presence of the HHV-6 genome in all individuals, with the active express

128 c cell of iciHHV-6+ individuals contains the HHV-6 genome integrated in the telomere of chromosomes.

129 Integration of the HHV-6 genome into TTAGGG telomere repeats was confirmed

130 neuroglial and inflammatory cells containing HHV-6 genome were present in acute-phase lesion tissue f

131 cytes, lymphocytes, and microglia containing HHV-6 genome within all lesions, whereas ICC showed only

132 n reaction (ISPCR) method was used to detect HHV-6 genome, in conjunction with immunocytochemical sta

133 The prevalence of HHV-6 genome-containing cells, including oligodendrocyte

134 results in the germ-line transmission of the HHV-6 genome.

135 telomere-loop (t-loop) formed within the CI-HHV-6 genome.

136 rom laser microdissected brain material, and HHV-6 genomic sequences were amplified by nested polymer

137 l experiments, a monoclonal antibody against HHV-6 gH was found to co-immunoprecipitate CD46.

138 hin all lesions, whereas ICC showed only the HHV-6 glycoprotein 116 antigen in some reactive astrocyt

139 rs of infants with transplacentally acquired HHV-6 had CI-HHV-6, and the mother's CI-HHV-6 variant wa

140 HHV-6 has evolved a unique mechanism of inhibition of T-

141 ) and CD8(+) T cells to human herpesvirus 6 (HHV-6) have not been previously investigated.

142 stein-Barr virus (EBV), human herpesvirus 6 (HHV-6), herpes simplex virus types 1 (HSV-1) and 2 (HSV-

143 Like the closely related HHV-6, HHV-7 suppresses the replication of CCR5-tropic (

144 he neurotropic human herpes viruses 6 and 7 (HHV-6, HHV-7) comprise a significant proportion of viral

145 Reactivations of HHV, including HHV-6, HHV-7, cytomegalovirus (CMV), and Epstein-Barr vi

146 to evaluate the viral reactivation rates of HHV-6, HHV-7, Epstein-Barr virus (EBV), and cytomegalovi

147 nfections with 5 human herpesviruses (HHVs) (HHV-6, HHV-7, HHV-8, varicella zoster virus [VZV], and E

148 ence, or level of DNAemia for infection with HHV-6, HHV-8, VZV, and EBV but not for infection with HH

149 Viremia with CMV, EBV, HHV-6, HSV-1, HSV-2, and VZV was detected in 60 (18%), 1

150 effect of inherited chromosomally integrated HHV-6 (iciHHV-6) in hematopoietic cell transplant (HCT)

151 Our results demonstrated increased levels of HHV-6 IgG, as well as IgM levels, in a subset of encepha

152 Serum HHV-6 immunoglobulin G antibody was measured by indirect

153 itance via gametocyte integration results in HHV-6 in every nucleated cell.

154 -6 makes it difficult to outline the role of HHV-6 in human disease.

155 The acquisition of HHV-6 in infancy is usually symptomatic and often result

156 CD4(+) T cells responding to HHV-6 in peripheral blood were observed at frequencies b

157 The detection of HHV-6 in specimens from patients diagnosed with encephal

158 r other agents, strongly suggests a role for HHV-6 in the pathogenesis of these central nervous syste

159 ejection), CMV and human herpesvirus type 6 (HHV-6) in bone marrow transplant patients (causing marro

160 Cell cycle arrest in HHV-6-infected cells was associated with a profound decr

161 Da protein band specifically associated with HHV-6-infected cells.

162 ellular antigens was dramatically altered in HHV-6-infected tissues: whereas CD4 was upregulated, bot

163 We show that the CD46 ectodomain blocked HHV-6 infection and bound a complex of gH-gL and the 80-

164 gration may confound laboratory diagnosis of HHV-6 infection and should be given due consideration.

165 nd HHV-7 have been suggested, and congenital HHV-6 infection does occur.

166 rscoring the need for diagnostic testing for HHV-6 infection even in the presence of ciHHV-6.

167 The frequent high level of HHV-6 infection in multiple sclerosis samples suggests a

168 Moreover, HHV-6 infection markedly enhanced the production of the

169 Primary HHV-6 infection occurred in 130 children, with cumulativ

170 Active HHV-6 infection occurs early after renal transplantation

171 HHV-6 infection of the skin-resident CD4(+) T cells was

172 ve placental infection along with congenital HHV-6 infection was identified.

173 who had other illnesses, those with primary HHV-6 infection were more likely to have fever (P=0.003)

174 Risk factors associated with active HHV-6 infection were receiving an organ from a living do

175 ing the transplacentally acquired congenital HHV-6 infection.

176 and from transplacental passage of maternal HHV-6 infection.

177 eplicate and cause transplacentally acquired HHV-6 infection.

178 logic course, and clinical manifestations of HHV-6 infection.

179 res are infrequently associated with primary HHV-6 infection.

180 n the understanding of the potential role of HHV-6 infection/reactivation in the activation of autoim

181 Higher incidence of human herpesvirus 6 (HHV-6) infection has been documented after umbilical cor

182 Congenital human herpesvirus 6 (HHV-6) infection results from germline passage of chromo

183 engue, and 260 cases of human herpesvirus 6 (HHV-6) infection.

184 e, HHV-7 infections occurred less often than HHV-6 infections (P< or =.002).

185 althy children < or =10 years old, HHV-7 and HHV-6 infections and their interaction by serologic asse

186 s and may cause most, if not all, congenital HHV-6 infections.

187 We show that HHV-6 infects human glial precursor cells in vitro.

188 c studies indicate that human herpesvirus 6 (HHV-6) infects 90 percent of children by two years of ag

189 disease virus (MDV) and human herpesvirus 6 (HHV-6), integrate their DNA into host chromosomes.

190 be made without first excluding chromosomal HHV-6 integration by measuring DNA load in CSF, serum, a

191 iquity of some, and possibly most, germ line HHV-6 integrations, the majority of ciHHV-6B (95%) and c

192 The telomere carrying the CI-HHV-6 is also prone to truncations that result in the fo

193 Taken together, the data suggest that HHV-6 is unique among human herpesviruses: it specifical

194 To investigate whether human herpesvirus-6 (HHV-6) is a causative agent of encephalitis, we examined

195 Human herpesvirus-6 (HHV-6) is a neurotropic virus that has been associated w

196 Human herpesvirus 6 (HHV-6) is a potentially immunosuppressive agent that has

197 Human herpesvirus 6 (HHV-6) is a ubiquitous T-lymphotropic betaherpesvirus th

198 Human herpesvirus 6 (HHV-6) is detected in the plasma of approximately 40% of

199 s a lymphotropic virus, human herpesvirus 6 (HHV-6) is highly neuropathogenic.

200 Human herpesvirus-6 (HHV-6) is known to reactivate after renal transplantatio

201 Human herpesvirus 6 (HHV-6) is susceptible to latency and reactivation in hem

202 other but divergent from that of other known HHV-6 isolates.

203 mes of the patients with CIHHV-6 (defined as HHV-6 levels >1 x 10(6) genomes/mL) were compared with t

204 The appearance and subsequent increase in HHV-6 load paralleled engraftment and an increase in whi

205 d outcome of the cellular immune response to HHV-6 makes it difficult to outline the role of HHV-6 in

206 Given this finding, we investigated whether HHV-6 may infect the CNS via the olfactory pathway.

207 y more common in MS plaques, suggesting that HHV-6 may play a role in MS pathogenesis.

208 arch has suggested that human herpesvirus-6 (HHV-6) may integrate into host cell chromosomes and be v

209 The genomic DNA of HHV-6, MDV, and several other herpesviruses harbors telo

210 ampered the elucidation of the mechanisms of HHV-6-mediated immune suppression.

211 actively explored how herpesviruses such as HHV-6 might be involved in MS disease pathogenesis.

212 Thus, by inhibiting T-cell activation, HHV-6 might limit its reactivation and thus minimize imm

213 We detected extra-chromosomal circular HHV-6 molecules, some surprisingly comprising the entire

214 V (n = 7), 100% for EBV (n = 2), and 67% for HHV-6 (n = 3).

215 aliva samples from the controls, but neither HHV-6 nor CMV were detected.

216 to the major immunoreactive region unique to HHV-6 occurred at significantly lower precursor frequenc

217 Integration of HHV-6 occurs not only in lymphocytes but also in the ger

218 ined serum immunoglobulin G (IgG) titers for HHV-6 of MS patients compared to those of control subjec

219 itu hybridization analysis showed integrated HHV-6 on chromosome band 17p13.3 in the donor and in the

220 ot support the hypothesis of reactivation of HHV-6 or HHV-7 in CFS.

221 nstrate the involvement, or lack thereof, of HHV-6 or other herpesviruses in this disease is through

222 viremia indicates primary infection, as with HHV-6, or reactivation, and if these differ clinically.

223 re consistent with transplacentally acquired HHV-6 originating from the transmission of reactivated c

224 Although HHV-6 persists within the human CNS and has been describ

225 igodendrocytes, in each lesion suggests that HHV-6 plays a role in the demyelinative pathogenesis of

226 t, changing the equivalent amino acid in the HHV-6 polymerase from alanine to valine alters polymeras

227 es were inhibited by PNU-183792, whereas the HHV-6 polymerase was not.

228 real-time quantitative human herpesvirus-6 (HHV-6) polymerase chain reaction assay was performed on

229 normally high death rate was observed in the HHV-6 positive population.

230 Fifteen percent (7/41) of HHV-6-positive patients presented clinical signs not rel

231 of PBMC and T cell cultures challenged with HHV-6 preparations indicated that gamma interferon (IFN-

232 Immunofluorescence against early and late HHV-6 proteins verified active translation of HHV-6 vira

233 study aimed to evaluate associations between HHV-6 reactivation and central nervous system dysfunctio

234 BT in 20 subjects with previously documented HHV-6 reactivation and persistent viremia.

235 HHV-6 reactivation has been associated with transplant r

236 ctivation, compared to cytokine levels after HHV-6 reactivation in the same patient.

237 The effect of HHV-6 reactivation on central nervous system function ha

238 HHV-6 reactivation or reinfection was suggested in 17% o

239 Here we demonstrate that HHV-6 reactivation persists for a very long time in half

240 HHV-6 reactivation was only observed in DRESS patients,

241 Among the various cADRs, HHV-6 reactivation was only observed in DRESS, but EBV a

242 e significantly lower in DRESS patients with HHV-6 reactivation when compared to those without HHV-6

243 cal trial to determine whether prevention of HHV-6 reactivation will reduce neurocognitive morbidity

244 s were significantly lower before and during HHV-6 reactivation, compared to cytokine levels after HH

245 To clarify the mechanism of HHV-6 reactivation, we immunologically investigated peri

246 r recipients confounds molecular testing for HHV-6 reactivation, which occurs in 30 to 50% of transpl

247 unrelated transplantation increased risk of HHV-6 reactivation.

248 es were significantly lower before or during HHV-6 reactivation.

249 reactivation when compared to those without HHV-6 reactivation.

250 as a cryptic and primary site for initiating HHV-6 reactivation.

251 ported the essential role of SCRs 2 and 3 in HHV-6 receptor activity.

252 This suggests the possibility that CI-HHV-6 replicates and may cause most, if not all, congeni

253 ant patients were prospectively followed for HHV-6 replication between February 2007 and February 200

254 he nasal cavity were demonstrated to support HHV-6 replication in vitro.

255 One placental sample had active HHV-6 replication.

256 T cells, which is an indispensable event for HHV-6 replication.

257 These findings revealed a unique pathway in HHV-6 replication: The virus causes Rb degradation and u

258 HHV-6 shedding rate and viral load were similar between

259 ssay that concurrently distinguishes between HHV-6 species (A or B) and identifies inherited ciHHV-6.

260 Human herpesvirus 6 (HHV-6) species have a unique ability to integrate into c

261 rrelates with disease course and evidence of HHV-6-specific immune responses in the CNS provide compe

262 ated with these epitopes were able to detect HHV-6-specific T cell populations.

263 The resulting HHV-6-specific T-cell lines obtained from MS patients ex

264 ve for viral antigen provided support for an HHV-6-specific tropism for hippocampal astrocytes.

265 divergent from the few modern nonintegrated HHV-6 strains for which complete sequences are currently

266 Viral strains belonging to both HHV-6 subgroups (A and B) were able to productively infe

267 cluding infections from two viruses (BKV and HHV-6) that had never been targeted previously with an o

268 ion of naive Jjhan and HEK-293 cell lines by HHV-6, the virus integrated into telomeres.

269 eleased from damaged skin and probably cause HHV-6 transmission to skin-infiltrating CD4(+) T cells,

270 lder siblings appear to serve as a source of HHV-6 transmission.

271 peptide corresponding to residues 1 to 13 of HHV-6 U24 in MS patients.

272 autoantigen for MS, and human herpesvirus-6 (HHV-6 U24, residues 4-10) that is a suspected viral agen

273 e increased antibody titers for both peptide HHV-6 (U24)(1-13) and peptide MBP(93-105) in the same pa

274 s recognizing both peptides, MBP(93-105) and HHV-6 (U24)(1-13), was significantly elevated in MS pati

275 Overall, these studies suggest that HHV-6 U51 is a positive regulator of virus replication i

276 ap, we characterized CD4 T cell responses to HHV-6 using peripheral blood mononuclear cell (PBMC) and

277 Collectively, these results support HHV-6 utilization of the olfactory pathway as a route of

278 Here we show that the U24 protein encoded by HHV-6 variant A downregulates cell surface expression of

279 d antigen in brain material confirmed active HHV-6 variant B infection, peak viral loads in cerebrosp

280 ired HHV-6 had CI-HHV-6, and the mother's CI-HHV-6 variant was the same variant causing the transplac

281 ntral nervous system diseases, suggesting an HHV-6 variant-specific tropism for glial cell subtypes.

282 These findings suggest that HHV-6 variants might be responsible for specific infecti

283 HHV-6 viral copy number and HHV-7 viral copy number in b

284 V-K18 env transcripts did not correlate with HHV-6 viral copy number or HHV-7 viral copy number in ei

285 te a difference in HERV-K18 env transcripts, HHV-6 viral copy number, and HHV-7 viral copy number bet

286 HERV-K18 env transcripts, HHV-6 viral copy number, and HHV-7 viral copy number did

287 We also explored the relationship between HHV-6 viral load and the presence of clinical signs.

288 (P=0.005), and pretransplantation recipient HHV-6 viral load more than 10,000 copies/mL plasma (P=0.

289 id not appear to be statistically related to HHV-6 viral load.

290 HV-6 proteins verified active translation of HHV-6 viral mRNA in oligodendrocytes.

291 Four (13%) showed concurrent HHV-6 viremia, 2 associated with primary HHV-7 infection

292 The acquisition of HHV-6 was associated with female sex (adjusted hazard ra

293 HHV-6 was detected in 111 (35%) of the 315 included pati

294 The study revealed that cell-free DNA of HHV-6 was detected more frequently in both serum and cer

295 HHV-6 was not detected.

296 Human herpesvirus 6 (HHV-6) was detected in specimens from patients hospitali

297 e sclerosis (MS) virus, human herpesvirus 6 (HHV-6), was sought in biopsy specimens of acute lesions

298 Patients with HHV-6 were more likely to develop delirium (adjusted odd

299 lovirus (CMV), Epstein-Barr virus (EBV), and HHV-6 were shed at high rates following primary infectio

300 Unlike HHV-6, which affects HIV-1 by upregulating RANTES, HHV-7

301 red in laboratory investigations associating HHV-6 with disease.