ライフサイエンスコーパス: HHV-6

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

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

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

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

5 vere pathological conditions associated with HHV-6.

6 alovirus (CMV) (18.3%), human herpesvirus 6 (HHV-6) (34.2%), human herpesvirus 7 (HHV-7) (20.5%) and

7 aliva and 3% in GCF; of human herpesvirus-6 (HHV-6) 6% in saliva and 2% in GCF; and HHV-7 44% in sali

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

9 Human herpesvirus-6 (HHV-6) A and B are ubiquitous betaherpesviruses, infecti

10 Here, we show that human herpesvirus 6 (HHV-6, A or B) RNA was detected in 6.1% of cases of pre-

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

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

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

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

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

16 ection do not suggest an association between HHV-6 and AD.

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

18 Concurrent HHV-6 and CMV viremia was associated with earlier onset

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

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

21 CMV, EBV, HHV-6 and HHV-7 are more prevalent in biliary fluid than

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

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

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

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

26 prophylaxis did not reduce the prevalence of HHV-6 and HHV-7 in bile, but it did reduce the presence

27 HHV-6 and HHV-7 might be associated with biliary complic

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

39 Human herpesvirus 6 (HHV-6) and cytomegalovirus (CMV) are population-prevalen

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

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

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

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

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

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

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

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

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

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

53 with understanding the cellular response to HHV-6 at the individual and population levels.

54 ier onset of HHV-6 viremia (p=0.004), higher HHV-6 AUC (p=0.043), and higher peak HHV-6 viral load (p

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

56 Detection of HHV-6 by FA-ME led to discontinuation of acyclovir withi

57 Chart review on 25 patients positive for HHV-6 by FA-ME was performed to determine clinical prese

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

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

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

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

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

63 The presence of chromosomally integrated HHV-6 (ciHHV-6) DNA was also investigated.

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

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

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

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

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

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

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

71 HHV-6 demonstrated little specificity to AD brains over

72 We screened for HHV-6 detection across three independent AD brain reposi

73 6 meningitis or meningoencephalitis based on HHV-6 detection in CSF, clinical presentation, and radio

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

75 erovirus, one cytomegalovirus (CMV), and two HHV-6 diagnoses.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 We identified three highly abundant HHV-6 encoded long non-coding RNAs, one of which generat

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

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

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

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

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

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

123 We detected intraparenchymal HHV-6 gene expression by RNA in situ hybridization in lu

124 issues from iciHHV-6 individuals do not show HHV-6 gene expression.

125 U90 and U100 were the most highly expressed HHV-6 genes in both iciHHV-6A- and iciHHV-6B-positive in

126 ed the highest tissue-specific expression of HHV-6 genes in two separate data sets.

127 Two HHV-6 genes, U90 (immediate early 1 protein) and U100 (g

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

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

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

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

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

133 Overall, our work reveals the complexity of HHV-6 genomes and highlights novel features conserved be

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

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

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

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

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

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

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

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

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

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

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

145 xhibited inherited, chromosomally integrated HHV-6 (iciHHV-6).

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

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

148 The presence of HHV-6 in bile was associated with non-anastomotic biliar

149 As testing for HHV-6 in cerebrospinal fluid (CSF) is more readily avail

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

151 -6 makes it difficult to outline the role of HHV-6 in human disease.

152 rmine the clinical significance of detecting HHV-6 in order to identify true infections and to ensure

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

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

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

156 e of herpesviruses, and human herpesvirus 6 (HHV-6) in particular, in AD.

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

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

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

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

161 Active HHV-6 infection occurs early after renal transplantation

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

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

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

165 h; 4 of these were treated specifically for HHV-6 infection, whereas therapy was discontinued in the

166 ing the transplacentally acquired congenital HHV-6 infection.

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

168 eplicate and cause transplacentally acquired HHV-6 infection.

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

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

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

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

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

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

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

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

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

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

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

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

181 and other human herpesviruses, but study of HHV-6 is at an earlier stage.

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

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

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

185 Human herpesvirus 6 (HHV-6) is an important cause of meningitis and meningoen

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

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

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

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

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

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

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

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

194 Human herpesvirus 6 (HHV-6) may be associated with LFUE, but studies are limi

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

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

197 Five patients were diagnosed with either HHV-6 meningitis or meningoencephalitis based on HHV-6 d

198 ts included in the study were diagnosed with HHV-6 meningitis/meningoencephalitis.

199 ed-chain RNA in situ hybridization to detect HHV-6 messenger RNA (U41 and U57 transcripts) in lung ti

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

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

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

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

204 e enterovirus (n = 38), human herpesvirus 6 (HHV-6) (n = 30), and Streptococcus pneumoniae (n = 14).

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

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

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

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

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

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

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

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

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

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

215 parameters were not generally predictive of HHV-6 positivity.

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

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

218 Fs), generating a complete unbiased atlas of HHV-6 proteome.

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

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

221 HHV-6 reactivation has been associated with transplant r

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

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

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

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

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

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

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

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

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

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

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

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

234 unrelated transplantation increased risk of HHV-6 reactivation.

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

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

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

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

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

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

241 One placental sample had active HHV-6 replication.

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

243 typing demonstrated that 70% of samples with HHV-6 RNA in the placenta exhibited inherited, chromosom

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

245 ed for LFUE compared to controls, suggesting HHV-6 should be evaluated in young children who present

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

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

248 We detected a low abundance of HHV-6-specific CD4 T cells in blood; however, the within

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

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

251 study provides a comprehensive assessment of HHV-6-specific T-cell responses that may inform the deve

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

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

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

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

256 limit of detection ranged from 14 copies/ml (HHV-6) to 191 copies/ml (BKV), and the lower limit of qu

257 transcript-analysis to experimentally define HHV-6 translation products.

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

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

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

261 In our institution, detection of HHV-6 using FA-ME led to faster establishment of disease

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

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

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

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

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

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

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

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

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

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

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

273 higher HHV-6 AUC (p=0.043), and higher peak HHV-6 viral load (p=0.006) vs HHV-6 viremia alone.

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

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

276 Average HHV-6 viral load was 213207 copies/106 cells in positive

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

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

279 viremia was associated with earlier onset of HHV-6 viremia (p=0.004), higher HHV-6 AUC (p=0.043), and

280 nd higher peak HHV-6 viral load (p=0.006) vs HHV-6 viremia alone.

281 HHV-6 viremia at any level developed in 42% (40/96).

282 ogic parameters and outcomes associated with HHV-6 viremia in high-risk donor CMV-seropositive and re

283 gh 100 days in the PET group were tested for HHV-6 viremia using a real-time quantitative PCR.

284 receiving valganciclovir as PET, high-grade HHV-6 viremia was associated with increased age and crit

285 ionship with CMV, risk factors and impact of HHV-6 viremia with outcomes through 12 months post-trans

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

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

288 Of 1,005 children tested by FA-ME, HHV-6 was detected in 25 (2.5%).

289 HHV-6 was detected in 34/51 cases (66.7%) and 19/51 cont

290 HHV-6 was detected in liver explants significantly more

291 HHV-6 was not detected.

292 Quantitative polymerase chain reaction for HHV-6 was performed on DNA from formalin-fixed paraffin-

293 articular, in patients younger than 3 years, HHV-6 was present in 13/27 cases (48.1%) and 2/27 contro

294 HHV-6 was present significantly more often in cases comp

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

296 his comprehensive evaluation, adenovirus and HHV-6 were associated with intussusception.

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

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

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

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