ライフサイエンスコーパス: HHV

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

2 HHV-6 demonstrated little specificity to AD brains over

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

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

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

6 HHV-6 was detected in liver explants significantly more

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

8 HHV-8 is a B-lymphotropic gamma-herpesvirus closely rela

9 HHV-8 uses langerin and the ephrin A2 receptor to infect

10 HHV-8-infected LC and iDDC had a reduced ability to stim

11 rus (VZV; also known as human herpesvirus 3 [HHV-3]).

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

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

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

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

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

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

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

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

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

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

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

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

24 The genomes of human herpesvirus 6A (HHV-6A) and HHV-6B have the capacity to integrate into t

25 e human roseoloviruses human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 comprise the Roseolovirus gen

26 tein-Barr virus [EBV], human herpesvirus 6A [HHV-6A], HHV-6B, herpes simplex virus 1 [HSV-1], HSV-2,

27 oseoloviruses human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 comprise the Roseolovirus genus of the

28 osely related to the roseoloviruses, HHV-6A, HHV-6B, and HHV-7, than to another murine betaherpesviru

29 ggest that MRV is a mouse homolog of HHV-6A, HHV-6B, and HHV-7.IMPORTANCE Herein we describe the comp

30 virus [EBV], human herpesvirus 6A [HHV-6A], HHV-6B, herpes simplex virus 1 [HSV-1], HSV-2, JC virus

31 Human herpesvirus 6A and 6B (HHV-6A and HHV-6B) are closely related viruses that infe

32 Human herpesviruses 6A and 6B (HHV-6A and HHV-6B) are human viruses capable of chromoso

33 Human herpesvirus 6B (HHV-6B) belongs to the beta-herpesvirus subfamily of the

34 Human herpesvirus 6B (HHV-6B) DNA is frequently detected in bronchoalveolar la

35 Human herpesvirus 6B (HHV-6B) DNA is frequently detected in human samples.

36 Human herpesvirus 6B (HHV-6B) frequently reactivates after allogeneic hematopo

37 recipients.IMPORTANCE Human herpesvirus 6B (HHV-6B) is a DNA virus that infects most children within

38 ry a copy of the human herpesvirus 6A or 6B (HHV-6A/B) in every cell of their body.

39 irus, BK polyomavirus, human herpesvirus 6B, HHV-6A, adenovirus, and Epstein-Barr virus between days

40 irus 6 (HHV-6) (34.2%), human herpesvirus 7 (HHV-7) (20.5%) and Epstein-Barr virus (EBV) (16.4%) were

41 The human herpesvirus-7 (HHV-7) U21 glycoprotein binds to class I major histocomp

42 With exception of HHV-7, HHV shedding was not significantly influenced by HIV RNA

43 could be infected with human herpesvirus 8 (HHV-8) (Kaposi's sarcoma [KS]-associated herpesvirus) an

44 Human herpesvirus 8 (HHV-8) encodes four viral interferon regulatory factors

45 Human herpesvirus 8 (HHV-8) infection occurs in early childhood and is associ

46 activation of recipient human herpesvirus 8 (HHV-8) infection or through donor-derived HHV-8 transmis

47 Human herpesvirus 8 (HHV-8) is an oncogenic virus causally related to AIDS-as

48 in-6 (vIL-6) encoded by human herpesvirus 8 (HHV-8) is believed to contribute via mitogenic, survival

49 Human herpesvirus 8 (HHV-8) is the causative agent of Kaposi sarcoma (KS) and

50 Human herpesvirus 8 (HHV-8) viral interleukin-6 (vIL-6) is a cytokine that is

51 Human herpesvirus 8 (HHV-8) viral interleukin-6 (vIL-6) localizes largely to

52 -zoster virus (VZV) and human herpesvirus 8 (HHV-8) were not or rarely detected in bile.

53 L-6 activity.IMPORTANCE Human herpesvirus 8 (HHV-8)-encoded viral interleukin-6 (vIL-6) was the first

54 (EBV) positive or human herpesvirus type-8 (HHV-8) positive.

55 Human herpes virus 8 (HHV-8), also known as Kaposi's sarcoma associated herpes

56 irus (KSHV; also called human herpesvirus 8 [HHV-8]), upon being reactivated, causes serious diseases

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

58 Additionally, HHV-6B can integrate into germ line chromosomes, resulti

59 , using phosphonoacetic acid, did not affect HHV-6A/B integration.

60 cidofovir has high in vitro activity against HHV-6B and other DNA viruses, but its in vivo activity f

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

62 s did not reduce the prevalence of HHV-6 and HHV-7 in bile, but it did reduce the presence of CMV and

63 HHV-6 and HHV-7 might be associated with biliary complications aft

64 genome imaging of the integrated HHV-6A and HHV-6B genomes using whole-genome optical site mapping t

65 t on the genetic structure of the HHV-6A and HHV-6B integration locus, demonstrating the utility of o

66 Human herpesvirus 6A and 6B (HHV-6A and HHV-6B) are closely related viruses that infect most hum

67 Human herpesviruses 6A and 6B (HHV-6A and HHV-6B) are human viruses capable of chromosomal integra

68 were probed for PCR reactivity to HHV-6A and HHV-6B.

69 genomes of human herpesvirus 6A (HHV-6A) and HHV-6B have the capacity to integrate into telomeres, th

70 s human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 comprise the Roseolovirus genus of the human Betah

71 d to the roseoloviruses, HHV-6A, HHV-6B, and HHV-7, than to another murine betaherpesvirus, mouse cyt

72 RV is a mouse homolog of HHV-6A, HHV-6B, and HHV-7.IMPORTANCE Herein we describe the complete genome

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

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

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

76 us-6 (HHV-6) 6% in saliva and 2% in GCF; and HHV-7 44% in saliva and 8% in GCF.

77 sociation between the rs73185306 C/T SNP and HHV-6A/B chromosomal integration (odds ratio, 0.90 [95%

78 respiratory failure, and the effect of anti-HHV-6B antivirals on these outcomes.

79 from 6 donors, retrospectively identified as HHV-8-positive, with a history of drug use disorder, wer

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

81 Human herpesviruses 6A/B (HHV-6A/B) can integrate their viral genomes in the telom

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

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

84 standing of the complex interactions between HHV-8 and immune cells that cause HHV-8-related MCD.

85 idence and risk factors of infection vary by HHV type.

86 ns between HHV-8 and immune cells that cause HHV-8-related MCD.

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

88 -blood samples from patients with concurrent HHV-6B viremia.

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

90 We describe 6 cases of donor-derived HHV-8 infection and KS investigated from July 2018 to Ja

91 8 (HHV-8) infection or through donor-derived HHV-8 transmission.

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

93 virus (EBV) were the most commonly detected HHV in semen of HIV-infected participants.

94 We detected HHV-6B(+) BALF from 147 of 553 (27%) individuals.

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

96 ect viral DNA is the mainstay for diagnosing HHV-6B infection, the characteristics of HHV-6B infectio

97 Autopsy revealed 3 distinct HHV-8-related entities: Kaposi sarcoma, HHV-8-associated

98 Diagnostic assays distinguishing HHV-6B reactivation from latency are limited.

99 ll, the data expand the number of documented HHV-6B CD4 T-cell antigens from approximately 11 to 60.

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

101 Each HHV causes a unique spectrum of disease depending on the

102 Each HHV has a distinct pattern of oral shedding which depend

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

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

105 ase (HDAC) inhibitor vorinostat disrupts EBV/HHV-8 latency, enhances chemotherapy-induced cell death,

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

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

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

109 er DNA viruses, but its in vivo activity for HHV-6B has not been demonstrated.

110 A RT-qPCR assay for HHV-6B U38 may be useful to identify lytic HHV-6B infect

111 We tested BALF for HHV-6B DNA using polymerase chain reaction in allogeneic

112 t the study of intravenous brincidofovir for HHV-6B prophylaxis.

113 Independent risk factors for HHV-8 incident infection included having a child who sha

114 Four of 6 donors had risk factors for HHV-8 infection reported in donor history questionnaires

115 The donor had multiple risk factors for HHV-8 infection.

116 hold members to investigate risk factors for HHV-8 transmission in Lusaka, Zambia.

117 remained associated with a lower hazard for HHV-6B plasma detection (hazard ratio, 0.40; 95% confide

118 We tested plasma for HHV-6B through week 6 post-HCT.

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

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

121 Testing donors and recipients for HHV-8 is currently challenging with no validated commerc

122 limited child feeding behaviors and risk for HHV-8 infection.

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

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

125 ne expression in the brain (specifically for HHV-6A), testis, esophagus, and adrenal gland.

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

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

128 currently no validated commercial tests for HHV-8 antibody screening.

129 immunocompromised patients who have frequent HHV-6B reactivation.

130 infect Langerhans cells, which support full HHV-8 lytic replication.

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

132 ative to the most common European haplogroup HHV, European haplogroups I, J, K, O-X, T, and U were as

133 one actively replicating human herpesvirus (HHV) in their mucosal secretions at any one time.

134 Human herpesvirus (HHV) infections are common during infancy.

135 lar tumor associated with human herpesvirus (HHV)-8 infection.

136 Human herpesviruses (HHV) establish lifelong latent infection and are transmi

137 ptomatic replication of human herpesviruses (HHV) is frequent in HIV-infected men and is associated w

138 HIV RNA and DNA from 7 human herpesviruses (HHVs) were measured by real-time polymerase chain reacti

139 Compared to other beta-herpesviruses, HHV-6B exhibits high similarity in capsid structure but

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

141 unction within the ER compartment.IMPORTANCE HHV-8 vIL-6 prosurvival (latent) and proreplication func

142 KORC1v2-associated vIL-6 function.IMPORTANCE HHV-8 vIL-6 promotes productive replication in the conte

143 V-6A/B-specific antibody response.IMPORTANCE HHV-6A and -6B are human herpesviruses that have the uni

144 indings establish the importance of vIL-6 in HHV-8 productive replication and the contributions of in

145 eceptor IGF2R, which is a positive factor in HHV-8 biology via these activities.

146 ies of vIRF-2 and vIRF-2-USP7 interaction in HHV-8 latent and lytic biology.IMPORTANCE Human herpesvi

147 180 "VLambda"-shaped CATCs are observed in HHV-6B, distinguishing from the 255 "Lambda"-shaped dime

148 mmatory and/or angiogenic viral proteins, in HHV-8-associated Kaposi's sarcoma, primary effusion lymp

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

150 llular and viral factors that play a role in HHV-6A/B integration.

151 ify vIRF-2 targeting of USP7 and its role in HHV-8 biology, expanding our understanding of the repert

152 s that these cells play an important role in HHV-8 infection and pathogenesis.

153 function, supporting their potential role in HHV-8 pathogenesis and KS.IMPORTANCE Here we show that H

154 ATC's binding to triplexes Ta, Tc, and Tf in HHV-6B.

155 After primary infection, HHV-6B persists as a chronic, latent infection in many c

156 ession, as well as the release of infectious HHV-6A/B from the integrated state.IMPORTANCE The analys

157 ine kinase ephrin A2 was required to inhibit HHV-8 infection of LC.

158 -DC-SIGN monoclonal antibody (MAb) inhibited HHV-8 infection of iDDC, as shown by low expression leve

159 on or targeting to the mitochondria inhibits HHV-8 replication-induced mitophagy and leads to an accu

160 n of vIRF-1/NIX-activated mitophagy inhibits HHV-8 productive replication.

161 of the world's population carries integrated HHV-6A/B genome in every cell of their body.

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

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

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

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

166 ng and analyzed for chromosomally integrated HHV-6A/B (ciHHV-6A/B).

167 red to as inherited chromosomally integrated HHV-6A/B (iciHHV-6A/B).

168 ects with inherited chromosomally integrated HHV-6B or latent infection with HHV-6B, and (iv) HHV-6B

169 uals with inherited chromosomally integrated HHV-6B.

170 spontaneous gene expression from integrated HHV-6A/B leads to an increase in antigenic burden that t

171 re employed genome imaging of the integrated HHV-6A and HHV-6B genomes using whole-genome optical sit

172 Our results offer insights into HHV-6B capsid assembly and the roles of its tegument pro

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

174 6B or latent infection with HHV-6B, and (iv) HHV-6B Z29 infected SupT1 CD4(+) T cells.

175 he presence of gene homologs to all 84 known HHV-7 open reading frames.

176 cells from 18 healthy donors with each known HHV-6B protein.

177 y have promoted the reactivation of a latent HHV-8 infection endowed with oncogenic potentialities an

178 rough reactivation of the recipient's latent HHV-8 infection, or less commonly through donor-derived

179 ression signatures were analyzed, low levels HHV-6A/B gene expression was found across multiple tissu

180 Limited HHV-8 antibody testing is available through some US refe

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

182 r HHV-6B U38 may be useful to identify lytic HHV-6B infection in nonplasma samples and samples from i

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

184 had an approximately 1 log(10) lower median HHV-6B BALF viral load, as well as a lower risk of overa

185 rs should be included in efforts to minimize HHV-8 transmission, and households with a large number o

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

187 egulator of key cellular pathways, modulates HHV-8 latent and lytic infection, and is targeted by vIR

188 Seminal replication of multiple HHVs is common in our HIV primary infection cohort.

189 No HHV-6B U38 transcripts were detected by RNA-seq or rever

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

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

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

193 azards models to evaluate the association of HHV-6B(+) BALF with overall mortality, death from respir

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

195 and angiogenesis that are characteristic of HHV-8-associated Kaposi's sarcoma, PEL and multicentric

196 ing HHV-6B infection, the characteristics of HHV-6B infection complicate efforts to distinguish betwe

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

198 of the human population carries one copy of HHV-6A/B integrated into every cell in their body, refer

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

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

201 With exception of HHV-7, HHV shedding was not significantly influenced by

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

203 ongly suggest that MRV is a mouse homolog of HHV-6A, HHV-6B, and HHV-7.IMPORTANCE Herein we describe

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

205 The cumulative incidence of HHV-6B plasma detection through day 42 post-HCT was sign

206 full reactivation.IMPORTANCE Inheritance of HHV-6A or HHV-6B integrated into a telomere occurs at a

207 , 1.49-7.14), having an increasing number of HHV-8-infected household members (HR, 1.27; 95% CI, 1.09

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

209 erapy should consider this expanded panel of HHV-6B antigens.IMPORTANCE Human herpesvirus 6 is highly

210 Predetermination of HHV-8 status can be useful when considering organ donors

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

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

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

214 mportant for the onset and/or progression of HHV-8-associated endothelial-cell and B-cell pathologies

215 F-1 in mitophagy activation and promotion of HHV-8 lytic replication via this mechanism.

216 However, there are numerous reports of HHV-8-unrelated PEL-like lymphomas with unknown aetiolog

217 use history, which may increase the risk of HHV-8 transmission to recipients.

218 Our results indicate that selection of HHV-6B ORFs for immunotherapy should consider this expan

219 actions, here we report atomic structures of HHV-6B capsid and capsid-associated tegument complex (CA

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

221 To investigate the trafficking of HHV-7 U21, we followed synchronous release of U21 from t

222 IMPORTANCE The analysis and understanding of HHV-6A/B genome integration into host DNA is currently l

223 a panel of vIL-6 variants and utilization of HHV-8 mutant viruses expressing selected variants in phe

224 6 meningitis or meningoencephalitis based on HHV-6 detection in CSF, clinical presentation, and radio

225 HCT to study the effect of brincidofovir on HHV-6B reactivation.

226 HV-6B viral polymerase gene U38 was the only HHV-6B transcript detected in all next-generation RNA se

227 tivation.IMPORTANCE Inheritance of HHV-6A or HHV-6B integrated into a telomere occurs at a low freque

228 dy responses against EBV and FLU antigens or HHV-6A/B gene products either not expressed or expressed

229 r virus [EBV], and influenza virus [FLU]) or HHV-6A/B antigens.

230 It has been implicated, along with other HHV-8 proinflammatory and/or angiogenic viral proteins,

231 ommon for CMV and EBV when compared to other HHVs.

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

233 ipients (64%) had evidence of posttransplant HHV-8 infection.

234 d studies of antiviral treatments to prevent HHV-6B reactivation.

235 agnostic, proteome-wide approach, we queried HHV-6B-specific CD4 T cells from 18 healthy donors with

236 as organ donors for HIV-positive recipients, HHV-8 prevalence among donors and recipients will likely

237 onclusion, brincidofovir prophylaxis reduced HHV-6B reactivation after allogeneic HCT in a post hoc a

238 and that vIRF-2 targeting of USP7 regulates HHV-8 productive replication.

239 ic burden that translates into a more robust HHV-6A/B-specific antibody response.IMPORTANCE HHV-6A an

240 more closely related to the roseoloviruses, HHV-6A, HHV-6B, and HHV-7, than to another murine betahe

241 inct HHV-8-related entities: Kaposi sarcoma, HHV-8-associated multicentric Castleman disease with mic

242 ted significantly increased rates of seminal HHV shedding compared with HIV-uninfected controls.

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

244 nd reproducible cell culture models to study HHV-6A/B integration.

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

246 el reverse transcription-PCR assay targeting HHV-6B U38, which identified U38 mRNA in all tested whol

247 itu hybridization, we could demonstrate that HHV-6A/B integrated in most human cell lines tested, inc

248 These data provide evidence that HHV-6B detection in BALF is associated with higher morta

249 These results indicate that HHV-8 can target both LC and iDDC for productive infecti

250 Taken together, our data show that HHV-8 utilizes alternate receptors to differentially inf

251 ogenesis and KS.IMPORTANCE Here we show that HHV-8, a DNA tumor virus that causes Kaposi's sarcoma, i

252 Here, we show that HHV-8-encoded viral interferon regulatory factor 1 (vIRF

253 We have previously shown that HHV-8 enters monocyte-derived dendritic cells (MDDC) thr

254 Retrospective serologic tests suggested that HHV-8 was likely transmitted by the seropositive donor a

255 The HHV-6B viral polymerase gene U38 was the only HHV-6B tra

256 , we used RNA sequencing to characterize the HHV-6B gene expression profile in multiple sample types,

257 In this study, we characterized the HHV-6A/B integration efficiencies in several human cell

258 A sequencing to characterize and compare the HHV-6B transcriptome in multiple sample types, including

259 We demonstrated substantial overlap in the HHV-6B transcriptome observed in in vivo and in vitro sa

260 a shed light on the genetic structure of the HHV-6A and HHV-6B integration locus, demonstrating the u

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

262 the typical findings of KS together with the HHV-8 positivity.

263 enic, survival, and angiogenic activities to HHV-8-associated Kaposi's sarcoma, primary effusion lymp

264 primary effusion lymphoma (PEL) cells and to HHV-8 productive replication, in part via promotion of E

265 f viral and cellular factors contributing to HHV-6A/B integration and the screening of drugs influenc

266 e viral and cellular factors contributing to HHV-6A/B integration remain largely unknown, mostly due

267 ation and IGF2R as a positive contributor to HHV-8 biology, thereby extending understanding of the me

268 of individual vIL-6-protein interactions to HHV-8 lytic biology.

269 s a favorable predisposing factor leading to HHV-6A/B integration.

270 NA samples were probed for PCR reactivity to HHV-6A and HHV-6B.

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

272 so considered to contribute significantly to HHV-8-associated pathogenesis, since vIL-6 can promote c

273 as impaired strategies to diagnose and treat HHV-6B-associated diseases.

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

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

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

277 Whether HHV-6B is a pulmonary pathogen is unclear.

278 Here we describe a novel mechanism by which HHV-6A, a member of the human herpesvirus family, may co

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

280 aposi sarcoma, but behaviors associated with HHV-8 transmission are not well described.

281 V infection, both situations associated with HHV-8-related diseases.

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

283 KS for recipients of organs from donors with HHV-8 infection risk could be useful for recipient manag

284 Second, cells were infected with HHV-6A/B and allowed to grow in bulk for 4 weeks or long

285 cts with large B cell lymphoma infected with HHV-6B, (iii) lymphoblastoid cell lines (LCLs) from subj

286 y integrated HHV-6B or latent infection with HHV-6B, and (iv) HHV-6B Z29 infected SupT1 CD4(+) T cell

287 Infection with HHV-8 did not alter the cell surface expression of lange

288 precursors support productive infection with HHV-8.

289 spleen (n = 9) samples from 32 patients with HHV-8 MCD and compared them with patients with KS (n = 2

290 ies were markedly decreased in patients with HHV-8 MCD and were undetectable in 6 of them.

291 Moreover, iNKT cells from patients with HHV-8 MCD displayed a proliferative defect after stimula

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

293 ung tissue in all three tested subjects with HHV-6B(+) BALF and sufficient tissue RNA preservation.

294 CI, 0.16-1.10), compared with subjects with HHV-6B(+) BALF not receiving antivirals.

295 Subjects with HHV-6B(+) BALF who received antivirals within 3 days pre

296 Subjects with HHV-6B(+) BALF, with or without copathogens, had signifi

297 % CI, 1.56-4.01) compared with subjects with HHV-6B(-) BALF.

298 transplant (HCT) recipients with and without HHV-6B plasma viremia, (ii) tumor tissue samples from su

299 in whole-blood samples from subjects without HHV-6B plasma detection or from latently infected LCLs.

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