ライフサイエンスコーパス: HHV

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

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

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

4 HHV-6B reactivation is well established as causing limbi

5 HHV-8 and RRV encode homologues of CD200, termed vCD200,

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

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

8 HHV-8-encoded viral interleukin-6 (vIL-6) is believed to

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

10 nfected with HIV are also infected with >/=1 HHV.

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

12 V), formally designated human herpesvirus 4 (HHV-4) and 8 (HHV-8), respectively, are viruses that can

13 tomegalovirus (HCMV, or human herpesvirus 5 [HHV-5]) is a large DNA-containing virus that belongs to

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

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

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

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

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

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

20 pathogens such as human herpesvirus (HHV) 6, HHV-7, and adenovirus, which are not often tested clinic

21 tissue lymphoma, human herpes virus (HHV)-6, HHV-7, chlamydia, Epstein-Barr virus (EBV) and bacterial

22 luate the viral reactivation rates of HHV-6, HHV-7, Epstein-Barr virus (EBV), and cytomegalovirus (CM

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

24 ation is infected with human herpesvirus 6A (HHV-6A), a betaherpesvirus family member.

25 Human herpesvirus 6A (HHV-6A), a member of the betaherpesvirus family, is asso

26 Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviru

27 Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviru

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

29 T cells infected with human herpesvirus 6A (HHV-6A), the E2F1 protein and its cofactor DP1 increased

30 Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviruses and a

31 Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviruses.

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

33 es, human herpesvirus-6A -6B and -7 (HHV-6A, HHV-6B and HHV-7) cause acute infection, establish laten

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

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

36 virus (EBV), cytomegalovirus (CMV), HHV-6A, HHV-6B, and HHV-8, using quantitative polymerase chain r

37 Human herpesvirus 6B (HHV-6B) commonly reactivates after umbilical cord blood

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

39 oloviruses, human herpesvirus-6A -6B and -7 (HHV-6A, HHV-6B and HHV-7) cause acute infection, establi

40 eport, we show that the human herpesvirus 7 (HHV-7) immunoevasin U21, itself a class I MHC-like prote

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

42 esignated human herpesvirus 4 (HHV-4) and 8 (HHV-8), respectively, are viruses that can cause a varie

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

44 mmatory tumor caused by human herpesvirus 8 (HHV-8) commonly observed in elderly men of Mediterranean

45 Here, we report that human herpesvirus 8 (HHV-8) gene product viral interferon regulatory factor 1

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

47 Human herpesvirus 8 (HHV-8) interleukin-6 (vIL-6) promotes cell proliferation

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 The contributions of human herpesvirus 8 (HHV-8) viral interleukin-6 (vIL-6) to virus biology rema

51 Human herpesvirus 8 (HHV-8) viral interleukin-6 (vIL-6), unlike cellular IL-6

52 sistently infected with human herpesvirus 8 (HHV-8), an oncogenic herpesvirus that has been detected

53 as hepatitis B virus or human herpesvirus 8 (HHV-8), establish persistent infections that cause chron

54 s (KSHV), also known as human herpesvirus 8 (HHV-8), is a cancer-related human virus, classified as a

55 ng infection, including human herpesvirus 8 (HHV-8), the causative agent of Kaposi's sarcoma and B ce

56 d with the exception of human herpesvirus 8 (HHV-8), these chimeric variants rescued the replication

57 coma is the most common human herpesvirus 8 (HHV-8)-related disease described after solid organ trans

58 acaribe arenavirus, and human herpesvirus 8 (HHV-8).

59 t is closely related to human herpesvirus 8 (HHV-8)/Kaposi's Sarcoma-associated herpesvirus (KSHV), a

60 EL) are associated with human herpesvirus-8 (HHV-8) and usually occur in immunocompromised individual

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

62 Kaposi sarcoma (KS), a human herpes virus 8 (HHV-8; also called KSHV)-induced endothelial tumor, deve

63 Human herpes virus-8 (HHV-8) drives the hypercytokinemia in all HIV-positive p

64 d herpesvirus (KSHV, or human herpesvirus-8 [HHV-8]) has another, alternative emergency escape replic

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

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

67 Here we characterize an HHV-8-unrelated PEL-like lymphoma in an elderly woman wh

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

69 eactivation of human herpesvirus (HHV)-6 and HHV-7 has been linked to various posttransplant adverse

70 d to be monitored in real-time for HHV-6 and HHV-7 viremia by polymerase chain reaction at regular in

71 strated from routine monitoring of HHV-6 and HHV-7 viremia in graft or patient outcome after liver tr

72 In the "monitoring" group, HHV-6 and HHV-7 viremia occurred in 23 of 64 patients (35.9%) and

73 otential utility of monitoring for HHV-6 and HHV-7 viremia remains unclear.

74 ly infected with viral homologs of HHV-6 and HHV-7, which we provisionally named MneHV6 and MneHV7, r

75 phalitis recognizing firstly that HHV-6A and HHV-6B are separate species with differing properties, a

76 al models for human herpesvirus (HHV)-6A and HHV-6B infections has been slow.

77 blish latency, and in the case of HHV-6A and HHV-6B, whole virus can integrate into the host chromoso

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

79 ve underscored the association of HHV-6B and HHV-7 primary infection with febrile status epilepticus

80 erpesvirus-6A -6B and -7 (HHV-6A, HHV-6B and HHV-7) cause acute infection, establish latency, and in

81 Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviruses and are highly pr

82 Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviruses.

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

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

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

86 , cytomegalovirus (CMV), HHV-6A, HHV-6B, and HHV-8, using quantitative polymerase chain reaction.

87 nclude Ebola virus, Tacaribe arenavirus, and HHV-8, and we propose ARB as a broad-spectrum antiviral

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

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

90 those seen in humans coinfected with HIV and HHV-8.

91 be subdivided into HHV-8-associated MCD and HHV-8-negative MCD or iMCD.

92 There is also a group of HIV-negative and HHV-8-negative patients with unknown etiology and pathop

93 nv transcripts, HHV-6 viral copy number, and HHV-7 viral copy number between CFS patients and healthy

94 Though the functions of RRV and HHV-8 vCD200 molecules have been examined in vitro, the

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

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

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

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

99 Both HHV-8 and RRV encode viral CD200 (vCD200) molecules that

100 oded miRNAs, although an miRNA(s) encoded by HHV-6A has yet to be reported.

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

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

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

104 investigations of the mechanisms that cause HHV-7 reactivation and associated disease.

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

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

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

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

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

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

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

112 ein-Barr virus (EBV), cytomegalovirus (CMV), HHV-6A, HHV-6B, and HHV-8, using quantitative polymerase

113 ologically similar to its human counterpart, HHV-7.

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

115 rr virus (EBV) (the most frequently detected HHV) might influence HIV DNA decay during antiretroviral

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

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

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

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

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

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

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

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

124 response, which was measured using anti-EBV/HHV antibodies, and the proportion of the homologous CD8

125 sons and the complete viral genome of either HHV-6A or HHV-6B is present in every nucleated cell in t

126 r CMV, 47% for EBV, 8% for HSV-1, and 0% for HHV-8.

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

128 incidence of postnatal infection was 76% for HHV-6B, 59% for CMV, 47% for EBV, 8% for HSV-1, and 0% f

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

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

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

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

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

134 suggest that viral miRNAs are important for HHV-6A and that they may serve as an important therapeut

135 new models have been established, mainly for HHV-6A, which reproduce some pathological features seen

136 ore, the lack of a relevant animal model for HHV-7 infection has hindered a better understanding of i

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

138 tic screening of organ donors/recipients for HHV-8 infection, HHV-8-related illness should be suspect

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

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

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

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

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

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

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

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

147 ll RNA species isolated from cells harboring HHV-6A to identify five novel small noncoding RNA specie

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

149 ectious pathogens such as human herpesvirus (HHV) 6, HHV-7, and adenovirus, which are not often teste

150 available to detect both human herpesvirus (HHV) and immune control of replication post-solid organ

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

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

153 eficiency virus (HIV) and human herpesvirus (HHV) infections persist lifelong, and almost all individ

154 Reactivation of human herpesvirus (HHV)-6 and HHV-7 has been linked to various posttranspla

155 uitable animal models for human herpesvirus (HHV)-6A and HHV-6B infections has been slow.

156 tomegalovirus (CMV), 44%; human herpesvirus [HHV] 6, 18%; HHV8, 6%; Epstein-Barr virus, 3%; herpes si

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

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

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

160 terminator for several human herpesviruses (HHVs), including HHV-2 (HSV-2), a common human immunodef

161 Like all herpesviruses, HHV-6A establishes a lifelong, latent infection in its h

162 In this review, we discuss how HHVs, and cytomegalovirus in particular, interact with c

163 ed proapoptotic protein negatively impacting HHV-8 latently infected primary effusion lymphoma (PEL)

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

165 vIL-6 function and associated mechanisms in HHV-8 biology.

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

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

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

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

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

171 xamined the role of vIL-6/gp130 signaling in HHV-8 productive replication in primary effusion lymphom

172 everal human herpesviruses (HHVs), including HHV-2 (HSV-2), a common human immunodeficiency virus (HI

173 organ donors/recipients for HHV-8 infection, HHV-8-related illness should be suspected in transplant

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

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

176 ARB inhibited HHV-8 replication to a similar degree as cidofovir.

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

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

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

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

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

182 MCD should be subdivided into HHV-8-associated MCD and HHV-8-negative MCD or iMCD.

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

184 equires infection with KS herpes virus (KSHV/HHV-8).

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

186 histochemistry staining confirmed that, like HHV-7, MneHV7 exhibits a natural tropism for salivary gl

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

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

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

190 CD134(+/neg-lo) cells contained little to no HHV-6B copies.

191 via ectopic cytokine secretion, and/or a non-HHV-8 virus.

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

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

194 advances have underscored the association of HHV-6B and HHV-7 primary infection with febrile status e

195 ction, establish latency, and in the case of HHV-6A and HHV-6B, whole virus can integrate into the ho

196 o) cells showed 0.308 versus 0.129 copies of HHV-6B/cell (P = .0002).

197 Diagnosis of HHV reactivation is conventionally based on quantitative

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

199 and provided a model to study the effects of HHV-6A on AIDS progression.

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

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

202 event may have deregulated the expression of HHV-6A or 19q genes or else disrupted telomere function.

203 on program appears to be a common feature of HHV biology.

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

205 irmed that the virus is a macaque homolog of HHV-7, which we have provisionally named Macaca nemestri

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

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

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

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

210 lls harbor significantly increased levels of HHV-6B, suggesting that CD134 (OX40) may facilitate vira

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

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

213 , 1.49-7.14), having an increasing number of HHV-8-infected household members (HR, 1.27; 95% CI, 1.09

214 Understanding the pathophysiology of HHV-6B encephalitis remains incomplete, especially regar

215 While the pathogenic potential of HHV-7 is unclear, it can reactivate HHV-6 from latency a

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

217 opresentation of 3 clinical presentations of HHV-8-mediated human disease in the post-transplant sett

218 re warranted for treatment and prevention of HHV-6B encephalitis after transplantation.

219 argeting to mDRM contributes to promotion of HHV-8 productive replication and inhibition of associate

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

221 Reactivation of HHV-6A is frequent within the immunosuppressed and immun

222 rum samples, we demonstrated reactivation of HHV-6B in 25% (4/16 recipients) of HCT recipients with d

223 t of high-density culture or reactivation of HHV-8 lytic replication in PEL cells, CatD depletion sub

224 ese observations suggest that replication of HHV may help maintain a larger HIV DNA reservoir, but th

225 Reports of HHV-6A or HHV-6B encephalitis in immunocompetent older c

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

227 pectives for studying the pathogenic role of HHV-6A in humans.

228 The PCR assay demonstrated shedding of HHV-7, EBV, HHV-6, and CMV, listed by order of magnitude

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

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

231 Reports of HHV-6A or HHV-6B encephalitis in immunocompetent older children/ad

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

233 he complete viral genome of either HHV-6A or HHV-6B is present in every nucleated cell in the body.

234 ng by contacts was associated with HHV-6A or HHV-6B transmission.

235 HSV-1 infection, unlike other HHV infections, caused acute clinical illness in these i

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

237 HSV-2 but endogenously coinfected with other HHVs.

238 hemophagocytic syndrome are other potential HHV-8-induced entities but are less frequently reported.

239 Except for HSV-1, primary HHV infections were subclinical.

240 Encephalitis due to primary HHV-6B infection in young children is commonly reported

241 n a negative-feedback manner, thus promoting HHV-8 productive replication.

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

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

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

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

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

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

248 There are limited published data surrounding HHV-8-related CD among HIV-negative patients.

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

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

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

252 The present study demonstrates that HHV-8-encoded vIRF-1 targets to the mitochondrial deterg

253 se findings provide additional evidence that HHV-6A may play a role in human immunodeficiencies.

254 HHV-6) encephalitis recognizing firstly that HHV-6A and HHV-6B are separate species with differing pr

255 Strikingly, we found that HHV-8 infection of androgen-sensitive prostate cancer ce

256 We hypothesized that HHV-6A, like other members of the human herpesvirus fami

257 We hypothesized that HHV-associated activation of HIV-infected CD4(+)T cells

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

259 Here we report that HHV-6A encodes at least one miRNA, which we named miR-U8

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

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

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

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

264 t in salivary gland tissues, suggesting that HHV-7 may also have a tropism for the peripheral nervous

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

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

267 Activated T-helper cells from the HHV-8-negative variant carriers showed reduced interfero

268 entire iciHHV-6A genome was absent from the HHV-8-unrelated-PEL-like lymphoma cells despite retentio

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

270 Whether release of the HHV-6A genome from the telomere contributed to lymphomag

271 viral miRNA candidate (miR-U86) targets the HHV-6A IE gene U86, thereby regulating lytic replication

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

273 tion and biological characterization of this HHV-6A-specific miRNA is the first step to defining how

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

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

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

277 No disease has been linked to HHV-6A, whereas HHV-6B may cause encephalitis.

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

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

280 C)-derived virus in Jjhan cells or wild-type HHV-6A strain U1102 virus in HSB2 cells and are associat

281 Sequential human herpes virus (HHV) reactivation is well known in drug reaction with eo

282 ymphoid tissue lymphoma, human herpes virus (HHV)-6, HHV-7, chlamydia, Epstein-Barr virus (EBV) and b

283 o disease has been linked to HHV-6A, whereas HHV-6B may cause encephalitis.

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

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

286 vere pathological conditions associated with HHV-6.

287 eal shedding by contacts was associated with HHV-6A or HHV-6B transmission.

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

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

290 Infection of T1H6-DC-SIGN cells with HHV-8 induces expression of beta-galactosidase, which wa

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

292 small fraction of individuals infected with HHV-8.

293 Primary infection with HHV-6B occurs in nearly all children and was first linke

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

295 precursors support productive infection with HHV-8.

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

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

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

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

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