ライフサイエンスコーパス: HHV-7

1 (Gcv) reduced the load of CMV and HHV-6 and HHV-7.

2 92 patients had at least 1 positive PCR for HHV-7.

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

4 +/- 8.2% by pretreatment with UV-inactivated HHV-7.

5 recovered after the cells were infected with HHV-7.

6 -associated virus type 2 rep gene homolog in HHV-7.

7 ere not susceptible to inhibitory effects of HHV-7.

8 ffected by the interaction between HHV-6 and HHV-7.

9 in saliva but has little effect on HHV-6 and HHV-7.

10 V-8, VZV, and EBV but not for infection with HHV-7.

11 hild had low-avidity antibodies to HHV-6 and HHV-7.

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

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

14 demonstrated that CD4INTRA co-localized with HHV-7 Ags within the same subcellular compartments of in

15 Exposure of macrophages to HHV-7 alone yielded no signs of virus replication or cyt

16 We studied the interactions between HHV-7 and a macrophage-tropic HIV-1 isolate (HIV-1BaL) i

17 d by 91.7 +/- 8.3% by pretreatment with live HHV-7 and by 91.8 +/- 8.2% by pretreatment with UV-inact

18 and reverse-transcriptase PCR for HHV-6 and HHV-7 and by quantitative PCR for HHV-6.

19 Significant production of HHV-7 and EBV was demonstrated in saliva samples from th

20 tinguish low-avidity antibodies to HHV-6 and HHV-7 and hence the respective primary infections.

21 herwise healthy children < or =10 years old, HHV-7 and HHV-6 infections and their interaction by sero

22 ected only twice and HHV-2, Cytomegalovirus, HHV-7 and HHV-8, only once.

23 tion of CD4, the cellular receptor shared by HHV-7 and HIV-1.

24 pre-exposed to either live or UV-inactivated HHV-7 and subsequently infected with HIV-1BaL, a signifi

25 y related human viruses human herpesvirus 7 (HHV-7) and human cytomegalovirus (HCMV).

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

27 VZV), human herpes virus-6, 7, and 8 (HHV-6, HHV-7, and HHV-8), and Epstein-Barr virus (EBV).

28 th Epstein-Barr virus/HHV-4, HHV-6A, HHV-6B, HHV-7, and KSHV.

29 ovirus (CMV), human herpesvirus (HHV)-6, and HHV-7-and their association with CMV disease and respons

30 megalovirus [CMV], EBV, human herpesvirus 7 [HHV-7], and HHV-8) were detected in 32 of 33 (97%) subje

31 were detected in one child with low-avidity HHV-7 antibody and high-avidity HHV-6 antibody.

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

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

34 Human herpesvirus 6 (HHV-6) and HHV-7 are closely related betaherpesviruses that encode

35 Although HHV-6 and HHV-7 are inhibited by several antiviral drugs in the la

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

37 cal and evolutionary divergence of HHV-6 and HHV-7 are notable structural differences in putative tra

38 Human herpesviruses 6 and 7 (HHV-6 and HHV-7) are prevalent lymphotropic viruses that infect mo

39 the mechanisms of interaction of HIV-1 with HHV-7, as well as with other pathogens that modulate HIV

40 nsidered for patients with serious HHV-6- or HHV-7-associated disease confirmed with accurate virolog

41 We prospectively studied HHV-6 and HHV-7 at multiple sites in pregnant women to determine t

42 was only marginally inhibited by exposure to HHV-7 before mitogen stimulation, indicating that the in

43 arly stages after infection, suggesting that HHV-7 blocks HIV-1 at the level of interaction with the

44 two children who had low-avidity antibody to HHV-7 but who were seronegative for HHV-6, only HHV-7 wa

45 An association was found between HHV-7, but not HHV-6, DNA detection and CMV disease, sug

46 We conclude that HHV-7 can provide a transacting function(s) mediating HH

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

48 ike molecules also play an important role in HHV-7-cell surface interactions required for infection a

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

50 (X4) HIV-1 was only minimally suppressed by HHV-7 coinfection.

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

52 otropic human herpes viruses 6 and 7 (HHV-6, HHV-7) comprise a significant proportion of viral infect

53 Reactivations of HHV, including HHV-6, HHV-7, cytomegalovirus (CMV), and Epstein-Barr virus (EB

54 which affects HIV-1 by upregulating RANTES, HHV-7 did not upregulate any CCR5-binding chemokine.

55 the HHV-6B genomes became prominent and the HHV-7 disappeared.

56 Treatment of HHV-6 and HHV-7 disease includes antiviral therapy and cautious re

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

58 ts were monitored weekly for CMV, HHV-6, and HHV-7 DNA and serological responses for 12 weeks after t

59 Finally, the minimal HHV-7 DNA element necessary for replicator activity was

60 Patients with detectable HHV-7 DNA had significantly higher peak plasma CMV loads

61 iated with CMV disease were the detection of HHV-7 DNA in peripheral blood leucocytes and donorrecipi

62 th the viral load, monitored by quantitative HHV-7 DNA polymerase chain reaction.

63 HHV-7 DNA was detected more frequently in PBMCs from pre

64 CMV, HHV-6, and HHV-7 DNA were detected within 8 weeks after transplanta

65 Human herpesvirus 7 (HHV-7) DNA sequences colinear with the HHV-6 lytic-phase

66 common, HHV-6A DNAemia was not observed, and HHV-7 DNAemia was prevalent.

67 HHV-6 and HHV-7 DNAemia were not significantly associated with cyt

68 vidity antibodies to both viruses, HHV-6 and HHV-7 DNAs were found, confirming dual primary infection

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

70 esvirus 6 variants A and B (HHV-6A and -6B), HHV-7 encodes a homolog of the alphaherpesvirus origin b

71 infection and that gB represents one of the HHV-7 envelope proteins involved in the adsorption of vi

72 attempt to identify the human herpesvirus 7 (HHV-7) envelope protein(s) involved in cell surface bind

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

74 vitro system for reactivation of HHV-6B and HHV-7 from latency.

75 However, extensive analysis of the HHV-7 genome has not been reported, and the precise phyl

76 he viral genome at the right (3') end of the HHV-7 genome.

77 ate loci of divergence between the HHV-6 and HHV-7 genomes, which occur at the genome terminal in the

78 ace binding, the extracellular domain of the HHV-7 glycoprotein B (gB) homolog protein was cloned and

79 Taken together, these findings suggest that HHV-7 gp65 may contribute to viral attachment to cell su

80 onses to HHV-6A (U1102)-, HHV-6B (Z29)-, and HHV-7 (H7SB)-infected cell lysates in healthy controls a

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

82 ransmission of human herpesvirus (HHV)-6 and HHV-7 have been suggested, and congenital HHV-6 infectio

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

84 ytomegalovirus, human herpesvirus 6 (HHV-6), HHV-7, HHV-8, and Epstein-Barr virus.

85 ns with 5 human herpesviruses (HHVs) (HHV-6, HHV-7, HHV-8, varicella zoster virus [VZV], and Epstein-

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

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

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

89 t the hypothesis of reactivation of HHV-6 or HHV-7 in CFS.

90 d CMV disease, suggesting a possible role of HHV-7 in its pathogenesis.

91 ovirus [CMV], human herpesvirus [HHV]-6, and HHV-7) in nonimmunocompromised hosts is rare.

92 A human herpesvirus 7 (HHV-7) indirect immunofluorescence antibody avidity test

93 HHV-7-induced CD4 downregulation was sufficient for HIV-

94 same cells strongly suggested that enlarged HHV-7-infected cells contained a single polylobated nucl

95 HHV-7-infected cells must therefore possess other means

96 (RNA) blot analysis with poly(A)(+) RNA from HHV-7-infected cells revealed that the cDNA insert hybri

97 nt kinase cdc2 and cyclin B was increased in HHV-7-infected cells with respect to the uninfected ones

98 intracellular CD4 (CD4INTRA) were reduced in HHV-7-infected cells with respect to uninfected controls

99 ctivity associated to cdc2 were decreased in HHV-7-infected cells with respect to uninfected cultures

100 To elucidate the origin of the enlarged HHV-7-infected cells, extensive electron and confocal mi

101 y analysis performed on nuclei isolated from HHV-7-infected cells, which showed multiple peaks with a

102 -6 oriLyt were replicated in both HHV-6- and HHV-7-infected cells.

103 cted bystander cells but not in productively HHV-7-infected cells.

104 ontaining these sequences were replicated in HHV-7-infected cord blood mononuclear cells but not in H

105 ion of HIV infection similar to that seen in HHV-7-infected tissues.

106 osphorylated p56lck levels were unchanged in HHV-7-infected versus uninfected cells.

107 findings, soluble heparin was found to block HHV-7 infection and syncytium formation in the SupT1 cel

108 In both coculture and cell-free HHV-7 infection experiments, a significant correlation w

109 front of the luciferase gene indicated that HHV-7 infection has a suppressive effect on CD4 transcri

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

111 Acute in vitro HHV-7 infection induced (1) the formation of giant multi

112 Here we show that HHV-7 infection results in premature degradation of majo

113 s likely to function in the normal course of HHV-7 infection to downregulate surface class I molecule

114 ls, which represent the hallmark of in vitro HHV-7 infection, arise from single CD4(+) T cells underg

115 Human herpesvirus 7 (HHV-7) infection of both primary CD4(+) T lymphocytes an

116 s are ubiquitous during childhood, few acute HHV-7 infections are identified.

117 Although both human herpesvirus (HHV) 6 and HHV-7 infections are ubiquitous during childhood, few ac

118 ratory tests for diagnosing active HHV-6 and HHV-7 infections include virus culture, antigen detectio

119 In children < or =24 months of age, HHV-7 infections occurred less often than HHV-6 infectio

120 al manifestations of primary and reactivated HHV-7 infections were similar, except that seizures occu

121 iously serologically proven primary HHV-6 or HHV-7 infections, eight had low-avidity antibody only to

122 ent HHV-6 viremia, 2 associated with primary HHV-7 infections.

123 se were primary and 7 (23%) were reactivated HHV-7 infections.

124 Human herpesvirus-6 (HHV-6) and -7 (HHV-7) infections typically are silent or manifested as

125 These data demonstrate that HHV-7 is a powerful inhibitor of HIV-1 infection in cell

126 HHV-7 is reactivated from latently infected peripheral b

127 e close biological relationship of HHV-6 and HHV-7 is reflected at the genetic level, where there is

128 HHV-7 is related to human herpesvirus 6 (HHV-6) in terms

129 These results indicate that HHV-7 is resistant to ganciclovir at levels that were ef

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

131 Human herpesvirus 7 (HHV-7) is a recently isolated betaherpesvirus that is pr

132 Human herpesvirus 7 (HHV-7) is a relatively recently discovered member of the

133 HHV-7, most (18 of 101 serum samples [20%]) HHV-7 low-avidity antibody was found in the second year

134 Lymphoproliferation to HHV-7 lysate was demonstrated in 23% of healthy controls

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

136 These results suggest that HIV-1 and HHV-7 may interfere in lymphoid tissue in vivo, thus pot

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

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

139 found in the first year of life, whereas for HHV-7, most (18 of 101 serum samples [20%]) HHV-7 low-av

140 ought to characterize the interaction of the HHV-7 OBP (OBP(H7)) with its cognate sites in the 600-bp

141 d by the T-lymphotropic human herpesvirus 7 (HHV-7) on the CD4(+) T-lymphoblastoid SupT1 cell line an

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

143 No significant reactivation of HHV-7 or CMV was demonstrated among the critically ill p

144 n to be essential for replicator function of HHV-7 oriLyt.

145 BP(H7)) with its cognate sites in the 600-bp HHV-7 oriLyt.

146 ociation with high levels of CMV, HHV-6, and HHV-7 (P<.001,.022, and.001, respectively) occurred main

147 the eight human herpesviruses; the HHV-6 and HHV-7 polymerases contain an alanine at this amino acid.

148 65 kDa in sucrose density gradient-purified HHV-7 preparations; treatment with PNGase F reduced this

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

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

151 nd X4 HIV-1 is explained by a suppression of HHV-7 replication in X4- but not in R5-coinfected tissue

152 and analysis of the complete DNA sequence of HHV-7 strain JI.

153 Like the closely related HHV-6, HHV-7 suppresses the replication of CCR5-tropic (R5) HIV

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

155 entified another virus, human herpesvirus 7 (HHV-7) that interferes with HIV type 1 (HIV-1) replicati

156 ave been putatively associated with HHV-6 or HHV-7, these associations are not well documented due to

157 onent of the receptor for the T-lymphotropic HHV-7, these findings suggest that heparin-like molecule

158 and the precise phylogenetic relationship of HHV-7 to the other human betaherpesviruses HHV-6 and hum

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

160 Here, we show that human herpesvirus 7 (HHV-7) U21 binds to and downregulates all of the human c

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

162 We identify and characterize a protein from HHV-7, U21, that binds to and diverts properly folded cl

163 Human herpesvirus 7 (HHV-7) uses CD4 as a cellular membrane receptor and ther

164 ith the T lymphotrophic human herpesvirus 7 (HHV-7), using the SupT1 lymphoblastoid T cell line as a

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

166 nv transcripts, HHV-6 viral copy number, and HHV-7 viral copy number did not correlate with CFS sympt

167 HHV-6 viral copy number and HHV-7 viral copy number in both PBMCs and saliva were no

168 ot correlate with HHV-6 viral copy number or HHV-7 viral copy number in either PBMCs or saliva.

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

170 in otherwise healthy children, suggest that HHV-7 viremia could represent primary or reactivated inf

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

172 It is unknown whether HHV-7 viremia indicates primary infection, as with HHV-6

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

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

175 Baseline and peak prevalences of HHV-7 viremia were 22% and 54%, respectively (P<.0001).

176 eks after transplantation, were analyzed for HHV-7 viremia.

177 nciclovir had no effect on the prevalence of HHV-7 viremia.

178 or =10 years old, 30 (1%) showed evidence of HHV-7 viremia; 23 (77%) of these were primary and 7 (23%

179 h were found at low rates in cervical swabs (HHV-7 vs. HHV-6 DNA, 3.0% vs. 7.5%; P=.19).

180 Rather, the inhibition of R5 HIV-1 by HHV-7 was associated with a marked downregulation of CD4

181 proviral DNA in macrophages pretreated with HHV-7 was completely inhibited during the early stages a

182 -7 but who were seronegative for HHV-6, only HHV-7 was found.

183 A 1.7-kb cDNA clone from HHV-7 was identified which contains a large open reading

184 re established: 1) productive infection with HHV-7 was required to obtain persistent down-modulation

185 he course of the week, the DNAs of HHV-6 and HHV-7 were detected significantly more often (97% to 99%

186 rpesvirus-6 (HHV-6) and human herpesvirus-7 (HHV-7) were measured in both saliva and PBMCs using TaqM

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

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

189 ntiserum also neutralized the infectivity of HHV-7, while matched preimmune serum did not do so.

190 linked human herpesviruses 6 (HHV-6) and 7 (HHV-7) with posttransplant cytomegalovirus (CMV) disease