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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 -6 oriLyt were replicated in both HHV-6- and HHV-7-infected cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 HHV-7 is reactivated from latently infected peripheral b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 65 kDa in sucrose density gradient-purified HHV-7 preparations; treatment with PNGase F reduced this

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 -7 but who were seronegative for HHV-6, only HHV-7 was found.

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

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

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

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

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

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

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

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