ライフサイエンスコーパス: HHV-8

1 ric (MCD) and linked to human herpesvirus 8 (HHV-8).

2 aposi's sarcoma-associated herpesvirus (KSHV/HHV-8).

3 us macaque homologue of human herpesvirus 8 (HHV-8).

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

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

6 organ failure have also been associated with HHV-8.

7 e are the major malignancies associated with HHV-8.

8 lethal KS in this child upon infection with HHV-8.

9 on > or = 1 day; heterosexual men also shed HHV-8.

10 infants also had evidence of infection with HHV-8.

11 precursors support productive infection with HHV-8.

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

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

14 small fraction of individuals infected with HHV-8.

15 tein-Barr virus (EBV; 64.8%), HSV-1 (13.0%), HHV-8 (3.2%), cytomegalovirus (2.4%), HSV-2 (0%), and va

16 We have developed a human herpesvirus 8 (HHV-8) 50% tissue culture infective dose (TCID50) assay

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

18 social behaviors that may modify the risk of HHV-8 acquisition.

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

20 Human herpesvirus 8 (HHV-8, also called Kaposi's sarcoma-associated herpes vi

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

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

23 s were collected daily during the study, and HHV-8 and CMV DNA were quantified by real-time PCR.

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

25 In this context, the risk of HHV-8 and its clinical disease is highest in immunocompr

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

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

28 Shedding of HHV-8 and shedding of cytomegalovirus were independent.

29 ortunity to study horizontal transmission of HHV-8 and understand the routes and sources of transmiss

30 ated herpesvirus (KSHV)/human herpesvirus 8 (HHV-8) and causes KSHV-like diseases in immunocompromise

31 ble association between human herpesvirus 8 (HHV-8) and prostate cancer, we evaluated HHV-8 seropreva

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

33 8), Kaposi's sarcoma-associated herpesvirus (HHV-8), and Epstein-Barr virus (EBV) are all members of

34 We compared T lymphocyte subsets among HIV-HHV-8+ and HIV-HHV-8- infected human individuals.

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

36 obtained from 517 Amerindians and tested for HHV-8 anti-latent nuclear antigen (anti-LANA) and antily

37 e used enzyme immunoassays (EIAs) to measure HHV-8 antibodies (K8.1 and open reading frame [ORF] 73 a

38 HHV-8 antibodies were detected by immunofluorescence wit

39 Serum samples were tested for HHV-8 antibodies with use of an enzyme immunoassay again

40 utive time points revealed sero-reversion of HHV-8 antibodies, with undetectable titers in some child

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

42 HHV-8 antibody titers in children followed at all consec

43 ) were more likely to die than recipients of HHV-8 antibody-negative blood (adjusted hazards ratio [A

44 6-month follow-up, we examined the effect of HHV-8 antibody-positive blood on transfusion recipients

45 ipt of multiple transfusions), recipients of HHV-8 antibody-positive blood stored </=4 days ("short-s

46 Transfusion with short-stored HHV-8 antibody-positive blood was associated with an inc

47 evaluated mortality following transfusion of HHV-8 antibody-positive blood.

48 recipients, 471 (43.1%) were transfused with HHV-8 antibody-positive blood.

49 f the effect of each additional short-stored HHV-8 antibody-positive transfusion was 1.79 (95% CI, 1.

50 n the United States, transmission routes for HHV-8 are uncertain.

51 ar B cells can be productively infected with HHV-8, as measured by an increase in viral DNA, the expr

52 ise in the incidence of human herpesvirus-8 (HHV-8)-associated Kaposi's sarcoma in both adults and ch

53 Management of HHV-8-associated diseases entails primarily a reduction

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

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

56 HHV-8-associated MCD may be considered as a single clini

57 ays an important role in the pathogenesis of HHV-8-associated MCD.

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

59 HHV-8 binding and infection were blocked by anti-DC-SIGN

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

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

62 Human herpesvirus 8 (HHV-8) causes Kaposi sarcoma.

63 Human herpesvirus 8 (HHV-8) causes Kaposi's sarcoma and pleural effusion lymp

64 Here we report that two of the HHV-8 chemokines, CCR8 agonists vCCL-1 and vCCL-2, have

65 s were disrupted by an human herpes virus-8 (HHV-8)-coded oncoprotein, vIRF1, and conferred resistanc

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

67 HHV-8 could also infect and replicate in B-cell lines tr

68 stein-Barr virus (EBV), human herpesvirus 8 (HHV-8), cytomegalovirus (CMV), and herpes simplex virus

69 Of the 44 MSM, 27 (61%) had HHV-8 detected in saliva on > or = 1 day; heterosexual m

70 Among MSM with HHV-8 detected in saliva, the median rate was 20% (range

71 The frequency of HHV-8 detection and quantity were correlated (r=0.62; P<

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

73 r alternatives for treatment, especially for HHV-8 diseases not responsive to immuno-minimization str

74 ated herpesvirus (KSHV)/human herpesvirus 8 (HHV-8) displays two distinct life stages, latency and ly

75 Although latent HHV-8 DNA can be detected in B cells from persons with t

76 s in host immune genes with the detection of HHV-8 DNA in PBMCs and with high lytic and latent antibo

77 Detection of HHV-8 DNA in PBMCs was not significantly related to any

78 We detected HHV-8 DNA in PBMCs with real-time amplification of the K

79 r latent antibody titers or the detection of HHV-8 DNA in peripheral blood mononuclear cells (PBMCs).

80 ntitative polymerase chain reaction measured HHV-8 DNA in saliva.

81 In analyses restricted to MSM, HHV-8 DNA was detected on 636 (22%) of 2897 days.

82 Polymerase chain reaction for HHV-8 DNA was positive on blood samples in all cases, wh

83 VZV and HHV-8 DNAemia were not detected.

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

85 Human herpesvirus 8 (HHV-8)-encoded viral interleukin-6 (vIL-6) has been impl

86 HHV-8-encoded viral Fas-associated death domain-like IL-

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

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

89 HHV-8 encodes a viral homolog of human IL-6, called vira

90 Human herpesvirus 8 (HHV-8) encodes a viral FLICE inhibitory protein (vFLIP),

91 Solid organ transplant recipients from HHV-8 endemic regions may develop HHV-8 reactivation or

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

93 us (KSHV; also known as human herpesvirus 8 [HHV-8]), Epstein-Barr virus (EBV), and murine gammaherpe

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

95 Zambia, to estimate the annual incidence of HHV-8 from birth through 48 months of age.

96 ange transporter that has been implicated in HHV-8 fusion to cells.

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

98 and unmasks the oncogenic potential of other HHV-8 genes in a paracrine fashion.

99 Although HHV-8 has not been linked etiologically to prostate canc

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

101 and survival of cells latently infected with HHV-8 in an autocrine manner via intracrine signaling an

102 is little information on the replication of HHV-8 in B cells.

103 innate and adaptive T cell responses against HHV-8 in immunocompetent individuals.

104 /microl had increased probability for having HHV-8 in saliva (P=0.009) compared with patients whose c

105 mic infection with human herpesvirus type 8 (HHV-8) in Amerindian populations is unknown.

106 pidemiologic studies designed to investigate HHV-8 incidence and transmission because it recruited an

107 is a paucity of data on human herpesvirus 8 (HHV-8) incidence and routes of infection, especially in

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

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

110 role in the treatment of conditions in which HHV-8-induced IL-8 production plays a pathogenic role.

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

112 ted herpesvirus (KSHV) (human herpesvirus 8 [HHV-8]) induces the host cell's preexisting FAK, Src, ph

113 lymphocyte subsets among HIV-HHV-8+ and HIV-HHV-8- infected human individuals.

114 cells displayed a strong reactivity against HHV-8-infected cell lines and prevented the release of i

115 , 1.49-7.14), having an increasing number of HHV-8-infected household members (HR, 1.27; 95% CI, 1.09

116 alphabeta+ T cells from HHV-8-infected individuals displayed a significantly hig

117 In vitro stimulation of PBMC from HHV-8-infected individuals with either infectious viral

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

119 rum levels comparable with those observed in HHV-8-infected patients, to contain elevated amounts of

120 of MCD, and LANA-1 immunostaining identified HHV-8-infected plasmablasts in 16 of 16 tested cases.

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

122 erify the observed association between acute HHV-8 infection and premature mortality.

123 Host genes important for control of HHV-8 infection are not well characterized.

124 However, HHV-8 infection bypassed AR signaling by promoting enhan

125 sauce plates was marginally associated with HHV-8 infection in children (P = .05).

126 oral, and biological factors associated with HHV-8 infection in children and adults to determine HHV-

127 rently selective protective immunity against HHV-8 infection in endothelial cells.

128 urrently no standard method of screening for HHV-8 infection in the transplant setting, although HHV-

129 Indeed, B cells are relatively resistant to HHV-8 infection in vitro.

130 the role of household members as a source of HHV-8 infection in young children and social behaviors t

131 osi's sarcoma and the role of antivirals for HHV-8 infection is being investigated.

132 ssion of DC-SIGN is essential for productive HHV-8 infection of and replication in B cells.

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

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

135 was performed by immunofluorescence assay of HHV-8 infection of immature dendritic cells at various T

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

137 nintegrin (DC-SIGN; CD209) is a receptor for HHV-8 infection of myeloid DCs and macrophages.

138 h little production of viral DNA, similar to HHV-8 infection of vascular endothelial cells.

139 Maternal HIV-1 and HHV-8 infection status were not independently associated

140 HHV-8 infection was associated with significant expansio

141 activated B cells was confirmed by blocking HHV-8 infection with endocytic pathway inhibitors.

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

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

144 Our study indicates that upon HHV-8 infection, the host responds by suppression of lyt

145 Primary HHV-8 infection, which is usually asymptomatic in immuno

146 nosuppression is the first line treatment of HHV-8 infection.

147 immune dysfunction and oncogenesis caused by HHV-8 infection.

148 immune genes could influence the control of HHV-8 infection.

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

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

151 the high prevalence of human herpesvirus-8 (HHV-8) infection in this region.

152 ted with the control of human herpesvirus 8 (HHV-8) infection in vivo.

153 Human herpesvirus 8 (HHV-8) infection is associated with Kaposi's sarcoma, pr

154 Human herpesvirus 8 (HHV-8) infection is endemic in sub-Saharan Africa.

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

156 ther evaluations of the relationship between HHV-8 infections and risk of advanced prostate cancer.

157 lso had associated human herpesvirus type 8 (HHV-8) infections.

158 ciated herpesvirus/human herpesvirus 8 (KSHV/HHV-8) interacts with cell surface alpha3beta1 integrin

159 Human herpesvirus 8 (HHV-8) interleukin-6 (vIL-6) is distinct from human and

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

161 rane domain, demonstrating that the entry of HHV-8 into B cells is related to DC-SIGN-mediated endocy

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

163 Our data suggest that HHV-8 is acquired primarily through horizontal transmiss

164 HHV-8 is an oncogenic gamma-herpesvirus that causes Kapo

165 HHV-8 is detected frequently and intermittently in the s

166 HHV-8 is latent in most PEL cells and, hence, resistant

167 These data imply that HHV-8 is not a major prevalent cause of prostate cancer.

168 Human herpes virus 8 (HHV-8) is a geographically limited virus that causes neo

169 persistent gamma-herpesvirus infection (EBV, HHV-8) is a significant problem in AIDS patients and tra

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

171 Human herpesvirus 8 (HHV-8) is endemic in Uganda and transmissible by blood.

172 ciated herpesvirus/human herpesvirus 8 (KSHV/HHV-8) is etiologically linked to Kaposi sarcoma (KS), p

173 -cell lymphoma in which human herpesvirus-8 (HHV-8) is found within all tumor cells and represents a

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

175 si's sarcoma-associated herpesvirus (KSHV or HHV-8) is the etiological agent of Kaposi's sarcoma, a h

176 Human herpesvirus 8 (HHV-8) is the etiological agent of Kaposi's sarcoma, pri

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

178 irus closely related to human herpesvirus 8 (HHV-8), is described here.

179 us (KSHV; also known as human herpesvirus 8 [HHV-8]) is the etiologic agent of Kaposi's sarcoma (KS)

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

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

182 Human herpesvirus 8 (HHV-8)/Kaposi's sarcoma-associated herpesvirus infection

183 ular neoplasm linked to human herpesvirus-8 (HHV-8/KS-associated herpesvirus [KSHV]) infection, is th

184 s 8/Kaposi's sarcoma-associated herpesvirus (HHV-8/KSHV), which are associated with several types of

185 the infection with the human herpesvirus 8 (HHV-8/KSHV).

186 entation of -798T/277A in subjects with high HHV-8 latent antibody titers (OR, 2.4 [95% CI, 1.1-5.2])

187 Compared with subjects with low HHV-8 latent antibody titers, analysis of inferred haplo

188 In 172 HHV-8 latent nuclear antigen (LANA)-seropositive adults

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

190 e promotion of proliferation and survival of HHV-8 latently infected primary effusion lymphoma cells.

191 Infection of DCs and macrophages with HHV-8 led to production of viral proteins, with little p

192 fection, and the risk is increased with high HHV-8 lytic or latent antibody titers or the detection o

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

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

195 turbed, such as after organ transplantation, HHV-8 may activate molecular pathways that drive oncogen

196 are single-gene inborn errors of immunity to HHV-8 may underlie classic KS in childhood.

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

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

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

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

201 pothesized that inborn errors of immunity to HHV-8 might underlie the exceedingly rare development of

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

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

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

205 ndritic cells (DC), is an entry receptor for HHV-8 on DC and macrophages.

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

207 ated herpesvirus (KSHV [human herpesvirus 8; HHV-8]) open reading frame 57 (ORF57) is a viral early p

208 lated expression of the human herpesvirus-8 (HHV-8 or KSHV)-encoded G protein-coupled receptor (vGPCR

209 Human herpes virus 8 (HHV-8) or Kaposi sarcoma-associated herpes virus is the

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

211 nfection in the transplant setting, although HHV-8 polymerase chain reaction is available to confirm

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

213 The role of antiviral drugs for HHV-8 prevention and treatment is yet to be defined.

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

215 iments that vGPCR is a positive regulator of HHV-8 productive replication and, through experimental u

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

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

218 ients from HHV-8 endemic regions may develop HHV-8 reactivation or primary infection and manifest wit

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

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

221 gle center 18 HIV-seronegative patients with HHV-8-related CD.

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

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

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

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

226 e similar to those described in HIV-positive HHV-8-related MCD.

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

228 al studies suggest that ganciclovir inhibits HHV-8 replication, but no randomized clinical trials hav

229 cantly reduces the frequency and quantity of HHV-8 replication.

230 Human herpesvirus-8 (HHV-8) replication is critical in the induction and main

231 erpesvirus (also called human herpesvirus 8 [HHV-8]) replication and transcription activator (RTA) is

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

233 The infection of B cells with HHV-8 resulted in increased expression of DC-SIGN and a

234 However, unlike what has been suggested for HHV-8, RRV R15- and ORF74-encoding transcripts are expre

235 rities between RTA and IRFs suggest that the HHV-8 RTA may usurp the cellular IRF pathway.

236 HHV-8 RTA was also able to activate two MHV-68 lytic pro

237 Here we report that HHV-8 RTA, not EBV RTA, was able to induce MHV-68 lytic

238 ciated herpesvirus/human herpesvirus 8 (KSHV/HHV-8) RTA is an important protein involved in the induc

239 ildren were at substantially higher risk for HHV-8 seroconversion (adjusted hazard ratio = 4.60, 95%

240 re not independently associated with risk of HHV-8 seroconversion in the child.

241 Rates of HHV-8 seroconversion in the transfusion and nontransfusi

242 1,532 child-years of follow-up, showed that HHV-8 seroconversion occurs early in life.

243 The incidence rate of HHV-8 seroconversion was 13.8 infections per 100 child-y

244 ansfusion in the United States by conducting HHV-8 serologic testing among participants of the Transf

245 s only 12 of 16 patients tested had positive HHV-8 serology at diagnosis.

246 dels were used to estimate the odds of being HHV-8 seropositive among intrafamilial pairs.

247 1259]), but this patient did not receive any HHV-8-seropositive blood units, suggesting that the infe

248 of 46 human immunodeficiency virus-negative, HHV-8-seropositive men collected saliva daily, and 25 re

249 lifetime sex partners and HIV infection) and HHV-8 seropositivity (P > .10).

250 HHV-8 seropositivity in children was independently assoc

251 nfection in children and adults to determine HHV-8 seroprevalence and potential routes of transmissio

252 HHV-8 seroprevalence by either assay was 75.4% (95% conf

253 Familial dependence in HHV-8 seroprevalence by either assay was found between m

254 8 (HHV-8) and prostate cancer, we evaluated HHV-8 seroprevalence in 2 case-control studies.

255 logic screening probably underestimates true HHV-8 seroprevalence in young Zambian children because o

256 HHV-8 seroprevalence increased from 16% among children a

257 HHV-8 seroprevalence tended to be lower in patients with

258 HHV-8 seroprevalence was 2.8% (29/1023) among blood dono

259 HHV-8 seroprevalence was examined according to sexual hi

260 neoplastic pathologies mirror the geographic HHV-8 seroprevalence, and certain groups of patients are

261 The quantity of HHV-8 shed was lower in nonwhites (P<.001) and younger p

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

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

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

265 data on the epidemiology and transmission of HHV-8 to young children in Zambia.

266 As in HHV-8, transcripts encoding RRV R15 and ORF74 are bicist

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

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

269 e suggests that, in this endemic population, HHV-8 transmission mainly occurs from mother to offsprin

270 Among men, HHV-8 transmission may occur through sexual activity, pa

271 s a paucity of knowledge about the routes of HHV-8 transmission to young children.

272 We investigated HHV-8 transmission via blood transfusion in the United S

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

274 Furthermore, we found that HHV-8 triggered epithelial-to-mesenchymal transition.

275 n between these 18 cases and 12 HIV-negative HHV-8-unrelated MCD cases showed marked discrepancies.

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

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

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

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

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

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

282 5 human herpesviruses (HHVs) (HHV-6, HHV-7, HHV-8, varicella zoster virus [VZV], and Epstein-Barr vi

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

284 acid identity with human CD200 (huCD200) and HHV-8 vCD200, respectively.

285 Collectively, our results demonstrate that HHV-8 vFLIP is an oncogenic protein that mimics the sign

286 Two main functions have been ascribed to HHV-8 vFLIP, inhibition of caspase 8/Fas-associated deat

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

288 ther infectious viral particles or different HHV-8 viral proteins resulted in gammadelta Vdelta1 T ce

289 The human herpesvirus 8 (HHV-8) viral G protein-coupled receptor (vGPCR) has been

290 Human herpesvirus 8 (HHV-8) viral interleukin-6 (vIL-6) mediates signaling th

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

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

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

294 r level of DNAemia for infection with HHV-6, HHV-8, VZV, and EBV but not for infection with HHV-7.

295 The infection of B cells with HHV-8 was blocked by the pretreatment of the cells with

296 HHV-8 was detected on 44% of swabs collected from partic

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

298 ms were reported on 10 (9%) of 114 days when HHV-8 was present, compared with 78 (9%) of 830 days wit

299 A total of 26 men infected with HHV-8 were randomized to receive 8 weeks of valganciclov

300 Human herpesvirus 8 (HHV-8), which is associated with the endothelial tumor K