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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

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