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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
17 ogenesis and KS.IMPORTANCE Here we show that HHV-8, a DNA tumor virus that causes Kaposi's sarcoma, i
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
24 standing of the complex interactions between HHV-8 and immune cells that cause HHV-8-related MCD.
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
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
40 utive time points revealed sero-reversion of HHV-8 antibodies, with undetectable titers in some child
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
49 f the effect of each additional short-stored HHV-8 antibody-positive transfusion was 1.79 (95% CI, 1.
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
54 enic, survival, and angiogenic activities to HHV-8-associated Kaposi's sarcoma, primary effusion lymp
58 inct HHV-8-related entities: Kaposi sarcoma, HHV-8-associated multicentric Castleman disease with mic
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
68 stein-Barr virus (EBV), human herpesvirus 8 (HHV-8), cytomegalovirus (CMV), and herpes simplex virus
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
76 s in host immune genes with the detection of HHV-8 DNA in PBMCs and with high lytic and latent antibo
79 r latent antibody titers or the detection of HHV-8 DNA in peripheral blood mononuclear cells (PBMCs).
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
97 Here, we report that human herpesvirus 8 (HHV-8) gene product viral interferon regulatory factor 1
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
104 /microl had increased probability for having HHV-8 in saliva (P=0.009) compared with patients whose c
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
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.
112 ted herpesvirus (KSHV) (human herpesvirus 8 [HHV-8]) induces the host cell's preexisting FAK, Src, ph
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
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.
126 oral, and biological factors associated with HHV-8 infection in children and adults to determine HHV-
128 urrently no standard method of screening for HHV-8 infection in the transplant setting, although HHV-
130 the role of household members as a source of HHV-8 infection in young children and social behaviors t
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
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
156 ther evaluations of the relationship between HHV-8 infections and risk of advanced prostate cancer.
158 ciated herpesvirus/human herpesvirus 8 (KSHV/HHV-8) interacts with cell surface alpha3beta1 integrin
161 rane domain, demonstrating that the entry of HHV-8 into B cells is related to DC-SIGN-mediated endocy
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
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
175 si's sarcoma-associated herpesvirus (KSHV or HHV-8) is the etiological agent of Kaposi's sarcoma, a h
177 s (KSHV), also known as human herpesvirus 8 (HHV-8), is a cancer-related human virus, classified as a
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
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
186 entation of -798T/277A in subjects with high HHV-8 latent antibody titers (OR, 2.4 [95% CI, 1.1-5.2])
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.
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
195 turbed, such as after organ transplantation, HHV-8 may activate molecular pathways that drive oncogen
197 spleen (n = 9) samples from 32 patients with HHV-8 MCD and compared them with patients with KS (n = 2
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
203 There is also a group of HIV-negative and HHV-8-negative patients with unknown etiology and pathop
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
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
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
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
224 organ donors/recipients for HHV-8 infection, HHV-8-related illness should be suspected in transplant
228 al studies suggest that ganciclovir inhibits HHV-8 replication, but no randomized clinical trials hav
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
234 However, unlike what has been suggested for HHV-8, RRV R15- and ORF74-encoding transcripts are expre
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%
244 ansfusion in the United States by conducting HHV-8 serologic testing among participants of the Transf
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
251 nfection in children and adults to determine HHV-8 seroprevalence and potential routes of transmissio
255 logic screening probably underestimates true HHV-8 seroprevalence in young Zambian children because o
260 neoplastic pathologies mirror the geographic HHV-8 seroprevalence, and certain groups of patients are
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
269 e suggests that, in this endemic population, HHV-8 transmission mainly occurs from mother to offsprin
273 rs should be included in efforts to minimize HHV-8 transmission, and households with a large number o
275 n between these 18 cases and 12 HIV-negative HHV-8-unrelated MCD cases showed marked discrepancies.
278 entire iciHHV-6A genome was absent from the HHV-8-unrelated-PEL-like lymphoma cells despite retentio
280 , cytomegalovirus (CMV), HHV-6A, HHV-6B, and HHV-8, using quantitative polymerase chain reaction.
282 5 human herpesviruses (HHVs) (HHV-6, HHV-7, HHV-8, varicella zoster virus [VZV], and Epstein-Barr vi
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
291 The contributions of human herpesvirus 8 (HHV-8) viral interleukin-6 (vIL-6) to virus biology rema
294 r level of DNAemia for infection with HHV-6, HHV-8, VZV, and EBV but not for infection with HHV-7.
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
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