Viral Interferon Regulatory Factor 1 of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Binds to, and Inhibits Transactivation of, CREB-Binding Protein

2000 ◽  
Vol 270 (1) ◽  
pp. 23-27 ◽  
Author(s):  
Taegun Seo ◽  
Daeyoup Lee ◽  
Bona Lee ◽  
Jae Hoon Chung ◽  
Joonho Choe
Keyword(s):  
Kaposi's Sarcoma ◽  
Binding Protein ◽  
Human Herpesvirus ◽  
Kaposi’S Sarcoma ◽  
Interferon Regulatory Factor ◽  
Human Herpesvirus 8 ◽  
Creb Binding Protein ◽  
Regulatory Factor ◽  
Herpesvirus 8 ◽  
Interferon Regulatory Factor 1

scholarly journals Modulation of Human Herpesvirus 8/Kaposi's Sarcoma-Associated Herpesvirus Replication and Transcription Activator Transactivation by Interferon Regulatory Factor 7

2005 ◽  
Vol 79 (4) ◽  
pp. 2420-2431 ◽  
Author(s):  
Jinzhong Wang ◽  
Jun Zhang ◽  
Luwen Zhang ◽  
William Harrington ◽  
John T. West ◽  
...  
Keyword(s):  
Gene Expression ◽  
Kaposi's Sarcoma ◽  
Human Herpesvirus ◽  
Interferon Regulatory Factor ◽  
Human Herpesvirus 8 ◽  
Viral Gene ◽  
Regulatory Factor ◽  
Transcription Activator ◽  
Herpesvirus 8 ◽  
Interferon Regulatory Factor 7

ABSTRACT Human herpesvirus 8 (HHV-8)/Kaposi's sarcoma-associated herpesvirus infection goes through lytic and latent phases that are regulated by viral gene products, but very little is known about the involvement of host proteins. The replication and transcription activator (RTA) is a viral protein sufficient to initiate lytic replication by activating downstream genes, including the viral early gene open reading frame 57 (ORF 57), which codes for a posttranscriptional activator. In this study, we demonstrate that cellular interferon regulatory factor 7 (IRF-7) negatively regulates this process by competing with RTA for binding to the RTA response element in the ORF 57 promoter to down-regulate RTA-induced gene expression. We also show that alpha interferon represses RTA-mediated transactivation and that repression involves IRF-7. Our study indicates that upon HHV-8 infection, the host responds by suppression of lytic gene expression through binding of IRF-7 to the lytic viral gene promoter. These findings suggest that HHV-8 has developed a novel mechanism to induce but then subvert the innate antiviral response, specifically the interferon-signaling pathway, to regulate RTA activity and ultimately the viral latent/lytic replicative cycle.

Detection of human herpesvirus 8 DNA and antibodies to latent nuclear and lytic-phase antigens in serial samples from aids patients with Kaposi’s sarcoma

2000 ◽  
Vol 16 (3) ◽  
pp. 247-251 ◽  
Author(s):  
Lı́gia Camera Pierrotti ◽  
Laura Masami Sumita ◽  
Wilton Santos Freire ◽  
Hélio Hehl Caiaffa Filho ◽  
Vanda Akico Ueda Fick de Souza
Keyword(s):  
Kaposi's Sarcoma ◽  
Human Herpesvirus ◽  
Kaposi’S Sarcoma ◽  
Human Herpesvirus 8 ◽  
Aids Patients ◽  
Herpesvirus 8 ◽  
Serial Samples

scholarly journals Activation of NF-κB by the Human Herpesvirus 8 Chemokine Receptor ORF74: Evidence for a Paracrine Model of Kaposi's Sarcoma Pathogenesis

2001 ◽  
Vol 75 (18) ◽  
pp. 8660-8673 ◽  
Author(s):  
Shibani Pati ◽  
Marielle Cavrois ◽  
Hong-Guang Guo ◽  
James S. Foulke ◽  
Jynho Kim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Kaposi's Sarcoma ◽  
Vascular Endothelial Cells ◽  
Inositol Phosphate ◽  
Human Herpesvirus ◽  
Kaposi’S Sarcoma ◽  
Lymphoid Cells ◽  
Human Herpesvirus 8 ◽  
Herpesvirus 8 ◽  
Latently Infected

ABSTRACT Infection with human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma (KS)-associated herpesvirus, is necessary for the development of KS. The HHV-8 lytic-phase gene ORF74 is related to G protein-coupled receptors, particularly interleukin-8 (IL-8) receptors. ORF74 activates the inositol phosphate/phospholipase C pathway and the downstream mitogen-activated protein kinases, JNK/SAPK and p38. We show here that ORF74 also activates NF-κB independent of ligand when expressed in KS-derived HHV-8-negative endothelial cells or primary vascular endothelial cells. NF-κB activation was enhanced by the chemokine GROα, but not by IL-8. Mutation of Val to Asp in the ORF74 second cytoplasmic loop did not affect ligand-independent signaling activity, but it greatly increased the response to GROα. ORF74 upregulated the expression of NF-κB-dependent inflammatory cytokines (RANTES, IL-6, IL-8, and granulocyte-macrophage colony-stimulating factor) and adhesion molecules (VCAM-1, ICAM-1, and E-selectin). Supernatants from transfected KS cells activated NF-κB signaling in untransfected cells and elicited the chemotaxis of monocytoid and T-lymphoid cells. Expression of ORF74 conferred on primary endothelial cells a morphology that was strikingly similar to that of spindle cells present in KS lesions. Taken together, these data, demonstrating that ORF74 activates NF-κB and induces the expression of proangiogenic and proinflammatory factors, suggest that expression of ORF74 in a minority of cells in KS lesions could influence uninfected cells or latently infected cells via autocrine and paracrine mechanisms, thereby contributing to KS pathogenesis.

Human herpesvirus 8 genoprevalence in populations at disparate risks of Kaposi's sarcoma

2006 ◽  
Vol 79 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Navdeep Kumar ◽  
Ken McLean ◽  
Naoki Inoue ◽  
David R. Moles ◽  
Crispian Scully ◽  
...  
Keyword(s):  
Kaposi's Sarcoma ◽  
Human Herpesvirus ◽  
Kaposi’S Sarcoma ◽  
Human Herpesvirus 8 ◽  
Herpesvirus 8

Human herpesvirus-8 and Kaposi's sarcoma: Relationship with the multistep concept of tumorigenesis

2001 ◽  
pp. 125-159 ◽  
Author(s):  
Michael Stürzl ◽  
Christian Zietz ◽  
Paolo Monini ◽  
Barbara Ensoli
Keyword(s):  
Kaposi's Sarcoma ◽  
Human Herpesvirus ◽  
Kaposi’S Sarcoma ◽  
Human Herpesvirus 8 ◽  
Herpesvirus 8
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