scholarly journals Human Herpesvirus-8 DNA Sequences in a Patient with Pemphigus Vulgaris, but Without HIV Infection or Kaposi's Sarcoma

1997 ◽  
Vol 108 (1) ◽  
pp. 118-119 ◽  
Author(s):  
Omeed M. Memar ◽  
Peter L. Rady ◽  
Randall M. Goldblum ◽  
Stephen K. Tyring
2002 ◽  
Vol 15 (3) ◽  
pp. 439-464 ◽  
Author(s):  
Dharam V. Ablashi ◽  
Louise G. Chatlynne ◽  
James E. Whitman, ◽  
Ethel Cesarman

SUMMARY Human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV), discovered in 1994, is a human rhadinovirus (gamma-2 herpesvirus). Unlike other human herpesviruses (herpes simplex virus, Epstein-Barr virus, varicella-zoster virus, cytomegalovirus, HHV-6, and HHV-7), it is not widespread in the general population and has many unique proteins. HHV-8 is strongly associated with all subtypes of Kaposi's sarcoma (KS), multicentric Castleman's disease, and a rare form of B-cell lymphoma, primary effusion lymphoma. In addition, HHV-8 DNA sequences have been found in association with other diseases, but the role of the virus in these diseases is largely unconfirmed and remains controversial. The seroprevalence of HHV-8, based on detection of latent and lytic proteins, is 2 to 5% in healthy donors except in certain geographic areas where the virus is endemic, 80 to 95% in classic KS patients, and 40 to 50% in HIV-1 patients without KS. This virus can be transmitted both sexually and through body fluids (e.g., saliva and blood). HHV-8 is a transforming virus, as evidenced by its presence in human malignancies, by the in vitro transforming properties of several of its viral genes, and by its ability to transform some primary cells in culture. It is not, however, sufficient for transformation, and other cofactors such as immunosuppressive cytokines are involved in the development of HHV-8-associated malignancies. In this article, we review the biology, molecular virology, epidemiology, transmission, detection methods, pathogenesis, and antiviral therapy of this newly discovered human herpesvirus.


1999 ◽  
Vol 43 (2) ◽  
pp. 377-380 ◽  
Author(s):  
Guy Boivin ◽  
Annie Gaudreau ◽  
Emil Toma ◽  
Richard Lalonde ◽  
Jean-Pierre Routy ◽  
...  

ABSTRACT Specific human herpesvirus 8 (HHV-8) DNA sequences were found in leukocytes of 12 of 29 (41.4%) AIDS subjects with Kaposi’s sarcoma (KS), whereas they were found in 4 of 43 (9.3%) AIDS subjects without KS (P = 0.003), although the peak HHV-8 DNA load in PCR-positive subjects with KS (mean, 425 copies per 0.2 μg of DNA) did not significantly differ from the one found in PCR-positive patients without KS (mean, 218 copies). The use of intravenous ganciclovir or foscarnet therapy to treat cytomegalovirus disease did not affect the HHV-8 DNA load in seven patients for whom serial samples were analyzed.


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

2001 ◽  
Vol 75 (18) ◽  
pp. 8660-8673 ◽  
Author(s):  
Shibani Pati ◽  
Marielle Cavrois ◽  
Hong-Guang Guo ◽  
James S. Foulke ◽  
Jynho Kim ◽  
...  

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.


2006 ◽  
Vol 79 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Navdeep Kumar ◽  
Ken McLean ◽  
Naoki Inoue ◽  
David R. Moles ◽  
Crispian Scully ◽  
...  

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