scholarly journals Visceral Kaposi's Sarcoma Related to Human Herpesvirus-8 in Liver Transplant Recipient: Case Report and Literature Review

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
H. Benhammane ◽  
G. Mentha ◽  
E. Tschanz ◽  
O. El Mesbahi ◽  
P. Y. Dietrich

Background. Kaposi’s sarcoma (KS) in transplant recipients is about 400 to 500 times rate in the general population. It is strongly associated to Human herpesvirus-8 (HHV-8) infection which has been found in 95% of KS lesions. The optimal approach to managing posttransplantation KS is to reduce or discontinue immunosuppressive therapy but this strategy carries a risk of the acute rejection of the graft. Recently, the use of an mTOR inhibitor has added new opportunities for KS treatment and prevention.Case Report. We report a case of 24 years-old Turkish woman with visceral HHV-8-associated Kaposi's sarcoma after orthotopic liver transplantation.Conclusion. Posttransplantation KS is considered an experimental model of virus induced tumor suggesting the usefulness of HHV-8 screening in transplant recipient and donor. Therapeutic approaches are complex and require a multidisciplinary team.

2003 ◽  
Vol 35 (1) ◽  
pp. 447-449 ◽  
Author(s):  
P.-M Huang ◽  
Y.-L Chang ◽  
J.-S Chen ◽  
H.-H Hsu ◽  
W.-J Ko ◽  
...  

2001 ◽  
Vol 33 (10) ◽  
pp. 1782-1785 ◽  
Author(s):  
Paolo Monini ◽  
Maria Caterina Sirianni ◽  
Marina Franco ◽  
Laura Vincenzi ◽  
Simone Topino ◽  
...  

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 ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document