HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplementary figures Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Xu, Y. Articles by Ganem, D. Search for Related Content PubMed PubMed Citation Articles by Xu, Y. Articles by Ganem, D. Agricola Articles by Xu, Y. Articles by Ganem, D.

Induction of chemokine production by latent Kaposi's sarcoma-associated herpesvirus infection of endothelial cells

Howard Hughes Medical Institute, G. W. Hooper Foundation and Departments of Microbiology and Medicine, University of California, San Francisco, CA 94143-0552, USA

Correspondence
Don Ganem
ganem{at}cgl.ucsf.edu

Infection with Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is linked strongly to development of KS, an endothelial neoplasm also characterized by striking neoangiogenesis and infiltration with inflammatory cells. To elucidate the links between endothelial infection and inflammation, primary human umbilical vein endothelial cells (HUVECs) were examined for the production of chemokines following latent KSHV infection. Several chemokines that are produced in the ground state, including MCP-1, NAP 2 and RANTES, are upregulated significantly by KSHV infection. Moreover, the chemokine CXCL16, which is nearly absent in uninfected cells, is induced significantly following infection. This induction is attributable primarily to expression of vFLIP, a known inducer of NF-B. CXCL16 induces the chemotaxis of activated T cells, whose products have been proposed to positively regulate KS tumour-cell survival and growth. Whilst CXCL16 has also been proposed as a direct endothelial chemoattractant and mitogen, neither proliferation nor chemotaxis of HUVECs was observed following CXCL16 exposure. These results suggest that CXCL16 induction by KSHV contributes to the inflammatory phenotype of KS, but plays little role in the recruitment of endothelial spindle cells.

Supplementary figures are available in JGV Online.

This article has been cited by other articles:

				S. Efklidou, R. Bailey, N. Field, M. Noursadeghi, and M. K. Collins vFLIP from KSHV inhibits anoikis of primary endothelial cells J. Cell Sci., February 15, 2008; 121(4): 450 - 457. [Abstract] [Full Text] [PDF]