Transformation of primary human endothelial cells by Kaposi's sarcoma-associated herpesvirus

Ornella Flore, Shahin Rafii, Scott Ely, John J. O'Leary, Elizabeth M. Hyjek and Ethel Cesarman ()
Additional contact information
Ornella Flore: Cornell University Medical College
Shahin Rafii: Cornell University Medical College
Scott Ely: Cornell University Medical College
John J. O'Leary: Cornell University Medical College
Elizabeth M. Hyjek: Cornell University Medical College
Ethel Cesarman: Cornell University Medical College

Nature, 1998, vol. 394, issue 6693, 588-592

Abstract: Abstract Kaposi's sarcoma-associated herpesvirus (KSHV), or human herpesvirus 8, is invariably present in Kaposi's sarcoma lesions1,2. KSHV contains several viral oncogenes and serological evidence suggests that KSHV infection is necessary for the development of Kaposi's sarcoma, but cellular transformation by this virus has not so far been demonstrated. KSHV is found in the microvascular endothelial cells in Kaposi's sarcoma lesions and in the spindle ‘tumour’ cells3,4, which are also thought to be of endothelial origin. Here we investigate the biological consequences of infecting human primary endothelial cells with purified KSHV particles. We find that infection causes long-term proliferation and survival of these cells, which are associated with the acquisition of telomerase activity and anchorage-independent growth. KSHV was present in only a subset of cells, and paracrine mechanisms were found to be responsible for the survival of uninfected cells. Their survival may have been mediated by upregulation of a receptor for vascular endothelial growth factor. Our results indicate that transformation of endothelial cells by KSHV, as well as paracrine mechanisms that are induced by this virus, may be critical in the pathogenesis of Kaposi's sarcoma.

Date: 1998
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/29093 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:394:y:1998:i:6693:d:10.1038_29093

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/29093

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().