: Kaposi's sarcoma (KS) is an endothelial neoplasm that is tightly linked to infection by KS-associated herpesvirus, KSHV. KSHV is a lymphotropic virus whose primary reservoir is the B cell. Spread to its endothelial targets in KS pathogenesis therefore requires reactivation from latently infected B cells and lytic replication. In addition, growing evidence suggests that the KSHV lytic cycle may be the source of paracrine factors that influence KS angiogenesis and inflammation, two of the histologic signatures of KS. In this application, experiments are proposed to examine the molecular basis of lytic KSHV reactivation and spread, by examining (i) the biochemical mechanisms by which the viral RTA protein, a key regulator of the latent-lytic switch, regulates viral gene expression and is itself regulated; (ii) the consequences of lytic viral reactivation on host cell survival and gene expression; and(iii) identifying host cell surface molecules involved in KSHV entry and spread.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA096491-05
Application #
7057833
Study Section
AIDS and Related Research 8 (AARR)
Program Officer
Read-Connole, Elizabeth Lee
Project Start
2002-05-01
Project End
2008-10-31
Budget Start
2006-05-01
Budget End
2008-10-31
Support Year
5
Fiscal Year
2006
Total Cost
$329,166
Indirect Cost
Name
University of California San Francisco
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
094878337
City
San Francisco
State
CA
Country
United States
Zip Code
94143