Latent KSHV infection increases the vascular permeability of human endothelial cells.

ABSTRACT: Kaposi sarcoma-associated herpesvirus (KSHV) is associated with 3 different human malignancies: Kaposi sarcoma (KS), primary effusion lymphoma, and multicentric Castleman disease. The KS lesion is driven by KSHV-infected endothelial cells and is highly dependent on autocrine and paracrine factors for survival and growth. We report that latent KSHV infection increases the vascular permeability of endothelial cells. Endothelial cells with latent KSHV infection display increased Rac1 activation and activation of its downstream modulator, p21-activated kinase 1 (PAK1). The KSHV-infected cells also exhibit increases in tyrosine phosphorylation of vascular endothelial (VE)-cadherin and β-catenin, whereas total levels of these proteins remained unchanged, suggesting that latent infection disrupte

SUBMITTER: Guilluy C 

PROVIDER: S-EPMC3217415 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature