Kaposi's Sarcoma-Associated Herpesvirus Latency-Associated Nuclear Antigen Prolongs the Life Span of Primary Human Umbilical Vein Endothelial Cells

Disruption of Kaposi's Sarcoma-Associated Herpesvirus Latent Nuclear Antigen Leads to Abortive Episome Persistence

“…LNA also dysregulates ␤-catenin pathways through the stabilization of ␤-catenin, by binding to the negative regulator glycogen synthase kinase 3␤ and causing a cell cycle-dependent nuclear accumulation of glycogen synthase kinase 3␤ (9). It has been reported that transduction with LNA promotes cell proliferation and prolongs the life span in primary human umbilical endothelial cells (38). Besides these functions, LNA is also likely to have an important role in KSHV episome persistence.…”

Role of Kaposi's Sarcoma-Associated Herpesvirus C-Terminal LANA Chromosome Binding in Episome Persistence

“…For example, expression of LANA inhibits p53-mediated apoptosis and also overcomes senescence in Saos2 cells induced by expression of retinoblastoma protein 1 (RB1) (21,60,63,66,71). LANA also induces B-cell hyperplasia and lymphomas in transgenic mice, and LANA prolongs the life span of primary endothelial cells (19,78). In addition, LANA modulates the Wnt signaling pathway by binding to and altering the activity of glycogen synthase kinase-3ß, resulting in increased levels of ß-catenin (22)(23)(24)48).…”

A Kaposi's Sarcoma-Associated Herpesvirus-Encoded Ortholog of MicroRNA miR-155 Induces Human Splenic B-Cell Expansion in NOD/LtSz-scid IL2Rγ null Mice

“…While ectopic expression has unmasked limited transforming potential for each of these genes, in vitro KSHV infection of either lymphoid or endothelial cells rarely leads to outgrowth of transformed cells (15,53). Since all KSHV miRNAs and the above proteins are coexpressed during latency, it is plausible that they work synergistically to deregulate host transcriptional networks promoting cell proliferation and transformation (4,24).…”