Ricerc@Sapienza

The Tyr705 STAT3 constitutive activation, besides promoting PEL cell survival, contributes to the maintenanceof viral latency. We found indeed that its de-phosphorylation by AG490 induced KSHV lytic cycle. Moreover,Tyr705 STAT3 de-phosphorylation, mediated by the activation of tyrosine phosphatases, together with the in-crease of Ser727 STAT3 phosphorylation contributed to KSHV lytic cycle induction by TPA. We then observedthat p53-p21 axis, essential for the induction of KSHV replication, was activated by the inhibition of Tyr705 andby the increase of Ser727 STAT3 phosphorylation.

Kaposi's Sarcoma-associated Herpesvirus (KSHV) is the causative agent of KS, an aggressive neoplasm that mainly occurs in immune-compromised patients. Spindle cells represent the main feature of this aggressive malignancy and arise from KSHV-infected endothelial cells undergoing endothelial to mesenchymal transition (EndMT), which changes their cytoskeletal composition and organization.

Background: Kaposi’s Sarcoma Herpesvirus (KSHV) is a gammaherpesvirus strongly linked to human cancer. The virus is also able to induce immune suppression, effect that contributes to onset/progression of the viral-associated malignancies. As KSHV may infect macrophages and these cells abundantly infiltrate Kaposi’s sarcoma lesions, in this study we investigated whether KSHV-infection could affect macrophage polarisation to promote tumorigenesis. Methods: FACS analysis was used to detect macrophage markers and PD-L1 expression.