Abstract
Kaposi’s Sarcoma‐Associated Herpesvirus (KSHV) is the etiological agent of Kaposi’s Sarcoma (KS), Primary Effusion Lymphoma (PEL), and Multicentric Castleman’s Disease (MCD). Upon primary infection, the KSHV genome primarily exists as a latent infection, tethered to the host chromatin as an episome. It is widely accepted that NFκB signaling promotes latency and that NFκB signaling is activated through expression of the viral FLICE Inhibitory Protein (vFLIP). Our objective is to reveal new insights into the regulation of KSHV latency. We have identified a putative SUMO Interaction Motif (SIM) in vFLIP and we hypothesize that the vFLIP SIM is required for maintaining latency. Mutation of this SIM abolishes the ability of vFLIP to activate NFκB signaling. We also observed reduced vFLIP degradation by the master lytic switch RTA, as well as increased lytic reactivation. Our data present a novel means by which KSHV vFLIP functions to maintain latency.
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