Oncogenic Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus on Cell Metabolism and Cell Transformation

Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) is a human double-stranded DNA virus that is responsible for the development of Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), multicentric Castleman's disease (MCD), and KSHV inflammatory cytokine syndrome (KICS). KSHV infection manipulates distinct cellular proteins and signaling pathways, resulting in immune escape, cell death inhibition, infinite cell growth, and cancer formation. Current treatments for KSHV-associated cancers are limited to conventional strategies targeting nonviral cancers which encounter limited efficacy and drug resistance. Understanding the molecular and cellular mechanisms underlying KSHV tumorigenesis is essential for the development of effective prevention and targeted therapeutics. In this review, we summarize recent studies and provide an updated understanding of the mechanisms employed by KSHV for metabolic reprogramming, cell immortalization, cell proliferation, and cell transition.