Regulating cellular plasticity to persist: a way for tumor viruses to triumph

Abstract

Viruses can cause cancer either by direct (e.g. expression of viral oncogenes) or indirect (e.g. immunomodulation) means. A pre-requisite to carcinogenesis is long-term infection of the natural niche, indicating an important link between the ability to establish persistent infections and eventual tumorigenesis. Persistently infected cells are thought to serve as the cells-of-origin in infection-associated cancers. As is the case with non-infectious cancers, it has been proposed that infected tissue stem cells may give rise to the cancer-initiating cells. Emerging evidence points to an alternative possibility that infected committed cells may acquire stem-like characteristics during infection, giving rise to tumor-initiating cells.

Here in this study, we summarize similarities and differences of the mechanisms used by human tumor viruses to evade the host immune system by promoting persistent infection and tumor formation. Moreover, we explore the possible benefit of infecting stem cells or reprogramming differentiated cells to more stem-like phenotypes by the human tumor viruses to aid the viral lifecycle and/or disease progression.