# Ubiquitination dynamics in human tumour viruses: Viral infection, oncogenesis and antiviral therapy

## TL;DR

This review explains how human tumor viruses use the ubiquitin system to survive, replicate, and cause cancer, highlighting potential new treatments.

## Contribution

The paper provides a comprehensive overview of how oncogenic viruses manipulate the host ubiquitination system for survival and oncogenesis.

## Key findings

- Viruses exploit the ubiquitin system to enhance survival and replication.
- Oncogenic viruses manipulate ubiquitination to evade immune responses and drive cancer.
- Understanding virus-host ubiquitination interactions may lead to new therapies.

## Abstract

The ubiquitin conjugation system is a critical regulator of cellular homeostasis and influences various cellular processes. Viruses, as obligate intracellular parasites, have evolved sophisticated strategies to utilise this system to enhance their survival, to either increase virus production or ensure the long‐term survival of the latently infected host. Viruses from almost all families, including RNA and DNA viruses, are challenged by ubiquitin‐mediated mechanisms at different stages of their life cycle and have evolved to exploit or bypass the host cell ubiquitination system for their own replication. In this review, we examine the diverse functions of the ubiquitin conjugation system during the different stages of viral infection, including viral entry, replication, gene expression, assembly and release. We discuss how human oncogenic viruses manipulate host ubiquitination pathways to maintain infection, evade immune responses and drive oncogenesis. Finally, we highlight new research aimed at uncovering the precise molecular interactions between oncoviruses and the host ubiquitination system, which will pave the way for the development of advanced therapeutic strategies to treat viral infections and cancer.

The ubiquitin system is essential for cellular homeostasis and regulates many processes. Viruses, including oncogenic ones, exploit or evade this system to survive and replicate. This review explores how human tumour viruses manipulate the ubiquitination system to complete their life cycle, evade immunity and promote cancer. Understanding these interactions could reveal new therapeutic targets for treating viral infections and virus‐mediated cancer.