Role of Oxidative Stress in the Epstein–Barr Virus Lifecycle and Tumorigenicity

Abstract

The Epstein–Barr virus (EBV) is an oncogenic virus with both latent and lytic states during its lifecycle. EBV employs a latency period as a strategy to avoid host immune surveillance and achieve lifelong persistent infection. However, the latent state may be interrupted and EBV may reactivate into a lytic replication cycle, exacerbating transmission and pathogenicity. The balance and transition between these two phases in the EBV lifecycle are complex, and reactive oxygen species play an important role. We reviewed the relationship between oxidative stress and lytic replication of EBV, and the role of oxidative stress in the development of EBV-related tumors. Further research is required to explore and develop tumor antioxidant therapy.

Plain language summary

The Epstein–Barr virus (EBV) is a virus that can cause cancer. Following infection, EBV can survive within cells in an inactive state known as a latent state. This latency can lead to a state of stress within cells because of the build-up of unstable molecules known as reactive oxygen species (ROS). These molecules can then trigger the activation of the virus, which can lead to the development of tumors. In this paper, we look at the relationship between ROS and EBV, and how they contribute to the development of tumors. We also provide insights into the current state of development of therapies for tumors linked to EBV infection.

Tweetable abstract

EBV disrupts oxygen homeostasis in host cells, leading to oxidative stress, reactivation, lysis, and accelerated replication and transmission. ROS play an important role in EBV regulation. Antioxidant therapy offers a new strategy for EBV-related tumors.

Keywords::

• Epstein–Barr virus
• latent infection
• lytic infection
• oxidative stress
• reactivation
• tumorigenesis

Author contributions

Z Zhao: writing – original draft preparation. W Liu and B Luo: writing – review and editing. All authors have read and agreed to the published version of the manuscript.

Financial & competing interests disclosure

This work was supported by the Natural Science Foundation of Shandong Province (ZR2020MH302 and ZR2021MC068). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was supported by the Natural Science Foundation of Shandong Province (ZR2020MH302 and ZR2021MC068). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.