Ferroptosis in viral infection: a potential therapeutic target

Abstract

Ferroptosis, known as a type of programmed cell death that is iron dependent, is characterized by intracellular iron accumulation, glutathione depletion, glutathione peroxidase inactivation and lipid peroxidation. More and more research in recent years has demonstrated the tight connection between viral infections and ferroptosis. This article reviews the potential role and mechanism of ferroptosis in viral infection, and these findings will help in the prevention and treatment of the virus.

Plain language summary

Ferroptosis is a newly discovered type of cell death. More and more studies have shown that ferroptosis is closely related to infection by a variety of viruses. This article reviews the potential role and mechanism of ferroptosis in viral infection.

Executive summary

Role of ferroptosis in SARS-CoV-2 infection

• Ferroptosis is associated with SARS-CoV-2 infection and may lead to multi-organ damage.

Role of ferroptosis in HIV-1 infection

• HIV-1 Tat protein mediates ferroptosis in microglia.

Role of ferroptosis in influenza virus infection

• Cell death caused by influenza virus can be partially salvaged by ferroptosis inhibitors while reducing viral titers and inflammatory responses.

Role of ferroptosis in HSV infection

• Herpes simplex virus type 1 infection leads to ferroptosis and ferroptosis inhibitors can effectively alleviate HSV-1 encephalitis.

Role of ferroptosis in the infection of other viruses

• Ferroptosis plays an important role in the infection of dengue virus and Epstein–Barr virus.

• The enteroviruses (CV-A16 and CV-B3) and coronaviruses (EV-A71 and EV-D68) can induce ferroptosis through ACSL4.

Keywords: :

• ferroptosis
• GPX4
• lipid peroxidation
• mitochondria
• ROS
• virus

Author contributions

LQ Ding wrote the manuscript, conceived the work and revised the manuscript.

Financial disclosure

This work was supported by the Initial Scientific Research Fund of PhD from Hubei University of Science and Technology (no. BK202120). The author has 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.

Competing interest disclosure

The author has no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Writing disclosure

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

Additional information

Funding

This work was supported by the Initial Scientific Research Fund of PhD from Hubei University of Science and Technology (no. BK202120).