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Updated: Sep 19, 2025
Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
Monkeypox virus induces ferroptosis to facilitate viral replication and promotes inflammatory responses
Xia Chuai1, Yuping Wang1,2, Chen Wang1
1State Key Laboratory of Virology and Biosafety, Wuhan Institute of Virology, Center for Biosafety Mega Science, Chinese Academy of Sciences, Wuhan, People's Republic of China.
Abstract:
Ferroptosis is an iron-dependent form of programmed cell death, which is characterized by iron overload and accumulation of lipid peroxidation. As a newly identified type of cell death, its involvement in poxvirus infection and pathogenesis remains unclear. Since MPXV shares biological and pathogenic similarities with other poxviruses, such as vaccinia virus (VACV), we used VACV-infected cell and mouse models to demonstrate that VACV infection induces ferroptosis both in vitro and in vivo. Inhibition of ferroptosis significantly reduce virus replication and alleviates the inflammatory response. Additionally, we observed that VACV infection upregulates prostaglandin-endoperoxide synthase 2 (PTGS2), which contributes to virus-triggered ferroptosis and inflammation. This study identifies a novel form of cell death triggered by poxvirus infection, shedding light on host-pathogen interactions and offering a potential therapeutic target for MPXV and other Orthopoxviruses.
Insights
Poxvirus infection triggers ferroptosis, a form of cell death involving iron and lipid peroxidation. Inhibiting this process reduces vaccinia virus replication and inflammation, revealing a new therapeutic target for orthopoxviruses.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Ferroptosis is iron-dependent programmed cell death involving lipid peroxidation.
- The role of ferroptosis in poxvirus infection and pathogenesis is not well understood.
- Monkeypox virus (MPXV) shares similarities with vaccinia virus (VACV).
Purpose of the Study:
- To investigate whether VACV infection induces ferroptosis.
- To determine the impact of ferroptosis inhibition on VACV replication and inflammation.
- To identify mechanisms linking VACV infection, ferroptosis, and inflammation.
Main Methods:
- VACV-infected cell and mouse models were used.
- Ferroptosis was assessed in infected cells and tissues.
- Virus replication and inflammatory markers were measured.
- The role of prostaglandin-endoperoxide synthase 2 (PTGS2) was investigated.
Main Results:
- VACV infection induces ferroptosis both in vitro and in vivo.
- Inhibiting ferroptosis significantly reduced VACV replication and inflammation.
- VACV infection upregulates PTGS2, contributing to ferroptosis and inflammation.
- This highlights a novel cell death pathway in poxvirus infection.
Conclusions:
- Poxvirus infection, specifically VACV, triggers ferroptosis.
- Targeting ferroptosis can reduce viral load and inflammation.
- PTGS2 is a key mediator of VACV-induced ferroptosis and inflammation.
- This offers a potential therapeutic strategy for orthopoxvirus infections like MPXV.
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