Key result
Viruses exploit mitochondria to induce oxidative stress, promoting their replication and controlling reactive oxygen species production to maintain a favorable redox environment.
Why the study?
Viruses exploit mitochondria to support their infection cycle, and induction of oxidative stress has emerged as a common viral strategy to promote replication.
This review highlights the mechanisms by which viruses manipulate mitochondrial oxidative stress to support their replication cycle.
May inform mitochondrial-targeted antivirals; leaves open clinical relevance in cardiac viral disease.
Through oxidative phosphorylation, mitochondria play a central role in energy production and are an important production source of reactive oxygen species (ROS). Not surprisingly, viruses have evolved to exploit this organelle in order to support their infection cycle. Beyond its role in the cellular antiviral response, induction of oxidative stress has emerged as a common strategy employed by many viruses to promote their replication. Here, we review the key molecular mechanisms employed by viruses to interact with mitochondria and induce oxidative stress. Furthermore, we discuss how viruses benefit from increased ROS levels, how they control ROS production to maintain a favorable redox environment, and how they cope with ROS-mediated cell death.
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Foo et al. (2022) conducted a review in Viral infection. Viral infection was evaluated. Viruses exploit mitochondria to induce oxidative stress, promoting their replication and controlling reactive oxygen species production to maintain a favorable redox environment.
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