Mitochondria in Viral Infections: Molecular Mechanisms and Therapeutic Targets.
- 1Department of Microbiology Chungnam National University School of Medicine Daejeon Republic of Korea.
- 2Department of Medical Science Chungnam National University School of Medicine Daejeon Republic of Korea.
- 3Brain Korea 21 FOUR Project for Medical Science Chungnam National University Daejeon Republic of Korea.
Abstract
Mitochondria are key regulators of cellular metabolism and innate immunity, and diverse viruses manipulate these organelles during infection. Viral proteins interact with respiratory chain complexes to regulate oxidative phosphorylation (OXPHOS) and reprogram host bioenergetics, thereby influencing viral replication or host antiviral responses. OXPHOS can be directly altered by viral factors or indirectly regulated through virus-induced changes in host metabolism and signaling. Beyond OXPHOS, viral infection perturbs mitochondrial metabolism, dynamics, calcium homeostasis, membrane potential, redox regulation, and apoptosis, linking mitochondrial alterations to viral replication and virus-associated cellular responses. This review focuses on how viruses regulate mitochondrial function, with particular emphasis on OXPHOS while addressing other mitochondrial processes in viral infection. We further distinguish mitochondrial alterations functionally linked to viral infection outcomes from those observed during infection without direct evidence of their effects on viral infection outcomes. Mitochondrial pathways have dual functions during infection, as viruses can hijack these pathways to promote infection, whereas hosts can utilize them to support antiviral responses. By integrating these mechanistic and experimental findings, this review highlights virus-specific patterns of mitochondrial regulation and their functional significance during infection. A mechanistic understanding of these mitochondrial responses provides a basis for identifying mitochondrial pathways as potential antiviral targets.
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BibTeX
@article{oh2026mitochondria,
title = {{Mitochondria in Viral Infections: Molecular Mechanisms and Therapeutic Targets.}},
author = {Ha Young Oh and Hye Jin Shin},
journal = {MedComm},
year = {2026},
month = nov,
doi = {10.1002/mco2.71127},
url = {https://europepmc.org/article/MED/42996889},
note = {CC BY},
}
RIS
TY - JOUR
TI - Mitochondria in Viral Infections: Molecular Mechanisms and Therapeutic Targets.
AU - Ha Young Oh
AU - Hye Jin Shin
PY - 2026
DA - 2026/11/05
JO - MedComm
DO - 10.1002/mco2.71127
UR - https://europepmc.org/article/MED/42996889
AB - Mitochondria are key regulators of cellular metabolism and innate immunity, and diverse viruses manipulate these organelles during infection. Viral proteins interact with respiratory chain complexes to regulate oxidative phosphorylation (OXPHOS) and reprogram host bioenergetics, thereby influencing viral replication or host antiviral responses. OXPHOS can be directly altered by viral factors or indirectly regulated through virus-induced changes in host metabolism and signaling. Beyond OXPHOS, viral infection perturbs mitochondrial metabolism, dynamics, calcium homeostasis, membrane potential, redox regulation, and apoptosis, linking mitochondrial alterations to viral replication and virus-associated cellular responses. This review focuses on how viruses regulate mitochondrial function, with particular emphasis on OXPHOS while addressing other mitochondrial processes in viral infection. We further distinguish mitochondrial alterations functionally linked to viral infection outcomes from those observed during infection without direct evidence of their effects on viral infection outcomes. Mitochondrial pathways have dual functions during infection, as viruses can hijack these pathways to promote infection, whereas hosts can utilize them to support antiviral responses. By integrating these mechanistic and experimental findings, this review highlights virus-specific patterns of mitochondrial regulation and their functional significance during infection. A mechanistic understanding of these mitochondrial responses provides a basis for identifying mitochondrial pathways as potential antiviral targets.
SN - 2688-2663
ER -