Year: 2026
Type: review
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.
Source: MedComm
DOI: 10.1002/mco2.71127
Authors: Ha Young Oh, Hye Jin Shin
Institution: Chungnam National University
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,500
Awards: G2636554128, G363200850, G4898484321
OpenAlex ID: W7225411352