Long-term persistence of mitochondrial dysfunctions after viral infections and antiviral therapies: A review of mechanisms involved.

Autor: Gay L; Pathogenesis and Control of Chronic and Emerging Infections, University of Montpellier, INSERM, Etablissement Français du Sang, University of Antilles, Montpellier, France., Desquiret-Dumas V; Department of Biochemistry and Molecular Biology, University Hospital of Angers, Angers, France.; MITOVASC Research Unit, CNRS 6015, INSERM U1083, University of Angers, Angers, France., Nagot N; Pathogenesis and Control of Chronic and Emerging Infections, University of Montpellier, INSERM, Etablissement Français du Sang, University of Antilles, Montpellier, France., Rapenne C; Department of Biochemistry and Molecular Biology, University Hospital of Angers, Angers, France.; MITOVASC Research Unit, CNRS 6015, INSERM U1083, University of Angers, Angers, France., Van de Perre P; Pathogenesis and Control of Chronic and Emerging Infections, University of Montpellier, INSERM, Etablissement Français du Sang, University of Antilles, Montpellier, France., Reynier P; Department of Biochemistry and Molecular Biology, University Hospital of Angers, Angers, France.; MITOVASC Research Unit, CNRS 6015, INSERM U1083, University of Angers, Angers, France., Molès JP; Pathogenesis and Control of Chronic and Emerging Infections, University of Montpellier, INSERM, Etablissement Français du Sang, University of Antilles, Montpellier, France.
Jazyk: angličtina
Zdroj: Journal of medical virology [J Med Virol] 2024 Sep; Vol. 96 (9), pp. e29886.
DOI: 10.1002/jmv.29886
Abstrakt: Mitochondria are vital for most cells' functions. Viruses hijack mitochondria machinery for misappropriation of energy supply or to bypass defense mechanisms. Many of these mitochondrial dysfunctions persist after recovery from treated or untreated viral infections, particularly when mitochondrial DNA is permanently damaged. Quantitative defects and structural rearrangements of mitochondrial DNA accumulate in post-mitotic tissues as recently reported long after SARS-CoV-2 or HIV infection, or following antiviral therapy. These observations are consistent with the "hit-and-run" concept proposed decades ago to explain viro-induced cell transformation and it could apply to delayed post-viral onsets of symptoms and advocate for complementary supportive care. Thus, according to this concept, following exposure to viruses or antiviral agents, mitochondrial damage could evolve into an autonomous clinical condition. It also establishes a pathogenic link between communicable and non-communicable chronic diseases.
(© 2024 The Author(s). Journal of Medical Virology published by Wiley Periodicals LLC.)
Databáze: MEDLINE
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