线粒体DNA
生物
线粒体
病毒学
抗病毒治疗
病毒复制
病毒
免疫学
遗传学
基因
慢性肝炎
作者
Laëtitia Gay,Valérie Desquiret‐Dumas,Nicolas Nagot,Clara Rapenne,Philippe Van de Perre,Pascal Reynier,Jacqueline María Valverde-Villegas
摘要
Abstract 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.
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