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Updated: May 1, 2026

Adenofection: A Method for Studying the Role of Molecular Chaperones in Cellular Morphodynamics by Depletion-Rescue Experiments
Published on: September 16, 2016
Effect of bovine adenovirus 3 on mitochondria
Sanjeev K Anand, Jaswant Singh, Amit Gaba
1Vaccine and Infectious Disease Organization -International Vaccine Center (VIDO- InterVac), University of Saskatchewan, Saskatoon, SK S7N 5E3, Canada. Suresh.tik@usask.ca.
Abstract:
Viruses alter the structure and the function of mitochondria for survival. Electron microscopy analysis of the cells infected with bovine adenovirus 3 revealed extensive damage to the inner mitochondrial membrane characterized by dissolution of the cristae and amorphous appearance of mitochondrial matrix with little or no damage to the outer mitochondrial membrane. There were fewer cristae with altered morphology. Potential patches of protein synthesis machinary around mitochondria could be observed at 12 hours post infection (hpi). At 24 hpi, the multi vascular bodies were evident throughout the infected cell. ATP production, mitochondrial Ca2+ and mitochondrial membrane potential (MMP) peaked at 18 hpi but decreased significantly at 24 hpi. This decrease coincided with the increased production of superoxide (SO) and reactive oxygen species (ROS), at 24 hpi indicating acute oxidative stress in the cells and suggesting a complete failure of the cellular homeostatic machinary. The results reveal an intericate relationship between Ca2+ homeostasis, the ATP generation ability of cells, SO and ROS production, and regulation of MMP following infection by bovine adenovirus 3.
Insights
Bovine adenovirus 3 infection severely damages mitochondria, disrupting cellular energy and homeostasis. This viral attack leads to oxidative stress and impaired mitochondrial function, crucial for virus survival.
Area of Science:
- Virology
- Cell Biology
- Mitochondrial Research
Background:
- Viruses manipulate host cell mitochondria for replication.
- Mitochondrial dysfunction is implicated in various viral infections.
Purpose of the Study:
- To investigate the impact of bovine adenovirus 3 on mitochondrial structure and function.
- To elucidate the relationship between viral infection, mitochondrial dynamics, and cellular homeostasis.
Main Methods:
- Electron microscopy was used to analyze mitochondrial ultrastructure in infected cells.
- Measurements of ATP production, mitochondrial calcium (Ca2+), mitochondrial membrane potential (MMP), superoxide (SO), and reactive oxygen species (ROS) were performed at different time points post-infection.
Main Results:
- Bovine adenovirus 3 infection caused significant damage to the inner mitochondrial membrane, including cristae dissolution and matrix changes.
- Mitochondrial Ca2+, ATP production, and MMP peaked at 18 hours post-infection (hpi) before declining sharply at 24 hpi.
- Increased SO and ROS production at 24 hpi indicated acute oxidative stress and failure of cellular homeostatic mechanisms.
Conclusions:
- Bovine adenovirus 3 infection profoundly alters mitochondrial structure and function.
- A complex interplay exists between Ca2+ homeostasis, ATP generation, oxidative stress, and MMP regulation during infection.
- Mitochondrial damage and dysfunction are critical components of the host-virus interaction in bovine adenovirus 3 infections.
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