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Viruses 2018, 10(5), 266; https://doi.org/10.3390/v10050266

Ectromelia Virus Affects Mitochondrial Network Morphology, Distribution, and Physiology in Murine Fibroblasts and Macrophage Cell Line

1
Division of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences—SGGW, Ciszewskiego 8, 02-786 Warsaw, Poland
2
Laboratory of Bioenergetics and Biomembranes, Department of Biochemistry, Nencki Institute of Experimental Biology, Polish Academy of Science, Pasteura 3, 02-093 Warsaw, Poland
3
Integrative and Mammalian Research Centre, Department of Biomedical Sciences, Ross University School of Veterinary Medicine, P.O. Box 334 Basseterre, Saint Kitts and Nevis
4
Molecular Biology Unit, Mossakowski Medical Research Centre, Polish Academy of Sciences, Pawińskiego 5, 02-106 Warsaw, Poland
In memoriam.
*
Author to whom correspondence should be addressed.
Received: 3 May 2018 / Revised: 14 May 2018 / Accepted: 14 May 2018 / Published: 16 May 2018
(This article belongs to the Special Issue Cytoskeleton in Virus Infections)
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Abstract

Mitochondria are multifunctional organelles that participate in numerous processes in response to viral infection, but they are also a target for viruses. The aim of this study was to define subcellular events leading to alterations in mitochondrial morphology and function during infection with ectromelia virus (ECTV). We used two different cell lines and a combination of immunofluorescence techniques, confocal and electron microscopy, and flow cytometry to address subcellular changes following infection. Early in infection of L929 fibroblasts and RAW 264.7 macrophages, mitochondria gathered around viral factories. Later, the mitochondrial network became fragmented, forming punctate mitochondria that co-localized with the progeny virions. ECTV-co-localized mitochondria associated with the cytoskeleton components. Mitochondrial membrane potential, mitochondrial fission–fusion, mitochondrial mass, and generation of reactive oxygen species (ROS) were severely altered later in ECTV infection leading to damage of mitochondria. These results suggest an important role of mitochondria in supplying energy for virus replication and morphogenesis. Presumably, mitochondria participate in transport of viral particles inside and outside of the cell and/or they are a source of membranes for viral envelope formation. We speculate that the observed changes in the mitochondrial network organization and physiology in ECTV-infected cells provide suitable conditions for viral replication and morphogenesis. View Full-Text
Keywords: mitochondrial network; ectromelia virus; mitochondrial membrane potential; reactive oxygen species; mitochondrial mass mitochondrial network; ectromelia virus; mitochondrial membrane potential; reactive oxygen species; mitochondrial mass
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Gregorczyk, K.P.; Wyżewski, Z.; Szczepanowska, J.; Toka, F.N.; Mielcarska, M.B.; Bossowska-Nowicka, M.; Gieryńska, M.; Boratyńska-Jasińska, A.; Struzik, J.; Niemiałtowski, M.G.; Szulc-Dąbrowska, L. Ectromelia Virus Affects Mitochondrial Network Morphology, Distribution, and Physiology in Murine Fibroblasts and Macrophage Cell Line. Viruses 2018, 10, 266.

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