作者: Jonna Nykky , Matti Vuento , Leona Gilbert
DOI: 10.1371/JOURNAL.PONE.0086124
关键词:
摘要: Proper functioning of the mitochondria is crucial for survival cell. Viruses are able to interfere with mitochondrial functions as they infect host Parvoviruses known induce apoptosis in infected cells, but role parvovirus induced cytopathy only partially known. Here we demonstrate confocal and electron microscopy that canine (CPV) associated outer membrane from onset infection. During viral entry a transient depolarization transmembrane potential increase ROS level was detected. Subsequently, homeostasis normalized shortly, detected by repolarization decrease ROS. Indeed, activation cell signalling through ERK1/2 cascade observed early CPV cells. At 12 hours post infection, concurrent expression non-structural protein 1, damage structure its were apparent. Results this study provide additional insight pathology also more general information virus-mitochondria association.