Role of Mitochondria in Parvovirus Pathology

Abstract

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

Transcriptome profiling indicating canine parvovirus type 2a as a potential immune activator

“…CPV-2a infection significantly activates host immune response-related signaling and CPV-2a is another potential immune cell activator, although further research is needed to investigate the effect on other cells lines and the underlying mechanisms. Yet, some studies mentioned that CPV-2a induces apoptosis [15,17], but our gene profiling data showed no connection between CPV-2a infection and apoptosis, which may be attribute to the virus types. This work extends our knowledge of CPV-2a-mediated cell infection and regulation.…”

“…VP2 is the main component to determine host range and mediate virus-receptor interaction during CPV-2 infection [13,14]. Parvovirus infection causes different effects on host cells, which depend on the species of virus and the cell lines [15]. CPV-2 is involved in induction of apoptosis in several cell lines, including Madin-Darby canine kidney (MDCK) cells [16,17].…”

Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection

“…The authors provide electron microscopic visuals of abnormal mitochondrial phenotypes that are similar to the ones we have included in our results including heterogeneously swollen mitochondria, membrane blebbing and disappearance of cristae. 58 Notably, the authors indicate activation of MEK/ERK signaling resulting from mitochondrial dysfunction in Parvovirus infection. We have previously demonstrated that VEEV infection leads to robust activation of the MEK/ERK signaling cascade, which is important for the virus to establish a productive infection.…”

The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability

“…Elevated levels of STAT-3 lead to the down-regulation of p53 [31] and hence, this may be a mechanism, by which B19 compromises the regulation of energy production within infected cells. The presence of NS1 leads to mitochondrial depolarization and elevated ROS production, which persists throughout the period of infection [119,120]. There is also evidence of decreased mitochondrial numbers in infected cells [121], which may reflect the fact that the survival of B19-infected cells is enabled by increased mitochondrial autophagy [122].…”