Classical swine fever virus induces oxidative stress in swine umbilical vein endothelial cells

@article{He2014ClassicalSF,
  title={Classical swine fever virus induces oxidative stress in swine umbilical vein endothelial cells},
  author={Lei He and Yanming Zhang and Yan-Qin Fang and Wulong Liang and Jihui Lin and Min Cheng},
  journal={BMC Veterinary Research},
  year={2014},
  volume={10}
}
BackgroundClassical swine fever virus (CSFV) infection causes significant losses of pigs, which is characterized by hemorrhage, disseminated intravascular coagulation and leucopenia. The swine vascular endothelial cell is a primary target cell for CSFV. The aim of this study was to determine the role of CSFV infection in inducing oxidative stress (OS) in vascular endothelial cells.ResultsWe demonstrated that CSFV infection induced oxidative stress in swine umbilical vein endothelial cells… 
View on Springer
ncbi.nlm.nih.gov
16 Citations
Background Citations
10
Methods Citations
1

16 Citations

Classical Swine Fever Virus Infection and Its NS4A Protein Expression Induce IL-8 Production through MAVS Signaling Pathway in Swine Umbilical Vein Endothelial Cells

It is demonstrated thatCSFV NS4A induced IL-8 production through enhancing MAVS pathway and promoted CSFV replication and it was discovered that CSF VNS4A was localized in the cell nucleus and cytoplasm, including endoplasmic reticulum (ER) and mitochondria.

Some epidemiology and immunopathology considerations of classical swine fever

Immunopathological understanding from molecular explanation in CSF is important in the conceptual contribution of the development of new prophylactic and therapeutic strategies that allow to control/ eradicate this disease.

Mitophagy Induced by Classical swine fever Virus Nonstructural Protein 5A Promotes viral replication.

It is revealed here that the CSFV nonstructural protein 5A (NS5A) plays a critical role in inducing cellular mitophagy, and the expression level of reactive oxygen species (ROS) was increased byCSFV NS5A protein, while NS 5A-induced mitophamy correlated with the quantity of ROS production.

CSFV induced mitochondrial fission and mitophagy to inhibit apoptosis

The preservation of mitochondrial proteins, upregulated apoptotic signals and decline of viral replication resulting from the silencing of Drp1 and Parkin in CSFV-infected cells suggested thatCSFV induced mitochondrial fission and mitophagy to enhance cell survival and viral persistence.

Apoptosis, Autophagy, and Pyroptosis: Immune Escape Strategies for Persistent Infection and Pathogenesis of Classical Swine Fever Virus

This review summarizes the known roles of apoptosis, autophagy, and pyroptosis in CSFV infection and how viruses manipulate these three cellular biological processes to evade the immune response.

Effects of astragalus polysaccharide on the adhesion-related immune response of endothelial cells stimulated with CSFV in vitro

The addition of APS to the culture can obviously regulate the expression of molecules related to the adhesion, growth, and immune response of ECs, as well as the production of cytokines, and may have the potential to be an effective component in vaccines against CSFV.

Peroxiredoxins—The Underrated Actors during Virus-Induced Oxidative Stress

It is demonstrated that peroxiredoxins scavenge hydrogen and organic peroxides at their physiological concentrations at various cell compartments, unlike many other antioxidant enzymes, and their recycling is discussed.

Inducible GBP5 Mediates the Antiviral Response via Interferon-Related Pathways during Influenza A Virus Infection

This study found that GBP5 expression was significantly elevated in influenza patients and influenza A virus-infected A549 human lung epithelial cells and inhibited virus replication through the activation of IFN signaling and proinflammatory factors.

CLASSICAL SWINE FEVER VIRUS DETECTION IN FETAL SWINE TISSUES BY IMMUNOHISTOCHEMISTRY

Results showed that CSFV antigen can be detected in formalin-fixed, paraffin-embedded fetal tissue specimens originating from naturally CSfV infected sows by using monoclonal antibody WH303, and Fetal kidneys proved to be a very useful organ for diagnosis of the CSF virus.

Probing the impact of quercetin-7-O-glucoside on influenza virus replication influence.

References

SHOWING 1-10 OF 44 REFERENCES

Classical swine fever virus NS5A protein localizes to endoplasmic reticulum and induces oxidative stress in vascular endothelial cells

It is suggested that CSFV NS5A plays important roles in the induction of oxidative stress and inflammatory response in vascular endothelial cells and provides an insight into the mechanism by which CSFCNS5A can alter intracellular events associated with the viral infection.

Attenuation of nitric oxide bioavailability in porcine aortic endothelial cells by classical swine fever virus

In conclusion, infection of PAECs with CSFV attenuated the expression of eNOS and reduced NO bioavailability through activation of the ERK and PI3/Akt pathways.

Proteomic analysis of primary porcine endothelial cells after infection by classical swine fever virus.

Classic swine fever virus NS2 protein leads to the induction of cell cycle arrest at S-phase and endoplasmic reticulum stress

The data suggest that CSFV NS2 protein modulate the cellular growth and cell cycle progression through inducing the S-phase arrest and provide a cellular environment that is advantageous for viral replication.

Classical swine fever virus infection protects aortic endothelial cells from pIpC-mediated apoptosis.

It is concluded that CSFV infection can inhibit apoptotic signalling at multiple levels, including at the caspase-8 and the mitochondrial checkpoints, and by supporting viral replication, endothelial cells may promoteCSFV pathogenesis.

Classical swine fever virus induces proinflammatory cytokines and tissue factor expression and inhibits apoptosis and interferon synthesis during the establishment of long-term infection of porcine vascular endothelial cells.

CSFV can actively block anti-viral and apoptotic responses and this may contribute to virus persistence and point to a central role for infection of vascular endothelial cells during the pathogenesis of the disease, where a proinflammatory and procoagulant endothelium induced by the virus may disrupt the haemostatic balance and lead to the coagulation and thrombosis seen in acute disease.

Up-regulation of integrin beta3 expression in porcine vascular endothelial cells cultured in vitro by classical swine fever virus.

Enhancement by Tumor Necrosis Factor Alpha of Dengue Virus-Induced Endothelial Cell Production of Reactive Nitrogen and Oxygen Species Is Key to Hemorrhage Development

It is shown by the presence of NS1 antigen and viral nuclei acid that dengue virus actively infects the endothelium at 12 h and 24 h after inoculation, and hemorrhage development and the severity of hemorrhage were greatly reduced in mice lacking iNOS or p47phox or treatment with oxidase inhibitor, pointing to the critical roles of reactive nitrogen and oxygen species in d Dengue hemorrhage.

Oxidative stress in human immunodeficiency virus infection

The data presented here lead to a better understanding of the consequences of oxidative stress on the pathophysiology of HIV infection and also enable the potential use of antioxidant molecules as therapeutic agents against AIDS.

Hepatitis C virus NS5A and core proteins induce oxidative stress-mediated calcium signalling alterations in hepatocytes.