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… 
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16 Citations
Background Citations
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Methods Citations
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16 Citations

The effect of classical swine fever virus NS5A and NS5A mutants on oxidative stress and inflammatory response in swine testicular cells.

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.

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.

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