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Pseudorabies virus infection inhibits autophagy in permissive cells in vitro
- Source :
- Scientific Reports
- Publication Year :
- 2017
- Publisher :
- Nature Publishing Group, 2017.
-
Abstract
- A large number of studies have demonstrated that autophagy is involved in the infection processes of different pathogens. Autophagy is now recognized as an essential component of innate and adaptive immunity. Several herpesviruses have developed various strategies to evade this antiviral mechanism. Pseudorabies virus (PRV) is a swine herpesvirus with a broad host range that causes devastating disease in infected pigs. In this study, we described the interaction between PRV and autophagy for the first time. PRV infection had a dual effect on the cell autophagy response; during the early period of infection, PRV virions induced autophagy without viral replication, and with viral protein expression, PRV reduced the basal level of autophagy in several permissive cells. We observed that inhibit the level of autophagy could increase the titer of infectious PRV. We also found that the conserved alphaherpesvirus US3 tegument protein may reduce the level of autophagy via activation of the AKT/mTOR pathways in PRV infected cells. These findings suggest that autophagy likely contributes to clearance of PRV, and that the virus has evolved strategies to antagonize this pathway.
- Subjects :
- 0301 basic medicine
Swine
Viral protein
animal diseases
viruses
Pseudorabies
Biology
Virus Replication
medicine.disease_cause
Article
Virus
Cell Line
Mice
Viral Proteins
03 medical and health sciences
Chlorocebus aethiops
Autophagy
medicine
Animals
Vero Cells
PI3K/AKT/mTOR pathway
Multidisciplinary
virus diseases
Viral Load
biochemical phenomena, metabolism, and nutrition
Acquired immune system
biology.organism_classification
Herpesvirus 1, Suid
Virology
030104 developmental biology
Viral replication
NIH 3T3 Cells
Vero cell
Signal Transduction
Subjects
Details
- Language :
- English
- ISSN :
- 20452322
- Database :
- OpenAIRE
- Journal :
- Scientific Reports
- Accession number :
- edsair.doi.dedup.....f1f5c1a0323fa2abee02fb13ff70bdb5
- Full Text :
- https://doi.org/10.1038/srep39964