Duck Tembusu virus NS3 protein induces apoptosis by activating the PERK/PKR pathway and mitochondrial pathway
Yuhong Pan1,2, Wenjun Cai1,2, Anchun Cheng1,2
1Research Center of Avian Disease, College of Veterinary Medicine, Sichuan Agricultural University , Chengdu, Sichuan, China.
Importance:
Duck Tembusu virus (DTMUV) is an emerging pathogenic flavivirus that replicates well in mosquito, bird, and mammalian cells. An in vivo study revealed that BALB/c mice and Kunming mice were susceptible to DTMUV after intracerebral inoculation. Moreover, there are no reports about DTMUV-related human disease, but antibodies against DTMUV and viral RNA were detected in the serum samples of duck industry workers. This information implies that DTMUV has expanded its host range and poses a threat to mammalian health. Thus, understanding the pathogenic mechanism of DTMUV is crucial for identifying potential antiviral targets. In this study, we discovered that NS3 can induce the mitochondria-mediated apoptotic pathway through the PERK/PKR pathway; it can also interact with voltage-dependent anion channel 2 to induce apoptosis. Our findings provide a theoretical basis for understanding the pathogenic mechanism of DTMUV infection and identifying potential antiviral targets and may also serve as a reference for exploring the pathogenesis of other flaviviruses.
Insights
Duck Tembusu virus (DTMUV) infection triggers apoptosis in mammalian cells via the NS3 protein. This research identifies key pathways for potential antiviral targets against this emerging flavivirus.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Duck Tembusu virus (DTMUV) is an emerging flavivirus with a broad host range, including birds and mammals.
- DTMUV infection poses a potential threat to mammalian health, necessitating research into its pathogenic mechanisms.
Purpose of the Study:
- To elucidate the pathogenic mechanism of DTMUV infection.
- To identify potential antiviral targets by understanding how DTMUV induces cell death.
Main Methods:
- Investigated the role of the DTMUV NS3 protein in inducing apoptosis.
- Examined the involvement of the PERK/PKR pathway and voltage-dependent anion channel 2 (VDAC2) in DTMUV-induced cell death.
Main Results:
- DTMUV NS3 protein induces mitochondria-mediated apoptosis.
- The PERK/PKR pathway is activated by NS3, contributing to apoptosis.
- NS3 interacts with VDAC2 to promote apoptotic cell death.
Conclusions:
- DTMUV NS3 protein is a key factor in inducing apoptosis through specific cellular pathways.
- Findings provide a basis for developing antiviral strategies against DTMUV.
- This study offers insights into the pathogenesis of other flaviviruses.
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