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A novel p53 paralogue mediates antioxidant defense of mosquito cells to survive dengue virus replication
- Source :
- Virology. 519:156-169
- Publication Year :
- 2018
- Publisher :
- Elsevier BV, 2018.
-
Abstract
- Mosquito cells allow dengue viruses (DENVs) to undergo replication without causing serious deleterious effects on the cells, leading to advantages for dissemination to other cells. Despite this, increased accumulation of reactive oxygen species (ROS) is usually detected in C6/36 cells with DENV2 infection as shown in mammalian cells. Uniquely, oxidative stress caused by the ROS is alleviated by eliciting antioxidant defense which leads to protection of mosquito cells from the infection. In the present study, a novel p53 paralogue (p53-2) was identified and proved to be regulated in C6/36 cells with DENV2 infection. With a gene-knockdown technique, p53-2 was demonstrated to transcribe catalase which plays a critical role in reducing ROS accumulation and the death rate of infected cells. Ecologically, a higher survival rate of mosquito cells is a prerequisite for prosperous production of viral progeny, allowing infected mosquitoes to remain healthy and active for virus transmission.
- Subjects :
- DNA Replication
0301 basic medicine
Antioxidant
Virus transmission
medicine.medical_treatment
Apoptosis
Cell Count
Dengue virus
Virus Replication
medicine.disease_cause
Microbiology
Dengue fever
03 medical and health sciences
Aedes
Virology
medicine
Animals
chemistry.chemical_classification
Regulation of gene expression
Reactive oxygen species
biology
Dengue Virus
Catalase
medicine.disease
Oxidative Stress
030104 developmental biology
Gene Expression Regulation
chemistry
Gene Knockdown Techniques
biology.protein
Insect Proteins
Tumor Suppressor Protein p53
Reactive Oxygen Species
Oxidative stress
Subjects
Details
- ISSN :
- 00426822
- Volume :
- 519
- Database :
- OpenAIRE
- Journal :
- Virology
- Accession number :
- edsair.doi.dedup.....f1807e903818d0d5841a7d0184b3f3bc
- Full Text :
- https://doi.org/10.1016/j.virol.2018.04.011