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Viral Tracing of Genetically Defined Neural Circuitry
Published on: October 17, 2012
Cellular chaperonin CCTγ contributes to rabies virus replication during infection
Jinyang Zhang1, Xiaopeng Wu, Jie Zan
1Key Laboratory of Animal Virology of Ministry of Agriculture, Zhejiang University, Hangzhou, People's Republic of China.
Journal of Virology
|May 3, 2013
Summary
Rabies virus utilizes the host chaperonin CCTγ to aid its replication. Inhibiting CCTγ significantly reduces rabies virus propagation, highlighting it as a potential therapeutic target.
Area of Science:
- Virology
- Molecular Biology
- Cellular Biology
Background:
- Rabies virus (RABV) poses a significant global health threat.
- The TRiC/CCT complex, a eukaryotic chaperonin, is crucial for protein folding.
- Understanding host-pathogen interactions is key to controlling viral infections.
Purpose of the Study:
- To investigate the role of neuronal CCTγ in neurotropic rabies virus (RABV) infection.
- To identify host factors involved in RABV replication.
- To explore the interaction between CCTγ and RABV proteins.
Main Methods:
- Utilized mouse N2a cells as a model system.
- Employed two-dimensional electrophoresis and mass spectrometry to identify altered proteins.
- Used confocal microscopy to visualize protein localization.
- Performed lentivirus-mediated RNA interference for gene knockdown.
Main Results:
- RABV infection altered 24 proteins, with 20 upregulated and 4 downregulated.
- Upregulated CCTγ colocalized with RABV nucleoprotein (N) and phosphoprotein (P) in Negri bodies (NBs).
- Knockdown of CCTγ significantly inhibited RABV replication.
Conclusions:
- Viral proteins N and P recruit CCTγ to NBs during RABV infection.
- Chaperonin CCTγ is a host factor essential for intracellular RABV replication.
- Viruses can exploit cellular chaperonins and compartmentalization for replication.
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