Cellular Chaperonin CCTγ Contributes to Rabies Virus Replication during Infection
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- Jinyang Zhang
- Key Laboratory of Animal Virology of Ministry of Agriculture, Zhejiang University, Hangzhou, People's Republic of China
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- Xiaopeng Wu
- Key Laboratory of Animal Virology of Ministry of Agriculture, Zhejiang University, Hangzhou, People's Republic of China
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- Jie Zan
- Key Laboratory of Animal Virology of Ministry of Agriculture, Zhejiang University, Hangzhou, People's Republic of China
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- Yongping Wu
- Key Laboratory of Animal Virology of Ministry of Agriculture, Zhejiang University, Hangzhou, People's Republic of China
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- Chengjin Ye
- Key Laboratory of Animal Virology of Ministry of Agriculture, Zhejiang University, Hangzhou, People's Republic of China
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- Xizhen Ruan
- Key Laboratory of Animal Virology of Ministry of Agriculture, Zhejiang University, Hangzhou, People's Republic of China
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- Jiyong Zhou
- Key Laboratory of Animal Virology of Ministry of Agriculture, Zhejiang University, Hangzhou, People's Republic of China
説明
<jats:title>ABSTRACT</jats:title> <jats:p>Rabies, as the oldest known infectious disease, remains a serious threat to public health worldwide. The eukaryotic cytosolic chaperonin TRiC/CCT complex facilitates the folding of proteins through ATP hydrolysis. Here, we investigated the expression, cellular localization, and function of neuronal CCTγ during neurotropic rabies virus (RABV) infection using mouse N2a cells as a model. Following RABV infection, 24 altered proteins were identified by using two-dimensional electrophoresis and mass spectrometry, including 20 upregulated proteins and 4 downregulated proteins. In mouse N2a cells infected with RABV or cotransfected with RABV genes encoding nucleoprotein (N) and phosphoprotein (P), confocal microscopy demonstrated that upregulated cellular CCTγ was colocalized with viral proteins N and P, which formed a hollow cricoid inclusion within the region around the nucleus. These inclusions, which correspond to Negri bodies (NBs), did not form in mouse N2a cells only expressing the viral protein N or P. Knockdown of CCTγ by lentivirus-mediated RNA interference led to significant inhibition of RABV replication. These results demonstrate that the complex consisting of viral proteins N and P recruits CCTγ to NBs and identify the chaperonin CCTγ as a host factor that facilitates intracellular RABV replication. This work illustrates how viruses can utilize cellular chaperonins and compartmentalization for their own benefit.</jats:p>
収録刊行物
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- Journal of Virology
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Journal of Virology 87 (13), 7608-7621, 2013-07
American Society for Microbiology