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Vimentin modulates infectious porcine circovirus type 2 in PK-15 cells

Porcine circovirus type 2 (PCV2) is the pathogen that causes postweaning multisystemic wasting syndrome, which leads to significant economic losses for swine farms worldwide. However, the infection mechanism of PCV2 is not completely understood yet. Vimentin is a part of the cytoskeleton network and...

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Detalles Bibliográficos
Autores principales: Wang, Zhi-Jian, Xu, Chang-Meng, Song, Zhong-bao, Wang, Mi, Liu, Qian-Yu, Jiang, Ping, Li, Yu-feng, Bai, Juan, Wang, Xian-Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier B.V. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7114564/
https://www.ncbi.nlm.nih.gov/pubmed/29079448
http://dx.doi.org/10.1016/j.virusres.2017.10.013
Descripción
Sumario:Porcine circovirus type 2 (PCV2) is the pathogen that causes postweaning multisystemic wasting syndrome, which leads to significant economic losses for swine farms worldwide. However, the infection mechanism of PCV2 is not completely understood yet. Vimentin is a part of the cytoskeleton network and plays an important role in several virus infections. It is not clear whether vimentin has a role in PCV2 infection nor how it affects PCV2 infection. In this study, the function of vimentin in PK-15 cells infected with PCV2 has been elucidated. We found that vimentin had a restrictive effect on the replication of PCV2 in PK-15 cells. Overexpression of vimentin by transferred pCAGGS-vimentin and down-regulation by the respective scrambled small interfering RNA showed that vimentin restricted the replication and virion production of PCV2. A special interaction between vimentin and PCV2 Cap protein was observed using laser confocal microscopy and immunoprecipitation assay. Moreover, overexpression of vimentin could decrease NF-κB activity and increase PCV2-induced caspase-3 activity in PK-15 cells. These data suggest that vimentin is involved in the replication of PCV2 and has a restrictive effect on it, which is helpful in the study of the replication mechanism of PCV2.