Abstract
Many viruses exploit the host cell division cycle to favour their own growth. Here we demonstrated that porcine circovirus type 2 (PCV2), which is a major causative agent of an emerging and important swine disease complex, PCV2-associated diseases, caused G0/G1 cell cycle arrest through degradation of cyclin D1 and E followed by reduction of retinoblastoma phosphorylation in synchronized PCV2-infected cells dependent upon virus replication. This induction of G0/G1 cell cycle arrest promoted PCV2 replication as evidenced by increased viral protein expression and progeny virus production in the synchronized PCV2-infected cells. To delineate a mechanism of miRNAs in regulating PCV2-induced G0/G1 cell cycle arrest, we determined expression levels of some relevant miRNAs and found that only miR-15a but not miR-16, miR-21, and miR-34a was significantly changed in the PCV2-infected cells. We further demonstrated that upregulation of miR-15a promoted PCV2-induced G0/G1 cell cycle arrest via mediating cyclins D1 and E degradation, in which involves PCV2 growth. These results reveal that G0/G1 cell cycle arrest induced by PCV2 may provide favourable conditions for viral protein expression and progeny production and that miR-15a is implicated in PCV2-induced cell cycle control, thereby contributing to efficient viral replication.
Highlights
Porcine circovirus type 2 (PCV2), a genus Circovirus of the family Circoviridae[1], has been shown to associate with a variety of clinical disorders, including postweaning multisystemic wasting syndrome (PMWS)[2,3], porcine dermatitis and nephropathy syndrome, reproductive failure, necrotizing tracheitis, congenital tremors as well as fetal myocarditis[4,5,6,7]
Increasing research evidence indicates that porcine circovirus type 2 (PCV2) infection regulates many host cellular signals and pathways, such as nuclear transcription factor kappa B (NF-κB)[15], extracellular signal-regulated kinase[16], c-Jun NH2-terminal kinases (JNK1/2) and p38 mitogen-activated protein kinase (MAPK)[17], and phosphatidylinositol 3-kinase (PI3K)/Akt[18], which contributed to PCV2 replication and PCV2-mediated apoptotic responses
We examined whether PCV2 infection affects the cell cycle progression and found that PCV2 replication induces cell cycle arrest in G0/G1 phase, which facilitates to producing favourable conditions for viral protein expression and virus production
Summary
Porcine circovirus type 2 (PCV2), a genus Circovirus of the family Circoviridae[1], has been shown to associate with a variety of clinical disorders, including postweaning multisystemic wasting syndrome (PMWS)[2,3], porcine dermatitis and nephropathy syndrome, reproductive failure, necrotizing tracheitis, congenital tremors as well as fetal myocarditis[4,5,6,7]. We examined whether PCV2 infection affects the cell cycle progression and found that PCV2 replication induces cell cycle arrest in G0/G1 phase, which facilitates to producing favourable conditions for viral protein expression and virus production.
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