| Literature DB >> 26093497 |
Yang Mu1, Liangliang Li2, Beibei Zhang3, Baicheng Huang4, Jiming Gao5, Xiangpeng Wang6, Chengbao Wang7, Shuqi Xiao8, Qin Zhao9, Yani Sun10, Gaiping Zhang11, Julian A Hiscox12, En-Min Zhou13.
Abstract
Cell apoptosis is common after infection with porcine reproductive and respiratory syndrome virus (PRRSV). PRRSV GP5 has been reported to induce cell apoptosis. To further understand the role of GP5 in PRRSV induced cell apoptosis, we established Marc-145 cell lines stably expressing full-length GP5, GP5(Δ84-96) (aa 84-96 deletion), and GP5(Δ97-119) (aa 97-119 deletion). Cell proliferation, cell cycle progression, cell apoptosis and virus replication in these cell lines were evaluated. Neither truncated nor full-length GP5 induced cell apoptosis in Marc-145 cells. However, GP5(Δ97-119), but not full-length or GP5(Δ84-96), induced a cell cycle arrest at the G2/M phase resulting in a reduction in the growth of Marc-145 cells. Additionally, GP5(Δ84-96) inhibited the replication of PRRSV in Marc-145 cells through induction of IFN-β. These findings suggest that PRRSV GP5 is not responsible for inducing cell apoptosis in Marc-145 cells under these experimental conditions; however it has other important roles in virus/host cell biology.Entities:
Keywords: Cell apoptosis; GP5; IFN; PRRSV; Virus replication
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Year: 2015 PMID: 26093497 DOI: 10.1016/j.virol.2015.05.019
Source DB: PubMed Journal: Virology ISSN: 0042-6822 Impact factor: 3.616