Transcriptome analysis reveals the host response to Schmallenberg virus in bovine cells and antagonistic effects of the NSs protein.
Transcriptome analysis reveals the host response to Schmallenberg virus in bovine cells and antagonistic effects of the NSs protein.
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DOI：
10.1186/s12864-015-1538-9
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发表时间：
2015-04-19
期刊：
影响因子：
4.4
通讯作者：
Kohl A
中科院分区：
文献类型：
--
作者：
Blomström AL;Gu Q;Barry G;Wilkie G;Skelton JK;Baird M;McFarlane M;Schnettler E;Elliott RM;Palmarini M;Kohl A
施马伦贝格病毒（Schmallenberg virus，SBV）是布尼亚病毒科（Bunyaviridae）正布尼亚病毒属（Orthobunyavirus）的成员，其引起反刍动物的畸形和流产。虽然，对于该科/属的其他成员，非结构蛋白NS已被证明是干扰素拮抗剂，但关于正布尼亚病毒NS蛋白在感染期间对宿主基因表达的总体抑制作用和靶点知之甚少。因此，使用RNA-seq，本研究描述了用施马伦贝格病毒（SBV）或用缺乏非结构蛋白NS的突变体（SBVdelNS）感染后原代牛细胞的转录组的变化，提供了NS表达对宿主细胞的影响的详细比较。来自所有样品（未感染的细胞、SBV和SBVdelNS）的序列读段与牛宿主参考基因组良好组装（平均87.43%的读段）。在用SBVdelNS感染期间，与未感染的细胞相比，649个基因差异表达（78.7%上调），其中许多是已知的抗病毒和IFN刺激的基因。另一方面，与未感染的对照细胞相比，只有9个基因在SBV感染的细胞中差异表达，证明NS对细胞基因表达的强烈抑制作用。然而，在SBV感染期间表达的大多数基因参与限制病毒复制和传播，表明SBV不能完全关闭宿主的抗病毒应答。在这项研究中，我们显示了SBV NS对感染细胞的转录组以及对野生型SBV的细胞应答的影响。虽然NS在关闭宿主先天反应的基因方面非常有效，但已鉴定出许多可能的抗病毒因子。因此，从这项研究的数据可以作为更详细的机制研究SBV和其他正布尼亚病毒的基础。
Schmallenberg virus (SBV) is a member of the Orthobunyavirus genus (Bunyaviridae family) causing malformations and abortions in ruminants. Although, as for other members of this family/genus, the non-structural protein NSs has been shown to be an interferon antagonist, very little is known regarding the overall inhibitory effects and targets of orthobunyavirus NSs proteins on host gene expression during infection. Therefore, using RNA-seq this study describes changes to the transcriptome of primary bovine cells following infection with Schmallenberg virus (SBV) or with a mutant lacking the non-structural protein NSs (SBVdelNSs) providing a detailed comparison of the effect of NSs expression on the host cell. The sequence reads from all samples (uninfected cells, SBV and SBVdelNSs) assembled well to the bovine host reference genome (on average 87.43% of the reads). During infection with SBVdelNSs, 649 genes were differentially expressed compared to uninfected cells (78.7% upregulated) and many of these were known antiviral and IFN-stimulated genes. On the other hand, only nine genes were differentially expressed in SBV infected cells compared to uninfected control cells, demonstrating the strong inhibitory effect of NSs on cellular gene expression. However, the majority of the genes that were expressed during SBV infection are involved in restriction of viral replication and spread indicating that SBV does not completely manage to shutdown the host antiviral response. In this study we show the effects of SBV NSs on the transcriptome of infected cells as well as the cellular response to wild type SBV. Although NSs is very efficient in shutting down genes of the host innate response, a number of possible antiviral factors were identified. Thus the data from this study can serve as a base for more detailed mechanistic studies of SBV and other orthobunyaviruses.
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