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首页> 外文期刊>Microbial Pathogenesis >Duckling short beak and dwarfism syndrome virus infection activates host innate immune response involving both DNA and RNA sensors
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Duckling short beak and dwarfism syndrome virus infection activates host innate immune response involving both DNA and RNA sensors

机译：Duckling Short Beak和Dwarfism综合征病毒感染激活涉及DNA和RNA传感器的主体先天免疫应答

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Duckling short beak and dwarfism syndrome virus (SBDSV), a newly identified goose parvovirus, causes devastating disease in domestic waterfowl and considerable economic losses to Chinese waterfowl industry. The molecular pathogenesis of SBDSV infection, nature and dynamics of host immune responses against SBDSV infection remained elusive. In this study, we systematically explored the relative mRNA expression profiles of major innate immune-related genes in SBDSV infected duck embryo fibroblasts. We found that SBDSV infection effectively activated host innate immune responses and resulted in significant up-regulation of IFN-beta and several vital IFN-stimulated genes (ISGs). These up-regulation responses were mainly attributed to viral genomic DNA and dsRNA replication intermediates. Importantly, the expression of cGAS was significantly induced, whereas the expression of other DNA receptors including DDX41, STING, ZBP1, LSM14A and LRRFIP1 have no significant change. Furthermore, SBDSV infection also activates the up-regulation of TLR3 and inhibited the expression of TLR2 and TLR4; however, no effect was observed on the expression of TLR1, TLR5, TLR7, TLR15 and TLR21. Intriguingly, SBDSV infection significantly up-regulated the expression of RNA sensors such as MDA5 and LGP2, and resulted in a delayed but significant up-regulation of RIG-I gene. Taken together, these data indicate that host multiple sensors including DNA sensor (cGAS) and RNA sensors (TLR3, MDA5 and LGP2) are involved in recognizing a variety of different pathogen associated molecular patterns (PAMPs) including viral genomic ssDNA and dsRNA replication intermediates, which trigger an effective antiviral innate immune response.
机译：鸭绒短喙和矮化综合征病毒（SBDSV）是一种新发现的鹅剖视血症，导致国内水禽的毁灭性疾病，对中国水禽行业的相当大的经济损失。对SBDSV感染的宿主免疫应答的SBDSV感染，性质和动态的分子发病机制仍然难以捉摸。在这项研究中，我们系统地探讨了SBDSV感染鸭胚成纤维细胞中主要先天免疫相关基因的相对mRNA表达谱。我们发现SBDSV感染有效地激活了主体先天免疫应答，并导致IFN-β和几个重要的IFN刺激基因（ISGS）的显着上调。这些上调响应主要归因于病毒基因组DNA和DSRNA复制中间体。重要的是，CGA的表达显着诱导，而其他DNA受体的表达，其中包括DDX41，STING，ZBP1，LSM14A和LRRFIP1的表达无明显变化。此外，SBDSV感染还激活TLR3的上调并抑制TLR2和TLR4的表达;然而，在TLR1，TLR5，TLR7，TLR15和TLR21的表达上没有观察到效果。有趣的，SBDSV感染显着上调RNA传感器如MDA5和LGP2的表达，并导致钻机I基因的延迟但显着上调。总之，这些数据表明，宿主多个传感器包括DNA传感器（CGA）和RNA传感器（TLR3，MDA5和LGP2）涉及识别各种不同的病原体相关分子模式（PAMP），包括病毒基因组SSDNA和DSRNA复制中间体。这引发了有效的抗病毒天生的免疫反应。

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