State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, 430070, Hubei, China; Laboratory of Animal Virology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, 430070, Hubei, China; Laboratory of Animal Virology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China; Key Laboratory of Development of Veterinary Diagnostic Products, Ministry of Agriculture, Wuhan, 430070, China.
Vet Microbiol. 2018 Feb;214:65-74. doi: 10.1016/j.vetmic.2017.12.007. Epub 2017 Dec 8.
Fowl adenovirus serotype 4 (FAdV-4), a member of the Aviadenovirus genus of the Adenoviridae family, causes hepatitis-hydropericardium syndrome (HHS) in chickens. It causes mortality of up to 80% in 3-6-week-old broilers, posing a substantial threat to the poultry industry. However, the specific host responses to the virus are not well understood. To better understand the interactions between the host and FAdV-4 and to explore the pathogenesis of this virus, a high-throughput RNA-seq technology was utilized with leghorn male hepatocellular (LMH) cells at 12, 24, and 48 h after FAdV-4 infection. We identified a total of 7000 differentially expressed genes (DEGs), which were enriched in a variety of biological processes and pathways using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Several immune related pathways, including Toll-like receptor (TLR) signaling pathway and cytokine-cytokine receptor interaction pathway, were activated after the FAdV-4 infection. The transcriptional data were validated by quantitative real-time PCR. The expression profiles of 10 genes involved in FAdV-4-infected chicken livers, including TLR2A, TLR3, TLR5, MyD88, IL12B, IL15, IL18, CCL20, TNFRSF21, and CD30, were consistent with RNA-seq profiles. By transfecting small interfering RNA into LMH cells, our results confirmed that MyD88 mediated FAdV-4-induced inflammation. To our knowledge, this was the first study to use transcriptome analysis to investigate host responses to FAdV-4 infection. These findings provide insights into the mechanisms of FAdV-4 pathogenesis and host-FAdV-4 interaction.
禽腺病毒血清型 4（FAdV-4）是腺病毒科禽腺病毒属的一员，可引起鸡的肝炎-心包积水综合征（HHS）。它可导致 3-6 周龄肉鸡的死亡率高达 80%，对家禽业构成了重大威胁。然而，宿主对病毒的具体反应尚不清楚。为了更好地了解宿主与 FAdV-4 的相互作用，并探索该病毒的发病机制，我们利用高通量 RNA-seq 技术，在 FAdV-4 感染后 12、24 和 48 小时，对来亨雄性肝细胞（LMH）细胞进行了研究。我们共鉴定了 7000 个差异表达基因（DEGs），通过基因本体论（GO）和京都基因与基因组百科全书（KEGG）通路富集分析，这些基因富集在多种生物学过程和通路中。在 FAdV-4 感染后，一些免疫相关通路被激活，包括 Toll 样受体（TLR）信号通路和细胞因子-细胞因子受体相互作用通路。通过定量实时 PCR 验证了转录数据。参与 FAdV-4 感染鸡肝脏的 10 个基因（TLR2A、TLR3、TLR5、MyD88、IL12B、IL15、IL18、CCL20、TNFRSF21 和 CD30）的表达谱与 RNA-seq 谱一致。通过转染小干扰 RNA 进入 LMH 细胞，我们的结果证实了 MyD88 介导了 FAdV-4 诱导的炎症。据我们所知，这是首次使用转录组分析来研究宿主对 FAdV-4 感染的反应。这些发现为 FAdV-4 发病机制和宿主-FAdV-4 相互作用的机制提供了新的见解。
