作　　者： (高琦）; (李海）; (闻晓波）; (刘胜旺）; (冉旭华）;

机构地区： 黑龙江八一农垦大学动物科技学院,黑龙江大庆163319 中国农业科学院哈尔滨兽医研究所兽医生物技术国家重点实验室／禽呼吸道传染病创新团队,黑龙江哈尔滨150069

出　　处： 《中国预防兽医学报》 2017年第8期605-610,共6页

摘　　要： 为探索SU6656对鸡传染性喉气管炎病毒(ILTV)感染的影响及调控机制,本研究应用鸡LMH细胞系感染ILTV LJS09株作为实验模型,测定了SU6656对ILTV增殖和毒力的影响,通过高通量RNA测序技术(RNA-Seq)在全基因组范围内检测宿主细胞基因转录谱表达,并利用荧光定量PCR对部分差异表达基因进行验证。进一步的GO功能分析显示,在宿主细胞应答ILTV感染过程中,SU6656所调控基因主要涉及氢离子跨膜运输、辅酶Q的结合、Fe^(2+)和S^(2+)聚集等功能。KEGG通路分析表明,氧化磷酸化通路在SU6656调控ILTV感染的过程中可能发挥重要作用。本研究为进一步解析ILTV感染及致病机制提供了重要依据。 Our functional studies using FITC-Annexin V/PI staining and ILTV-specific RT-qPCR revealed that SU6656 could promot ILTV virulence and repress ILTV replication significantly in LMH cells.To explore the regulation mechanisms to ILTVhost by SU6656,genome-wide transcription profiles of LMH cells infected with ILTV was detected using RNA sequencing technology（RNA-seq）.Gene Ontology analysis of the genome-wide transcriptional expression data identified hydrogen ion transmembrane transporter activity,ubiquinone binding and Fe2＋/S2＋ clustering as the main cellular processes and functions altered by SU6656 during ILTV infection.Further KEGG pathway analysis indicated oxidative phosphorylation pathway was a key molecular event in the regulation of ILTV-host interaction by SU6656.Our present study provided fundamental data for further illustration of the molecular mechanisms of ILTV-host interaction.

关 键 词： 传染性喉气管炎病毒 病毒与宿主互作