SU6656对鸡传染性喉气管炎病毒与宿主细胞互作分子网络的影响

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、Fe2+和S2+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 ILTV-host 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.