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Identification of Differentially Expressed Genes in Ducks in Response to Avian Influenza A Virus Infections

机译:鉴定鸭子中差异表达基因的抗病患者感染禽流感

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Avian influenza (AI) viruses are highly contagious viruses that infect many bird species and are zoonotic. Ducks are resistant to the deadly and highly pathogenic avian influenza virus (HPAIV) and remain asymptomatic to the low pathogenic avian influenza virus (LPAIV). In this study, we identified common differentially expressed genes (DEGs) after a reanalysis of previous transcriptomic data for the HPAIV and LPAIV infected duck lung cells. Microarray datasets from a previous study were reanalyzed toidentify common target genes from DEGs and their biological functions. A total of 731 and 439 DEGs were identified in HPAIV- and LPAIV-infected duck lung cells, respectively. Of these, 227 genes were common to cells infected with both viruses, in which193 genes were upregulated and 34 genes were downregulated. Functional annotation of common DEGs revealed that translation related gene ontology (GO) terms were enriched, including ribosome, protein metabolism, and gene expression. REACTOME analyses alsoidentified pathways for protein and RNA metabolism as well as for tissue repair, including collagen biosynthesis and modification, suggesting that AIVs may evade the host defense system by suppressing host translation machinery or may be suppressed before being exported to the cytosol for translation. AIV infection also increased collagen synthesis, showing that tissue lesions by virus infection may be mediated by this pathway. Further studies should focus on these genes to clarify their roles in AIV pathogenesis and their possible use in AIV therapeutics.
机译:禽流感(ai)病毒是一种感染许多鸟类的高度传染性病毒,并且是人畜共患病毒。鸭子对致命和高度致病的禽流感病毒(HPAIV)有抵抗力,并且对低致病性禽流感病毒(LPAIV)保持无症状。在这项研究中,我们在HPAIV和LPAIV感染鸭肺细胞的先前转录组数据的再分析后鉴定了常见的差异表达基因(DEGS)。来自先前研究的微阵列数据集重新达到了来自DEG的常见目标基因及其生物学功能。分别在HPAIV和LPAIV感染鸭肺细胞中鉴定了总共731和439次。其中,227个基因对两个病毒感染的细胞常见,其中将上调193个基因,下调34个基因。常见的常见次数的功能注释揭示了翻译相关基因本体(GO)术语富集,包括核糖体,蛋白质代谢和基因表达。反应分析了蛋白质和RNA代谢以及组织修复以及包括胶原蛋白生物合成和修饰的组织修复,表明AIV可以通过抑制宿主转移机械来避免主导系统,或者可以在出口到翻译之前抑制。 AIV感染还增加了胶原蛋白合成,表明病毒感染的组织病变可以通过该途径介导。进一步的研究应关注这些基因,以澄清其在AIV发病机制中的作用及其在AIV治疗中的可能使用。

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