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目的:运用生物信息学方法探讨甲型流感病毒所致肺损伤的可能机制。方法:从Gene Expression Ominbus（GEO）数据库中选择基因表达谱GSE57455、GSE63786和GSE64800，通过GEO2R工具在线分析，筛选出差异表达基因（DEGs），基于STRING构建蛋白互作网络图，筛选出显著模块；并对获取的DEGs进行Gene Ontology（GO）分析和Kyoto Encyclopedia of Genes and Genomes（KEGG）通路富集分析。通过Cystoscape软件筛选出具有高度连接性的关键基因，并构建生物学功能图。结果:筛选得到119个交集DEGs，其中上调基因有106个，下调基因13个。GO分析显示，DEGs显著富集于免疫应答、细胞分裂等生物学过程中；显著富集于细胞外间隙、胞外区部分等细胞组成上；显著富集于趋化因子活性、细胞因子受体结合等分子功能上。KEGG通路富集显示，DEGs显著富集于细胞因子及受体相互作用信号通路、趋化因子等信号通路。同时，共筛选得到7个关键基因：FIGNL1、GBP5、ICOS、ARG1、IRF7、CYSLTR1和SLMAF8，其富集作用主要在免疫应答、精氨酸代谢、B细胞反应等生物学功能。结论:FIGNL1介导的肺组织细胞受损、IRF7和GBP5介导的Ⅰ型IFN反应、ARG1介导的精氨酸代谢以及ICOS、CYSLTR1和SLAMF8介导的趋化因子和炎性因子的活化与甲型流感病毒所导致的肺损伤密切相关。“,”Objective:To explore the possible mechanism of lung injury caused by influenza A virus through bioinformatics.Methods:The gene expression profiles GSE57455, GSE63786, and GSE64800 were selected from the Gene Expression Ominbus (GEO) database, and differentially expressed genes (DEGs) were screened out through the GEO2R tool. A protein interaction network map was constructed based on STRING, and significant modules were screened out. The obtained DEGs were performed by Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The highly connected key genes were screened out by Cystoscape software to construct the biological function map.Results:A total of 119 intersection DEGs were selected, of which 106 genes were up-regulated and 13 genes were down-regulated. GO analysis showed that DEGs significantly enriched in biological processes such as immune response and cell division; significantly enriched in extracellular space, extracellular region, and other cell components; significantly enriched in chemokine activity, cytokine receptor binding and other molecular functions. KEGG pathway enrichment showed that DEGs significantly enriched in signal pathways such as cytokines and receptor interaction signal pathways, chemokines. At the same time, 7 key genes were screened including FIGNL1, GBP5, ICOS, ARG1, IRF7, CYSLTR1 and SLMAF8, which enriched in biological functions such as immune response, arginine metabolism, and B cell response.Conclusions:FIGNL1-mediated lung tissue damage, IRF7 and GBP5-mediated type Ⅰ interferon response, ARG1-mediated arginine metabolism, and activation of chemokines and inflammatory factors mediated by ICOS, CYSLTR1 and SLAMF8 are closely related with lung injury caused by influenza A virus.