Fig. 1: Human lncRNA AVAN is identified to participated in controlling IAV infection. | Cell Death & Differentiation

Fig. 1: Human lncRNA AVAN is identified to participated in controlling IAV infection.

From: Long noncoding RNA AVAN promotes antiviral innate immunity by interacting with TRIM25 and enhancing the transcription of FOXO3a

Fig. 1

A Cluster heat map showing differentially expressed lncRNAs in IAV-infected patient neutrophils compared with recovery-stage samples based on RNA-seq data (FC > 2; p < 0.05). B Cluster heat map showing 26 lncRNA candidates selected via in silico analysis from the RNA-seq data (FC > 2; p < 0.05). The expression of 26 lncRNA candidates in neutrophils (C) from healthy volunteers and A549 (D) stimulated with BJ501 (MOI = 0.5) or mock for 12 h by qRT-PCR analysis (n = 3; means ± SEM; *p < 0.05; **p < 0.01; ***p < 0.001). E, F GSEA analysis of AVAN related gene coexpression networks from the sequencing data. G AVAN upregulation in IAV-H7N9-infected patient (n = 3; means ± SEM; **p < 0.01). H AVAN expression in IAV-infected patient neutrophils by qRT-PCR analysis (healthy controls = 18; patients = 63; *p < 0.05). The efficiency of AVAN overexpression (I) or knockdown (K) was determined by qRT-PCR in BJ501-uninfected or -infected A549 cells (n = 3; means ± SEM; **p < 0.01; ***p < 0.001). BJ501 replication in AVAN-overexpression (J) and AVAN-knockdown (L) A549 cells examined by the TCID50 assay (MOI = 1). The virus titers in supernatants were measured at 24 h post infection (n = 3; means ± SEM; **p < 0.01; ***p < 0.001).

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