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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: HBV-driven host chromatin accessibility changes affect liver metabolic pathways, iron homeostasis and promote a preneoplastic phenotype

Fig. 8

The transcriptional signature of HBV-infection in vitro persists in CHB patients. a) Venn diagram of the 208 genes differentially expressed in the RNA-seq from CHB patients [32] and co-regulated in ATAC-seq/RNA-seq from HBV-infected PHHs. Most of the genes differentially expressed in HBe pos and HBe neg chronic hepatitis (CH) vs non-HBV infected healthy livers (HL) and HBV inactive carriers (IC; e.g., HBe neg chronic infection (CI)) vs HL shows that most DEGs are shared (n = 167), 24 DEGs unique to HBe pos and HBe neg CH groups and 17 DEGs exclusive of the HBe neg CI patients. b) Upper panel: Heatmap of the 191 ATAC-seq/RNA-seq co-regulated genes that are differentially expressed in CH patients (HBe pos and HBe neg CH; purple) vs non-HBV infected healthy livers (HL, dark yellow). Lower Panel: Heatmap of the 184 ATAC-Seq/RNA- seq co-regulated genes that are differentially expressed in HBV inactive carriers (IC; e.g., HBe neg chronic infection (CI); light purple) vs non-HBV infected healthy livers (HL, dark yellow). Normalized counts are represented with a color scale from blue (negative) to red (positive). c) KEGG pathways (Release 86.1; yellow bars) and HALLMARK MSigDB modules significantly enriched from the 191 genes differentially expressed in CH vs HL (full bars) and the 184 genes differentially expressed in IC vs HL (striped bars) (ShinyGO 0.76 tool) and sorted by–Log (FDR) values. Fold enrichment ranks the relative number of genes included in each enriched pathway (see Tables S12 and S13)

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