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. 2018 Apr 24;11(3):743–754. doi: 10.1016/j.tranon.2018.03.013

Figure 1.

Figure 1

Reciprocal interactions of PML and HBsAg is closely associated with metabolic reprogramming in a chronic HBV mouse model. (A) Representative double-stained images of PML and HBsAg in liver-specific HBsAg-transgenic mice (HBsAgtg/0) at different ages. Note that correlation of the evolving pathology in mice with reciprocal interactions between PML and HBsAg recapitulates the chronic human HBV-infected liver pathogenesis observed in Figure 1C. (B) Comparison of proteomic profiling between young and aged HBsAgtg/0 mice. The enriched genes, whose expression was 2-fold up-regulated or down-regulated in more than 50% of the genetically engineered mice (n = 10 for each genotype) compared to the average expression of the same genes in sex- and age-matched wild-type mice (n = 5 for each group), were categorized by gene ontology (GO) analysis. Note that the major GO pathways affected in young mice with HBsAg-dominant expression and older mice with PML-dominant expression are involved in immune response and energy metabolism, respectively.