“…The previous study primarily focused on the correlations between APOH and HBV infection and elucidated that HBV and its large surface antigen directly upregulates APOH expression, which inhibits HBsAg secretion and induces hepatocyte ER stress [ 7 , 8 ]. Further studies clarified that ApoH gene knockout mouse appears spontaneous steatohepatitis and APOH deficiency disrupted hepatic lipid metabolism and gut microbiota homeostasis [ 9 , 10 ]. Based on these complied results, APOH might be a hinge point in fatty liver disease incidence and progression during chronic HBV infection and we focus on this direction in the present study.…”