Global death rates from chronic liver diseases (CLD) continue to rise, highlighting the need for a better understanding of pathogenic mechanisms to inform the development of novel therapies. However, CLD development and evolution is a highly complex process, involving multiple interacting hepatic cell types. The field has therefore often relied on in vivo rodent models to study disease pathogenesis. Whilst potentially useful for studying certain aspects of pathophysiology, these models lack the chronicity and complexity of human disease and do not incorporate human-specific factors such as genetics and metabolism.

Global death rates from chronic liver diseases (CLD) continue to rise, highlighting the need for a better understanding of pathogenic mechanisms to inform the development of novel therapies. However, CLD development and evolution is a highly complex process, involving multiple interacting hepatic cell types. The field has therefore often relied on in vivo rodent models to study disease pathogenesis. Whilst potentially useful for studying certain aspects of pathophysiology, these models lack the chronicity and complexity of human disease and do not incorporate human-specific factors such as genetics and metabolism.

Monitoring and retention in care remain suboptimal for patients diagnosed with chronic hepatitis B (CHB) infection with only a minority receiving cons...