Insulin Resistance Rewires Hepatocyte Antiviral Pathways and Hepatitits B virus HBV Replication Mechanistic Insights Into a Major East London Health Inequality

Chronic hepatitis B (CHB) is a viral infection that affects many people in East London, particularly those from Bangladeshi, Pakistani, Chinese, African and Middle Eastern communities. These same communities are more likely to experience metabolic health problems such as insulin resistance and fatty liver disease. When hepatitis B and metabolic disease occur together, people develop more severe liver damage, but we do not yet understand why.

This project aims to understand how insulin resistance, a condition where the body becomes less responsive to insulin and the liver comes under extra metabolic stress, changes the way liver cells defend themselves against hepatitis B. Liver cells normally have built‑in antiviral systems that help control the virus, but these systems may not work properly when cells are stressed by fat and altered metabolism.

Using laboratory models of human liver cells, the student will study how insulin resistance affects antiviral defences and how this influences hepatitis B replication. The student will also examine whether stressed liver cells release signals that change how immune cells respond to the virus. Existing liver research datasets will be analysed to link laboratory findings to patient biology.

The student will be supported by a strong supervisory team: Dr Upkar Gill (hepatitis B/antiviral immunity), Professor William Alazawi (metabolic liver disease), and Professor Clare Jolly (virus–cell interactions and immune responses).

Understanding how metabolic health affects hepatitis B could lead to better ways to identify high‑risk patients and develop more personalised treatments for the communities most affected in East London.

Aims:

Work Package 1 (WP1): IR and hepatocyte antiviral signalling

Work Package 2 (WP2): Impact of IR on HBV replication

Work Package 3 (WP3): Hepatocyte–immune crosstalk under metabolic stress

Work Package 4 (WP4): Integration with single‑cell human datasets