Understanding how Type 2 diabetes mellitus increases susceptibility to intracellular pathogens

Project Overview

Research Background

People with diabetes have an increased risk of infection and / or worse clinical outcomes from a number of global intracellular pathogens including Mycobacterium tuberculosis, Burkholderia pseudomallei (the Gram-negative bacterial cause of melioidosis) and Hepatitis B.  77% of people with diabetes now live in low and middle-income countries, and the understanding the collision of this non-communicable disease with major global outbreak pathogens is an international public health priority. Defining biomarkers and the mechanisms behind this increased susceptibility is essential to allow development of new effective vaccines and therapeutics for this at-risk population.

Project objectives

This project will seek to define biomarkers of susceptibility and outcomes of infection in diabetes. An extensive biobank of samples from people with and without diabetes, during infection and in health is available, and there will be the opportunity to develop new experimental models to evaluate the mechanism behind the susceptibility. Experiments will be carried out in the University of Oxford laboratories, with potential to spend time at the Mahidol-Oxford Tropical Medicine Research Unit (MORU) in Bangkok, Thailand.

Training Opportunities

Through this project the student will:

host response to infection, including flow cytometry, chip cytometry, cell metabolism studies and host transcriptomics


Immunology & Infectious Disease and Tropical Medicine & Global Health


Project reference number: 964

Funding and admissions information


Name Department Institution Country Email
Professor Susanna J Dunachie FRCP FRCPath Tropical Medicine Oxford University, Peter Medawar Building GBR susie.dunachie@ndm.ox.ac.uk
Professor Paul Klenerman Experimental Medicine Division Oxford University, Peter Medawar Building GBR paul.klenerman@medawar.ox.ac.uk

There are no publications listed for this DPhil project.