Viral infections including HIV and SARS-CoV-2 are known to increase the risk of certain chronic diseases including cardiovascular disease (CVD). People with HIV have twice the risk of developing CVD than the general population despite effective anti-viral therapy, and CVD is now one of the greatest causes of disease and death in this population.
How viral infections such as HIV increase the risk of CVD is not fully understood but may be related to systemic inflammation and immune activation that persist despite effective viral control/clearance, effects of anti-viral medications, or long-lasting impacts of viral replication on cells such as monocytes, which are involved in the early stages of cardiovascular disease.
This project aims to understand the mechanisms of how viral infections can potentiate the development of CVD, with a particular focus on the role monocytes may play in this process.
2022–ongoing.
We are utilising clinical cohort samples, transcriptomic and proteomic approaches together with novel in vitro assays of atherosclerotic processes to investigate:
This work will help determine how viral infections may potentiate CVD, which will identify processes that can be targeted therapeutically. Identifying biomarkers to predict those at risk of a cardiovascular event will help prevent CVD in the millions of people worldwide who live with a chronic viral infection.