Getting to the heart of cardiovascular disease in viral infections
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.
Objective
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.
Timeline
2022–ongoing.
Approach
We are utilising clinical cohort samples, transcriptomic and proteomic approaches together with novel in vitro assays of atherosclerotic processes to investigate:
- What atherosclerotic pathways and processes are modified by viruses?
- Can we identify biomarkers that predict a cardiovascular event in people with viral infections like HIV?
- How do viral infections alter the atherosclerosis-promoting functions of monocytes?
- What treatments are effective at preventing CVD in people with a history of viral infection?
- Do viruses and healthy ageing act through similar or different pathways to increase CVD risk?
Community impact
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.
Student opportunities
Getting to the heart of cardiovascular disease in HIV
People with HIV have twice the risk of developing cardiovascular disease (CVD) compared to the general population. This is despite effective anti-viral therapy. CVD is now one of the greatest causes of disease and death in this population.
How HIV increases the risk of CVD is not fully understood. However, it may be related to systemic inflammation and immune dysfunction that persist despite effective viral control. Monocytes are a type of immune cell involved in the early stages of atherosclerosis, which drives most CVD.
We've found that HIV enhances the atherosclerosis-promoting activities of monocytes. We hypothesise that this may contribute to increased CVD risk in this population.
This project aims to investigate how monocytes contribute to increased atherosclerosis in people with HIV. It also aims to identify therapeutic strategies to mitigate these effects.
To answer these questions, we're utilising clinical cohort samples together with our novel in vitro assay of atherosclerotic processes.
This project utilises the following techniques:
- cell culture
- flow cytometry
- digital microscopy
- RNASeq analysis
- PCR.
Partners
Partners and collaborators
- Infectious Diseases Unit, Alfred Hospital and Monash University
- Austin Health
Project contacts
Associate Professor Anna Hearps
Deputy Program Director, Disease Elimination; Head, Infection, Inflammation and Innate Immunity
Project team