Details
- Close date
- No date set
- Academic background
- Health Sciences, Sciences
- Host campus
- Dunedin
- Qualification
- Master's, PhD
- Department
- Physiology
- Supervisor
- Associate Professor Martin Fronius
Overview
The recent COVID-19 pandemic caused by the SARS-CoV-2 virus is a considerable challenge for your lives. Severe Sars-CoV-2 infections can cause respiratory distress including pulmonary oedema. ENaC in the alveolar epithelium is a major player for fluid homeostasis in the alveolar region and impaired ENaC function is associated with the formation of pulmonary oedema. This indicates that symptoms in COVID-19 can be caused by impaired ENaC function. Intriguingly, Sars-CoV-2 has developed a new sequence in its spike protein that is unique in viruses and this sequence is identical to a peptide sequence only found in the human alpha ENaC subunit (among 23,000 other human proteins). This sequence is a recognition site for proteases. Proteolytic cleavage of viral spike protein is essential for cell infection and also for normal ENaC function. This finding further supports the hypothesis that COVID-19 symptoms are due to impaired ENaC function due to interference of the virus with host proteases.
The project will study ENaC function in pulmonary epithelial and endothelial cells that have been exposed to virus proteins. Results from this study could be a breakthrough for our understanding of the COVID-19 pathophysiology and allow the development of improved treatment options in COVID-19 patients with severe respiratory distress.
Useful information
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