Precision Diagnostics: COVID-19 Severity Assessment via Advanced Plasma Biomarkers

24023-05:  Precision Diagnostics: COVID-19 Severity Assessment   via Advanced Plasma Biomarkers

Inventor: Marko Radic, Ph.D.

•COVID-19 patients who died had extensive damage to the elastin fibers in the lungs.
•This suggests that neutrophil activity and elastin degradation play a crucial role in pulmonary fibrosis development.
•High levels of neutrophil elastase-alpha-1 antitrypsin (NE-A1AT) complexes in the plasma of COVID-19 patients could potentially be a biomarker for long COVID-19 disease.
•Targeting neutrophil activity and elastin degradation could help improve long COVID symptoms.
 
Technology: Dr. Radic’s team examined lung tissue from people who died of COVID-19 and found significant damage to the elastic fibers in the lungs. This loss of elasticity was linked to the activity of immune cells called neutrophils, which released the enzyme neutrophil elastase (NE), a potent protease that degrades the extracellular matrix (ECM). This damage occurred before scar tissue (fibrosis) buildup, suggesting it plays a crucial role in lung destruction.

An inhibitor regulates the activity of NE-alpha-1 anti-antitrypsin (A1AT), which forms a NE-NE-A1AT complex and blocks its activity. Plasma samples from hospitalized patients had approximately 30 times higher NE-A1AT complexes than plasmas from healthy donors, suggesting that such complexes may indicate host tissue damage due to inflammation in respiratory lung infections. Thus, a blood test for this complex could be used to diagnose lung damage or predict long-term lung problems (long COVID) after the acute infection.

The elastolytic activity is crucial in exacerbating pulmonary pathogenesis in COVID-19 patients, especially in the pathologic development of pulmonary fibrosis. Dysregulated neutrophil activity and NETosis lead to elastin degradation, ECM remodeling, and fibrotic changes in COVID-19.

Understanding how neutrophils contribute to lung damage in COVID-19 could identify novel therapeutic targets and prevent pulmonary fibrosis in COVID-19 patients. This could improve patient outcomes during acute and long-term COVID-19 phases.

Applications:

1. Diagnostic marker for lung damage and long COVID

2. Therapeutic target for fibrosis and long COVID

3. Potential for personalized medicine

Value Proposition:

1. Improved diagnosis and treatment of lung damage and long COVID.

2. Develop new therapeutic approaches for fibrosis in COVID-19 and other diseases 

3. Personalize treatment for patients based on their individual needs.

4. Contribute to the development of new anti-fibrotic drugs.

Publication: Biomolecules 

Status: The protocol has been finalized. UTRF is seeking licensees for this tech on a tech-specific or exclusive basis. Further collaboration may be possible.

 
Patent Information: