To assess blood levels of vasoactive mediators that may regulate pulmonary endothelial permeability and contribute to multi-organ injury in patients with COVID-19 disease and to correlate the levels of these mediators with disease outcomes such as ICU admission, length of ventilatory support, respiratory failure, kidney failure, heart failure, and death.

When patients are sick with other lung infections (pneumonias) caused by viruses or bacteria there are changes in a pathway that regulates the "leakiness" the tiny airspaces inside the lungs. Even bigger changes in this pathway are seen when patients develop severe breathing difficulties (acute respiratory distress syndrome) similar to what is seen in patients who get really sick with COVID-19 disease.

There are important changes in this pathway that occur in patients who have preexisting cardiovascular (heart) disease who do not have lung infections. The investigator will evaluate these levels in patients with COVID-19 because the investigator believes that this baseline difference in pathway regulation may be one reason patients with heart disease who contract COVID-19 get sicker than patients without heart or vascular disease.

The investigator will also assess the levels of components of this pathway in patients who are less sick with those who became sick enough to require a tube to help them breathe because this is important to determine if COVID-19 lung disease has a similar effect on this pathway as other lung infections like flu and bacterial pneumonias.

Inclusion Criteria:

• Positive test for COVID-19 (SARS-CoV-2 infection)
• >=18 years
• Blood (plasma) specimen(s) available in the CCTS biorepository

Exclusion Criteria:

• <18 years
• Lack of blood specimen

Patients who have available specimens in the UAB CCTS Biorepository for COVID-19 patients. (IRB-300005127: COVID-19 Enterprise Biorepository.)