Coronaviruses are highly pathogenic to humans and can cause respiratory and intestinal infections. They are large, enveloped, single-stranded RNA viruses that can cause respiratory, gastrointestinal, and neurological disease. SARS-CoV-2 has a diameter of 60 to 140 nm and distinctive spikes that range in size from 9 to 12 nm. This gives the virus the appearance of a solar corona, which is how it got its name.
When a host is first infected, SARS-CoV-2 targets the epithelial cells that line the nasal passages, bronchi, and lungs. It does this using the viral structural spike protein that binds to the angiotensin-converting enzyme 2 (ACE2) receptor. Like other viruses that can cause respiratory dysfunction, SARS-CoV-2 can cause profound lymphopenia (reduced white blood cell count) by infecting and killing T lymphocyte cells, a major component of the immune system that is responsible for defending the body against foreign pathogens.
In later stages of infection, the integrity of cell barriers is compromised. It is at this stage when viral replication begins to accelerate: the virus infects pulmonary capillary endothelial cells and rapidly proliferates, exacerbating the inflammatory response. This leads to excessive recruitment of immune cells, especially monocytes and neutrophils, to the lungs. In more severe cases of SARS-CoV-2, activation of coagulation and clotting factors will occur. Inflamed lung tissues and pulmonary endothelial cells may result in high incidences of circulatory complications, such as deep vein thrombosis, pulmonary embolism, and thrombotic arterial complications in critically ill patients.