Viruses require a host (animal, plant cell, yeast) to reproduce. They are not like bacterial organisms that can divide on their own. Viruses require a host cell to manufacture more of themselves to spread and survive. In order for them to get into a cell they must first bind to a host cell and be brought into the cell for infection to occur. This assumes they are not recognized as a pathogen and destroyed before infection can occur.

COVID-19 and SARS, both bind to a particular protein called Angiotensin Converting Enzyme II (ACE2). This protein is like the door to the cell and, unfortunately, COVID-19 and SARS, are attracted to this doorway and can sometimes push their way through if they are not identified by immune system first. A recent study published states “the cells with ACE2 expression may act as target cells and thus are susceptible to 2019-nCoV infection; such cells include type II alveolar cells (AT2) of the lungs” (Zou et al., 2020).

One of the purposes of ACE2 is vascular constriction, defined as tightening of blood vessels. As more and more cells become infected, the ACE2 function is destroyed and increased fluid accumulation occurs in the lung tissue along with the influx of a specific type of immune cell called neutrophils. Neutrophils are an important component of a robust immune system, however, if their recruitment is overdone, the inflammation they attract can lead to a downward spiral of the recovery efforts and ultimately destruction of lung tissue (Lai et al., 2020).

The specific type of lung cells that have ACE2 present are alveolar type II cells and are particularly important for maintenance of oxygen exchange in the body. Without these cells, the lungs are unable to exchange carbon dioxide (our natural waste product) for fresh oxygen. If enough of alveolar type II cells are damaged, the person may develop acute respiratory distress and ultimately can lead to death.