How Coronavirus Kills?

For the majority of COVID-19 cases, symptoms are either non-existent or similar to those of flu. However, a minority of infections can be far more dangerous, developing into a case of severe pneumonia that can be fatal, particularly for the elderly and for those with underlying health problems.

After gaining access to the lungs, Sars-CoV-2 enters the cells of the alveoli (the sites where oxygen and carbon dioxide are exchanged) and hijacks their cellular machinery in order to replicate. This process kills some cells, however it is the body’s own immune response that causes most of the damage. Blood vessels dilate and become more permeable to allow more immune cells to access the site of infection, which leads to the accumulation of fluid inside the alveoli. This reduces the efficiency of gas exchange between the alveoli and the blood. The fluid also increases the surface tension in the alveoli, and can cause them to collapse, further impeding gas exchange and making it harder to breathe.

Ventilators are used either to apply a positive pressure to help keep the airways and alveoli open, or to more forcefully push oxygen into the lungs. A sufficient drop in oxygen carried by the blood can lead to organ damage, however this is not the only threat posed by a coronavirus infection.

In the most severe cases, a coronavirus infection can lead to the dreaded cytokine storm, in which large numbers of white blood cells release inflammatory molecules (cytokines), which in turn activate more white cells. Furthermore, the cell debris and protein-rich fluid in the alveoli can leak into the blood and be carried around the body. In both cases, the result is a widespread inflammatory response called systemic inflammatory response syndrome.

When inflammation is localised to one place, it usually serves to help the immune system fight an infection. However, when inflammation occurs throughout the body, the result is catastrophic, leading to life-threatening low blood pressure (septic shock) and multiple organ failure. For many COVID-19 patients, this is the cause of death.

In truth, however, scientists are still struggling to understand many of the effects of coronavirus outside of the lungs. While the cytokine storm could be responsible for damage to other organs, these sites might also be attacked directly. The virus could, for example, attack cells in the lining of the heart and blood vessels, or in the neural cortex and brainstem, as all of these sites express ACEII receptors, the structure to which Sars-CoV-2 binds before entering a cell.

Until we better understand how COVID-19 causes these complications, particularly to the cardiovascular system, it is difficult to predict who will be more severely affected. Further study of the virus’s effects outside of the lungs will thus be essential as the pandemic continues to progress.