Until 2019 there were 4 Coronaviruses known to infect humans. They accounted for about 20% of colds. Last year the SARS-CoV-19 Coronavirus jumped from wild animals (probably from bats) to humans as a result of a new mutation in the virus surface protein (spike protein) which allowed this virus to enter human cells very efficiently. The virus surface (this is the spike protein) binds on to a receptor on the surface of lung cells, which is why major respiratory infection can result.
We make a family of proteins called Interferons whose function is to fight off viral infections. One of these is particularly important to counteract the Coronavirus. An important effect of the SARS-CoV-19 Coronavirus infection is to shut off production of this particular Interferon; which allows the virus to overcome human resistance to the infection. This is one reason why we see so many severely infected people and why there are more deaths than we see, for instance, in Influenza. Rare cases exist where this Interferon is not made at all because of a mutated and defective gene. In this instance, the infection is often fatal. There are also a number of functional gene variations for components of Interferon signaling pathways in cells which may reduce the biological effectiveness of Interferon – and these variations also lead to more severe disease. An unknown autoimmune disease affecting men was discovered in which antibodies against the cell surface receptor for interferon blocks its action on cells. Here again more severe and potentially fatal disease is seen. We have now learned that steroid treatment can save the lives of individuals with this disease by suppressing production of this antibody.