SARS-CoV-2, the Coronavirus that causes COVID-19 and is responsible for the 2020 pandemic, is known to enter cells via the ACE2 receptor (see this video on the Renin-Angiotensin system).
In addition to ACE2, there are other receptors that either facilitate entry into cells (making the virus more infectious) or increase its pathogenicity (causing more severe symptoms).
Neuropilin-1 And Its Role in Virus Cell Entry
The other receptor that helps entry is neuropilin-1, which is more abundant in the upper respiratory tract. It is what makes SARS-CoV-2 highly infectious (see video). That may explain the the first phase of infection and spread while asymptomatic or having mild symptoms. Finding a way to block that receptor (without severe side effects) may reduce the viral load in the body, and cause the disease to be milder.
Heparan Sulfate and Immune System Causing Pathogenicity
Another receptor in human cells is heparan sulfate. A recent study shows that the virus binds to that glycoprotein, and therefore triggers a chain reaction of the complement system part of the innate immune system. This could cause many of the inflammatory complications of the disease. Finding a way to prevent this chain reaction (by blocking Factor D) means that the disease is milder than if it gets triggered. Again, potential severe side effects need to be taken into account.
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