The disease might very likely be mild as some past exposure creates immunity that reduces the likelihood of hospitalisation and death
It is controversial whether viruses are alive, but – like all living things – they do evolve. This fact has become abundantly clear during the pandemic, as new variants of concern have emerged every few months. Some of these variants have been better at spreading from person to person, eventually becoming dominant as they out-compete slower versions of SARS-CoV-2, the virus that causes COVID-19. This improved spreading ability has been ascribed to mutations in the spike protein – the mushroom-shaped projections on the surface of the virus – that allow it to bind more strongly to ACE2 receptors. ACE2 are receptors on the surface of our cells, such as those that line our airways, that the virus attaches to in order to gain entry and start replicating.
These mutations allowed the alpha variant, and then the delta variant, to become globally dominant. And scientists expect the same thing to happen with omicron. The virus cannot, however, improve indefinitely. The laws of biochemistry mean that the virus will eventually evolve a spike protein that binds to ACE2 as strongly as possible. By that point, the ability of SARS-CoV-2 to spread between people will not be limited by how well the virus can stick to the outside of cells. Other factors will limit virus spread, such as how fast the genome can replicate, how quickly the virus can enter the cell via the protein TMPRSS2, and how much virus an infected human can shed. In principle, all of these should eventually evolve to peak performance.
