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In the same way that zebras haven’t evolved eyes at the back of their heads to avoid predators, it’s plausible that SARS-CoV-2 can’t pick up the mutations required to reach a theoretical maximum as those mutations need to occur all at once, and that is just too unlikely to emerge.Įlectron micrograph of a B.1.1.7 variant coronavirus. Perhaps Omicron won’t get any better because it is limited by genetic probability. Besides this, improvements could be made to other aspects of the virus life cycle, such as genome replication, as I mentioned above.īut let’s assume for a second that Omicron is the variant with maximized spreading ability. So-called “gain-of-function” studies, which look at what mutations SARS-CoV-2 needs to spread more efficiently, have identified plenty of mutations that improve the spike protein’s ability to bind to human cells that Omicron doesn’t have. Has Omicron reached this peak? There is no good reason to assume that it has.
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In principle, all of these should eventually evolve to peak performance. 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. 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. The laws of biochemistry mean that the virus will eventually evolve a spike protein that binds to ACE2 as strongly as possible. The virus cannot, however, improve indefinitely. And scientists expect the same thing to happen with Omicron. These mutations allowed the Alpha variant, and then the Delta variant, to become globally dominant. 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. 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. 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 fact has become abundantly clear during the pandemic, as new variants of concern have emerged every few months. It is controversial whether viruses are alive, but – like all living things – they do evolve.