It is controversial whether viruses survive, but – like all living things – they evolve. This fact has become perfectly clear during the pandemic, as new forms of anxiety emerge every few months. Some of these variants have been more effective in spreading from person to person, eventually competing with the slower versions of SARS-CoV-2 that causes COVID-19.
This improved proliferative ability has been attributed to mutations in the spike protein—the spike protein is a mushroom-shaped bulge on the surface of the virus—that helps it bind more strongly to ACE2 receptors. ACE2 are receptors on the surface of our cells, binding to which the virus starts the process of entering our body and multiplying.
These mutations caused the alpha version and then the delta version to become globally dominant. And scientists expect the same thing to happen with Omicron. However, the virus cannot cure itself indefinitely. The laws of biochemistry mean that the virus will eventually develop a spike protein that binds to ACE2 as tightly as possible.
Until that time, the ability of SARS-CoV-2 to spread between people will not be limited by how well the virus can stick outside cells. Other factors will limit the spread of the virus, 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 remove. In theory, all of this should eventually develop for peak performance.
Has Omicron reached this peak? Although there is no good reason to believe that this is so. So-called “gain-of-function” studies, which look at which mutations are needed for SARS-CoV-2 to spread more efficiently, have identified a number of mutations that affect the spike protein’s ability to function in human cells. Improves binding ability that Omicron does not have.
In addition, other aspects of the virus’s life cycle can be improved, such as genome replication, as I mentioned above.
But let’s assume for a second that Omicron is the version with maximum diffusion potential. Perhaps none would be better than Omicron because its genetic potential is limited.
After infection with any virus, the immune system adapts by making antibodies that stick to the virus to neutralize it, and kill T-cells that destroy the infected cells.
Antibodies are protein fragments that stick to the specific molecular shape of the virus, and killer T-cells also recognize infected cells via molecular shape. Therefore SARS-CoV-2 can evade the immune system by mutating enough that its molecular shape changes beyond recognition by the immune system.
This is why Omicron is so clearly successful in infecting people with previous immunity, either from vaccines or from other forms of infection – mutations that give Spike a chance to bind to ACE2, allowing antibodies to bind to the virus and It also reduces the ability to neutralize it.
Data from Pfizer suggests that T-cells should respond similarly to Omicron as in previous variants, which aligns with the observation that Omicron has a low mortality rate in South Africa, where most people have immunity.
The important thing for humanity is that the infection of the past still prevents serious illness and death. This leaves us in a position where the virus can replicate itself and become re-infected, but we don’t become as seriously ill as the first time.
This is where the most likely future for this virus lies. Even if it behaves like a professional gamer and eventually maxes out all its stats, there’s no reason to think it won’t be controlled and cleared by the immune system. Mutations that improve its proliferative ability do not greatly increase deaths.
We can have Covid season every winter, just like we have flu season now. Influenza viruses can have a similar pattern of mutations over time, known as “antigenic drift”, leading to reinfection.
Not every year’s new flu virus will necessarily be better than last year’s, just substantially different. Perhaps the best evidence of this phenomenon for SARS-CoV-2 is that 229E, a coronavirus that causes the common cold, already does so.
So Omicron won’t be the final version, but it could be the final form of concern. If we are lucky, and the course of this pandemic is hard to predict, SARS-CoV-2 will likely become a permanent virus that mutates slowly over time.