Whether or not a virus is alive is arguable, but like all living things, it evolves. This fact was fully revealed during the pandemic as follows: New mutant strains of concern Appears every few months.
Some of these variants have excellent human-to-human transmission and eventually dominate because they compete with the slower version of SARS-CoV-2, the virus that causes COVID-19. This improved diffusivity is due to mutations in peplomer proteins (mushroom-shaped protrusions on the surface of the virus) that allow them to bind more strongly to the ACE2 receptor. ACE2 is a receptor on the surface of cells, such as cells that line the airways, where the virus attaches to it to invade and initiate replication.
These mutations have led to the global dominance of alpha variants and then delta variants. And scientists expect the same to happen with Omicron.
However, the virus cannot be improved indefinitely. The law of biochemistry means that the virus will eventually evolve a peplomer that binds to ACE2 as strongly as possible. By that time, the ability of SARS-CoV-2 to spread among people is not limited by how well the virus can attach to the outside of the cell. Other factors limit the spread of the virus, such as the rate at which the genome can replicate, the rate at which the virus invades cells via the protein TMPRSS2, and the amount of virus that infected humans can release. As a rule, all of this should eventually evolve into the best performance.
Did Omicron reach this peak? There is no good reason to assume it has. For so-called “gain of function” studies that look for mutations needed for SARS-CoV-2 to spread more efficiently, Identify many mutations This enhances the ability of peaplomers to bind to human cells, which Omicron does not have. In addition to this, as mentioned above, other aspects of the viral life cycle can be improved, such as genomic replication.
But let’s assume for a moment that Omicron is a variant with maximum diffusivity. Perhaps Omicron is limited by genetic probabilities, so it can’t get any better. Just as zebras haven’t evolved their eyes behind their heads to avoid predators, SARS-CoV-2 believes they can’t pick up the mutations needed to reach their theoretical maximums. Will be. Once, and it is very unlikely to appear. Even in scenarios where Omicron is the optimal variant to spread among humans, new variants will emerge to process the human immune system.
After being infected with a virus, the immune system adapts by making antibodies that attach to the virus and neutralize the virus, and killer T cells that destroy the infected cells. Antibodies are fragments of proteins that attach to a particular molecular shape of a virus, and killer T cells also recognize infected cells through the molecular shape. Therefore, SARS-CoV-2 can evade the immune system by mutating it sufficiently so that its molecular shape changes beyond the perception of the immune system.
This is why Omicron is clearly successful in infecting people with previous immunity from either vaccines or other mutant infections – allowing spikes to bind more strongly to ACE2. mutation Reduces antibody capacity It binds to the virus and neutralizes it.Pfizer’s Data suggests T cells should respond to Omicron as in previous variants, consistent with observations that South Africa has low mortality. Most people have immunity..
Important to humanity, past exposures still seem to prevent serious illness and death, leaving us a “compromise” in which the virus can replicate and reinfect. It’s not as serious as it was the first time.
Here is the most probable future of this virus. Even if it behaves like a pro gamer and ultimately makes the most of all the statistics, there is no reason to think that it will not be controlled and cleared by the immune system. Mutations that improve their ability to spread do not significantly increase death. This maximized virus simply mutates randomly and changes over time, making it impossible to recognize the adapted defenses of the immune system, allowing a wave of reinfection.
As with the current flu season, there can be a COVID season every winter. Influenza viruses “may have similar mutation patterns over time.Antigenic drift, Which leads to reinfection. The new flu virus each year is not necessarily better than last year, it is quite different. Perhaps the best evidence of this contingency for SARS-CoV-2 is the cold-causing coronavirus 229E. This already does..
Therefore, Omicron is not the final mutant, but it may be the final mutant of concern.If we are lucky and it is difficult to predict the course of this pandemic, SARS-CoV-2 is probably Endemic virus It changes slowly over time.
The disease is very likely to be mild, as past exposures create immunity and reduce the chances of hospitalization or death. Most people are first infected as a child, but this can occur before and after the vaccine, and subsequent reinfections are largely unnoticed. Only a small group of scientists track the genetic changes in SARS-CoV-2 over time, making the variant of concern a thing of the past – at least until the next virus jumps over the species barrier.
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