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Ben Krishna postdoctoral researcher in Virology and Immunology at the University of Cambridge argues in an interesting article in The Conversation about how the Omicron variant may not be the last of the coronavirus, but it may be the last one to be of serious concern before the virus finally becomes endemic and concerns us once a year, like the flu virus.
An undeniable fact of the pandemic is the constant variations of the coronavirus. Some variants are more efficient in their human-to-human transmission and eventually become dominant, displacing more "sluggish" variants of SARS-CoV-2. The improved transmissibility of the virus is attributed to mutations in the spike protein of the virus that allows it to better bind to ACE2 receptors on the surface of human cells, such as those found in the airways of the respiratory system. After binding to our cells, the virus enters the body and begins to replicate.
Mutations in the virus have made alpha and delta variants dominant, and the same is now expected to happen with Omicron.
However, as Dr Krishna points out, the virus cannot improve its profile - that is, mutate - in perpetuity. According to the laws of biomechanics the virus will at some point create a spike protein capable of binding very effectively to ACE2 receptors. However, by then other factors will have come to the fore that will limit the transmissibility of the virus, such as the speed of genome replication, the speed of entry of the virus into cells via the TMPRSS2 protein, and the amount of viral load transmitted by an infected host. Theoretically all of these factors can evolve and reach their peak value.
The question is whether Omicron has reached this tipping point. The available evidence reveals that Omicron does not have all the required "trump cards" in protein-spike binding capacity that the scientists' computational models reveal to be required for a powerful and infectious mutation.
But suppose Omicron has reached its peak transmission capacity. It may not be improved further, just as zebras did not develop eyes on the back of their heads even though they would have helped them avoid their predators, explains Dr Krishna. Also even in a scenario where omicron would be the best - most infectious - variant, new variants would emerge to invade the human immune system.
After infection with any virus, the immune system adapts by creating antibodies that stick to the virus to neutralize it as well as T-cell killers that destroy infected cells. The antibodies are pieces of protein that stick to the specific molecular shape of the virus and the T-cell killers recognise the infected cells through the molecular shape as well. SARS-CoV-2 can therefore only fool the immune system through mutations in its molecular shape so it cannot be recognized.
\NThe virus's high mutability is why Omicron infects people with prior immunity - either from vaccines or natural infection. Mutations that allow the spike protein to bind more strongly to ACE2 receptors also reduce the ability of antibodies to bind to the virus and neutralize it. Pfizer's data suggest that killer T-cells respond in a similar way against Omicron as to previous variants, which aligns with the observation that Omicron has a lower mortality rate in South Africa, where most people are immune.
It remains important for humanity that prior exposure to the virus still protects against severe disease and death, leaving us with a "compromise" where the virus replicates and reinfects, but we don't get as badly ill as the first time.
The likely scenario
What is the most likely future for SARS-CoV-2? No matter how "cleverly" it behaves, there is no reason to believe that it will not eventually be controlled and driven out of the immune system. Mutations that improve its ability to spread don't increase deaths much. Then this virus would mutate sporadically, changing enough over time that it would not be detected by the immune system's adaptive defenses, allowing waves of reinfection, which has happened with past major epidemics worldwide.
Somehow we can have "Covid season" like we have flu season every year. Influenza viruses have a similar pattern of mutation over time, known as "antigenic drift" (a term used to describe one of the ways in which influenza viruses change to create new strains), leading to reinfections. Each year's new strains of influenza virus are not necessarily more improved than last year's, just quite different. Perhaps the best evidence for this scenario for SARS-CoV-2 is that human coronavirus 229E, a coronavirus that causes the common cold, already does this.
Therefore, Omicron will not be the final variant, but it may be the last "variant of concern." If we are lucky SARS-CoV-2 will likely become an endemic virus that mutates slowly over time.
The illness will most likely be mild as some prior exposure builds immunity that reduces the likelihood of hospitalization and death. Most people will be infected for the first time in childhood, which could happen before or after vaccination, and subsequent reinfections will hardly be noticed. Only a small group of scientists will monitor the genetic changes in SARS-CoV-2 over time, and the variants of concern will be a thing of the past - at least by the time a new virus breaks the 'species barrier' and triggers a new pandemic.
Source: ygeiamou.gr
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