Most developments can be interpreted a lot better afterwards than when we are in the middle of it. This applies to most social developments as well as to the evolutionary development of the coronavirus. At the beginning of 2022, within this article, I already made a serious attempt to interpret the potential evolutionary development of the coronavirus. The Omikron variant had only recently appeared on the scene and there was still plenty of uncertainty about the course of the corona pandemic. I now dare to interpret the evolutionary development of the coronavirus and the future course of the corona pandemic with a lot more certainty. While I assumed in the cited article that a new variant could just pop up that could revive the pandemic, I now consider such a scenario a lot more unlikely. This of course has everything to do with the relatively mild properties of Omikron.
Evolutionary trend towards faster spread
Evolutionarily, new virus variants tend to spread more quickly than previous variants. Such an evolution is in fact a precondition for successful displacement of previous variant(s). Faster spread comes down to (a combination of) a higher risk of infection, a shorter incubation time, reduced pathogenicity or partial circumvention of previously built up immunity. The Omikron variant appears to have walked these paths simultaneously to supplant previous variants. This has led, among other things, to the fact that Omikron is substantially less pathogenic than previous variants.
In principle, the emergence of a new variant which no longer shows any overlap with previous variants in terms of immune response, this new variant no longer has to compete with previous variants in terms of spreading speed. In which case it would be lifted completely out of competition. In essence, in that case, a completely new virus has emerged that could revive the corona pandemic. Based on my analysis below, I now consider such a ‘worst case’ scenario a lot more unlikely. In an evolutionary sense, the Omikron variant has clearly taken paths towards reduced pathogenicity in addition to a higher spreading rate. I have listed the main mechanisms that have led to this below.
Higher infection risk
Over time, accidental mutations have resulted in variants that attach preferentially or more emphatically to our upper lung epithelium or tissue. This means a higher risk of infection and therefore a faster spread and displacement compared to previous variants. In this specific case, this higher infection risk also leads to a reduced pathogenicity. Infection of the upper lung epithelium, in contrast to infection of the lower lung epithelium, is less likely to cause serious respiratory complaints or difficulties.
Shorter incubation time
In addition, accidental mutations have resulted in the incubation period (the time between infection and subsequent infectivity) being more or less halved compared to the original virus. This also leads to a faster spread and a crowding out compared to previous variants.
The reduced pathogenicity of Omikron variants also means that infected persons potentially continue to be infected for longer. This is because they are sometimes barely aware of their contagiousness or associate the virus with a regular cold. Ergo: a faster spread and a crowding out compared to previous variants.
Bypassing previously built up immunity
Partly bypassing previous immunity builds allows Omikron variants to compete more effectively with previous variants, resulting in a faster spread and crowding out compared to previous variants.
Other mechanisms that increase the rate of spread
Mutations that in any other way lead to a higher rate of spread – for example due to the release of more virus particles, longer survival on surfaces, etc. – also lead to successful displacing previous variants.
The current corona variants have adapted to their human host
It is precisely this evolutionary displacement potential of faster diffusion that leads to a natural selection pressure whereby random mutations having the aforementioned consequences are selected over mutations with a neutral or opposite effect. The current variants have thereby adapted to their human host and have gradually developed a gene configuration that guarantees a faster spread with regard to this human host.
Nevertheless, it cannot be ruled out that mutations arise that completely lift the coronavirus out of the competition by completely bypassing the existing immunity. However, the more the coronavirus has adapted to its human host, the more unlikely it will be that it will lead to another pandemic. After all, the paths already taken have already resulted in the disease becoming a lot less serious, with which the virus apparently develops into a regular cold. On the one hand, due to the reduced pathogenicity in itself and, on the other hand, because of the typical infection of the higher lung epithelium, which also contributes to reduced pathogenicity.
Even if a variant emerges that completely circumvents the existing immunity, that variant will still carry a significant part of the characteristics that made Omikron the dominant variant. Existing properties cannot simply be undone on the basis of accidental mutations. In addition, those existing traits will also serve and benefit the new variant just as they do the current Omikron variants.
Almost all human viruses once started as zoonoses
The main difference of Omikron with the original Wuhan virus is that the original variant jumped directly from the animal world to humanity. Such so-called zoonoses have adapted to their animal host, but not yet to humanity. This means that the virus jumps with a set of traits that are more or less optimized for infection and transmission in the animal host. On the one hand, this can lead to the virus having no or insufficient possibilities for infection and subsequent transmission to its new human host. In that case, the further spread will come to a screeching halt and it will not or hardly spread further within the human population.
If, on the other hand, the animal virus does have sufficient possibilities for infection and subsequent transmission to its new human host, we speak of an actual spreading zoonosis. Although a virus generally does not benefit from making its host seriously ill – after all, this ultimately hinders its spread – the characteristics of each zoonosis are completely unpredictable. After all, the virus has adapted to its animal host and it is impossible to say in advance how such properties relate within a human host. This is why zoonoses move on a spectrum from potentially completely harmless to extremely sickening or deadly.
Endemic viruses are often relatively mild
Viruses that humanity has been carrying for a long time (in this case endemic viruses), have usually already evolved towards a relatively mild appearance due to the five potential development paths described earlier. For example, think of measles, chickenpox, rubella, scarlet fever, mumps, various colds, etcetera. Relatively mild infections (always barring individual exceptions) with an extremely high risk of infection without exception. This is due to the fact that these viruses have been circulating within the human population for a long time and have therefore adapted to our physical characteristics in terms of optimal spreading speed and usually associated reduced pathogenicity.
Something similar now seems to be the case with the coronavirus. In itself it is remarkable that this process has largely taken place within two years. This gives a completely different view on the becoming endemic of zoonoses. Previously, virologists were convinced that such processes would take at least decades. In general, viral infections seem to adapt more strongly to our physical characteristics than bacterial infections do. This is undoubtedly due to the fact that viral infections are directly dependent on our (genetic) biology, as opposed to bacterial infections, which (can) be a lot more independent of our (genetic) biology. This is of course even more true for parasitic infections.
The reason that potentially pandemic diseases such as Ebola, Marburg, HIV, etc. manifest themselves so severely is largely due to the fact that they do not or hardly or not yet survive long enough to adapt sufficiently to their new human host. Or in the event that a virus cannot adapt sufficiently to its new human host on typical genetic grounds, the human host has not yet sufficiently adapted to the virus through natural selection (ie death and infertility). Left or right, the impact of zoonoses over longer periods of time within a population of hosts will usually decrease sharply because the relative pathogenicity of the virus decreases over time. This is simply how natural selection works!
Why the Flu is no exception to this
The fact that the Flu does not seem to keep up with this development towards milder forms has everything to do with the fact that severe influenza pandemics are simply the result of the flu viruses jumping over and over from the original hosts (ie poultry, poultry, pigs) to humanity. To a certain extent, flu viruses can therefore be regarded as separate zoonoses that regularly make the transition back to humanity.
[Fotocredits – Halfpoint / dottedyeti © Adobe Stock]