3 Reasons COVID (including Omicron) is going to become less severe
With all the hoopla going around saying omicron is less severe, some of us want to look at the bigger picture. Where are we going? Do viruses tend to become less severe over time? This article gives an easy-to-digest evolutionary perspective to that question.
First, a virus doesn’t have goals. It doesn’t care to kill or spread. However, if a virus does not spread, it dies; therefore alive viruses are viruses that must be able to spread. The more it spreads, the more alive it is. We saw that with the wild type, alpha, delta, and now omicron. The dominant variant is the one that spreads the most, and others fall away.
What about killing? It’s not necessary, but not selected against either. Herpes does a great job at spreading, but doesn’t do much apart from hang around in our cells and give us the occasional cold sore. On the other hand, the plague was a fast moving killer.
In order to know whether a virus will tend to evolve towards deadlier versions of itself, we need to analyze the relationship between lethality and transmission. After all, viruses are evolving increased transmission, and therefore changes in lethality must come in two forms: those that affect transmission, and those that are affected by transmission. There’s a third factor which is how our immune systems respond to the virus, also explained below.
Factor 1: Lethality Affecting Transmission
First, consider a quick killer version of COVID-19. A short incubation, and before one so much as develops a cough, lung failure happens and it’s lights out. You wouldn’t see as many people while shedding, which would have a negative effect on transmissibility. The original SARS is a good example for a virus being too deadly for its own good.
On the other hand, a harmless COVID would largely be tolerated, the way we tolerate colds, and it would be given free pass to circulate in the human population, the same way we don’t do much about colds.
Conclusion: A lower lethality favors spreading in humans.
Factor 2: Transmission Affecting Lethality
This part is a bit more complicated, but I’ll try to break it down using some analogies. In order to improve its spread, a virus tries to replicate more in our upper airways (throats, noses) in order to facilitate ejection into the environment. Lethality is somewhat a function of how well the virus invades our lower airways (lungs). So are the two related?
Well, the cells in both lower and upper tracts share a lot of similarities, but they do have their fair share of differences as well. Remember, the virus is optimizing its performance for the upper airways, and doesn’t really care about how it spreads in the lower airways, since that’s not how it spreads.
Consider Mark, a beginner runner training for 100 meter dashes. Every so often, he also runs 400 meter races, but he has no time to train for the 400 meters. At first, he noticed that even though his training was for the 100 meters only, with a focus on speed rather than stamina, his times on the 400 meter race were also improving thanks to the increased speed. As Mark began winning more races in the 100 meters, he began learning specialized techniques, like how to expend the maximal energy in the 70–100m phase to get a final push, and how to maximize the initial acceleration, with little regard to making that acceleration last more than a few seconds. He began competing at a national level on the 100 meter race, and winning. But he was no longer able to do so well on the 400 m race, he found that with his new techniques, his energy was totally expended at the 100m mark, and he would be slow for the remaining 300. Mark just learned that if two tasks are similar, you can improve on both by training one of them only to a certain extent, before having to specialize. The graph below shows Mark’s performance as a function of training for the 100 meter races. See how at first, his 400m results also go up as Mark becomes a better overall runner by training for the 100m, but they then gradually decline due to Mark learning techniques that are not applicable to 400m races.
Viruses work in the same way. Nose cells and lung cells are human cells, so when the original animal-based coronavirus crossed to humans, and began learning how to spread (ie, infecting the nose cells better), this probably translated to better replication in the lung cells, in the same way Mark’s early improvements in the 100 meter race helped him in the 400 m. Real data shows that the earlier variants, alpha and delta, are indeed somewhat deadlier than the wild type itself.
However, to really increase spreading in the upper respiratory tract, early data shows that omicron might be sacrificing its ability to target the lower areas (which again, is not so relevant to transmission so the virus neither tries to increase nor decrease it). If this is the case, then there is indeed hope that this trend takes hold.
Conclusion: A virus may eventually favor evolving to better suit transmission at the cost of lethality, even if it initially evolves more lethality.
Factor 3: Déjà vu
COVID mutates, but it’s no shape shifter. For all its attempts at immune evasion, the combined effects of vaccine and natural immunity are going to leave us more ready for the next time it comes knocking. It doesn’t have to become intrinsically less deadly; it’s just that we’re better at handling it.
Evolution and history are on our side. So is medicine and science. We’re up against a fierce foe, but we’re quite a piece of work ourselves.
