COVID from the virus’s point of view

Photo by Anna Shvets on

There are a lot of headlines and news and predictions about where COVID has come from and where it is going.  While lots of good studies have been done and lots has been learned, I want to suggest that a lot can be learned by just looking at this pandemic from the virus’s point of view.  While I am not a virologist myself, it is fairly easy to image how this can happen and what is to the virus’s advantage and disadvantage in surviving and thriving.

Let’s start with a pre-COVID virus in a bat.  From the virus’s perspective it is all about the success of propagating its RNA, its reproductive molecule.  A virus is barely more than an RNA molecule packed with a minimum of reproductive machinery and a protective coating that doubles as a docking molecule looking for a cell type in a host to attach to.  Success for a virus is spreading itself far and wide.  The more hosts the better, the more copies the better.  Its method of reproduction is fairly simple and fairly prone to error, which is actually to its advantage since this allows it to mutate to overcome various barriers to its spread.

So, a COVID-like virus in a bat is happily reproducing and mutating and spreading around among bats.  A number of these viruses end up in humans and chickens and pigs by the natural processes of moving through the air.  But this does the virus no good since those protective coats cannot bind or attach to any cell types in humans, chickens, or pigs.  But then, by random chance, its RNA gets mutated in just one or two places and the shape of the protective coat, we now know to call them the spike proteins, changes just enough to stick to a cell type in the lungs of pigs.  (Of course, I am fabricating some of this because we do not know the exact path of the evolution of COVID, but this is a common pathway for a number of these flu-like viruses.)  Now here is where it gets complex.  The $10 question is whether the pigs get sick?  Does it really matter to the propagation and success of the virus whether its host gets sick and maybe dies?  Only partially.  Think like a virus.  If the pig gets sick enough to cough and sneeze and spew clouds of viruses into its environment, then yes, it is an advantage.  It the pig rolls over and dies within two days of catching the bug without barely a cough, then it is probably no advantage to the evolving virus.  Hence, we see a lot of successful viral diseases that involve clear modes of dispersal such as the common colds with lots of sneezing or certain stomach bugs that cause copious diarrhea or vomiting.

Photo by CDC on

In another interesting and devious twist, consider when most of our viral diseases are most contagious.  Is it when we have been diagnosed and are sick in our beds and masked up and isolated?  No.  Most often, we are unknowingly spreading the disease in the earliest days when we don’t even know we have it, in the pre-symptomatic period.  If you are thinking like a virus, this is genius.

So, back to our pigs who are in close contact with their human owners and are being taken to markets with even more humans and pigs and are being sold and transported around the country.  You already know the next step.  Another mutation happens and those viruses that the pigs were transmitting to their owner without much problem suddenly become a problem because the mutated spike protein can now attach to the cells of the human lung.  It is amazing to think that this disease, now officially called COVID-19, probably came about by a change of one or two molecules with one or two viruses within one pig in China in the summer of 2019, or some other equally improbable event.

This first variant of COVID-19 that attacked humans may not have been very effective.  It might not have bound very well and might not have used the human reproductive machinery very well.  But slowly with additional mutations it probably got more effective until it reached the point of being recognized and being named the alpha variant.

Now we can see that in the lifecycle of the virus there are several problems to be overcome and optimized.  Hosts must be infected; viruses need to be reproduced efficiently, and they have to be spread widely.  To be infected, a host must take in the virus to the cell to which the virus attaches, and it has to attach firmly.  The fewer inhaled viruses that can kick off an infection the better.  The omicron variant seems to be particularly good at infection.  Next the host cells need to be co-opted to make more viruses.  The more the better.  Again, it appears that delta and now omicron have become increasingly productive of new viruses.  As for the spread, we are now learning that the R0 of omicron is probably higher than delta.  The R0, or R-naught, is the average number of people that one infected person infects.  Both delta and omicron seem to be running about 3-7.  These are wide ranges, but it means that if a person is infected with omicron, they will infect about 3-7 more before becoming non-infective.  This explains why COVID is traveling so fast right now.

But what about severe illnesses and deaths?  Doesn’t this matter to the virus?  It certainly matters to us.  As I explained above, it is all about propagation, and sickness only helps the virus if it helps propagation.  And dead people don’t propagate viruses.  So, this gives us some hint on how this virus might evolve.  If you were the virus, would choose to infect people and give them no symptoms while you went through your lifecycle and spread, or would you choose to kill off a large fraction of your hosts after they have been quarantined in a hospital for two weeks?  I vote for fewer symptoms and fewer deaths.  I suspect that the pre-symptomatic but infectious phase is going to get longer and longer while the sick but not spreading phase is going to get shorter and shorter.  Deaths that don’t help spread viruses will also probably go down.  This a conjecture, but I have read that most virologists agree with this probable scenario.  Omicron seems to be headed in this direction with more infections and less lethality.

But this should not make us complacent.  This is a very smart virus with a long-term plan to take over the world.  It will patiently lay in wait until we are not watching and then a mutant might spring up that is much more infectious and also, for a short time, much more lethal.  And we can also expect variants to emerge that resist or avoid the vaccines but are still very infectious.  Omicron also seems to be taking us down that road.

So, in thinking like a virus we have learned a couple things.  Viruses are wicked smart but not necessarily committed serial murderers.  They just want to take over the world.  Please keep up those vaccinations and boosters.  Please encourage worldwide vaccinations.  Please keep those masks up.

This link can help find a vaccine near you in the US.

Photo by Gustavo Fring on

One thought on “COVID from the virus’s point of view

  1. Do you think that this will be like HIV, ever mutating and avoiding a one-size-fits-all vaccine? Smallpox and polio never mutated which is why a vaccine ultimately takes care of it? Do you predict that Covid will be like the influenza virus that changes just a bit each year?


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