Mutations in Coronavirus

A friend posted this. Not sure if it is accurate or wishful thinking. Any evidence that this is why the death rate seems to be lower?

It seemed reasonable, and it would be an additional reason for a lower death rate besides just better theraputics.

No on ‘accurate’, yes on ‘wishful thinking’. The underlying article looks fine, but the blog post about it says things that aren’t in the paper and that don’t have any support. Unfortunately, those bits are the supposed good news. Problems with the blog:

  1. There is no general trend in viruses toward lower pathogenicity, at least not on a relevant timescale (i.e. tens of years). Viruses can evolve to become less pathogenic and they can evolve to become more pathogenic; sometimes the same virus will do both in turn. Since SARS-CoV-2 already causes mostly zero or mild symptoms, especially in those who are most likely to be out and about infecting others, there is very little selective pressure toward lower pathogenicity. The only mutation in this virus known to affect its phenotype increases transmissibility, with little effect on virulence.
  2. The APOBEC enzymes that are (probably) mutating SARS-CoV-2 are also present in bats, the presumed normal host for the virus. So this isn’t some new effect that’s started occurring since the virus changed hosts.
  3. There is no suggestion in the paper, or in any data I’ve seen, that deleterious mutations (including those caused by APOBEC enzymes) are accumulating as the virus spreads in humans. That seems to be an invention of the blog writer. It’s a routine fact that deleterious mutations occur as viruses spread, and that natural selection weeds them out.

Thanks! That was my suspicion, but good to hear from someone who knows the subject.

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I am no viral expert but we know that mutations and different strains of the various viruses occur and it is highly likely that Covid 19 will do the same. That will be crucial to track for the future for when we get a vaccine. it could happen that new strains may differ in their effects and severity. It may not impossible to track each strain so we will always need the uttermost precautions for a long time to come. Do not listen to any voices that say we can or have conquered the virus.

I agree that this virus is likely not going to be conquered, but we will have to learn how to co-exist as it becomes endemic.

So really no vaccine would be of any use?

No, what it means is a vaccine is very important in making it possible to return to a new normal, as the virus is likely going to be hanging around. We just have to deal with it.


There’s the potential that the first one(s) available may reduce the distribution of a later one that is appreciably more effective.

But if the virus is going to continue to mutate, then how can the vaccine help? Will they have to make more and more types of vaccines?

The same way the measles vaccine helps while the measles virus continues to mutate. By preventing infection for many years. Maybe someday measles will mutate enough that we need a new vaccine, at which time they’ll add a new vaccine.


I was thinking, and I would like feedback from our biologists like @glipsnort here – I was putting two and two together, namely the so called inoculum effect (by which I mean this idea that the severity of an illness depends on the amount of initial exposure to the virus) and high rates of random mutations in viruses.

Could it be that the reasons why you have this “inoculum effect” is not because the actual numbers of viruses you are exposed to is so important but rather the higher likelihood of being exposed to a particularly virulent version of the virus when you are exposed in higher amounts. You see the thing about the “inoculum effect” which didn’t quite add up for me was that viruses multiply quite rapidly and so I couldn’t see why starting numbers should be all that important.

I had another idea as well, but it took me a while to figure out out to express it. If viruses mutate so close to population lethal rates, it suggests that despite their ability to multiply they have a hard time establishing a stable population in the host, in which case the exposure to higher amounts of the virus would get the virus over this hurdle and thus be more likely to affect the host more severely.

Or… am I just over thinking this and this is just a matter of getting a large enough population going before the body has time to build up defenses? Or… is it perhaps a combination of all three?

The advantage of the first idea is that it would explain the difficulty in getting evidence for this “inoculum effect” since it would be purely statistical. Some people with low exposure would still get really sick and some people with high exposure might still only have a mild case of the illness.

So in other words what you are saying is that the mutations are insignificant and the immune system’s reaction will continue to produce the right antibodies.

By “infection” do you mean the entrance of the pathogen into the body OR do you mean the pathogen gains some foothold and causes disease? I imagine you mean the latter. However, the vaccine doesn’t prevent infection. The vaccine only allows our body to develop the antibodies. It still takes the immune system to fight the pathogen and prevent infection, does it not?

That is really semantics, in that the immune system is of course the machine, but the vaccine provide the programming instructions.

For SARS-CoV-2, yes. So far.

I should have said ‘preventing disease’. An infection starts and is quickly suppressed by the immune system.

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Didn’t I read somewhere that the mutated strain that is now predominant likely makes it more transmissible (maybe more easily aerosolized) but not more serious disease? That would not necessarily have any immune response implications, would it?

Sorry, but that would imply that without the vaccine the immune system would have no instructions.
The reality is that the immune system doesn’t need the vaccine to fight the pathogen and win. Our immune system is awesome and can fight any and every pathogen when it is working to full capacity. Both my sisters had the measles and I lived in the same room as them and never got sick AND had not had any vaccine at that time.

Yes jpm’s analogy was not the best.

What the vaccines do is provide a way for your immune system to develop the “programming” (i.e. antibodies) without the person getting sick. They are typically composed of nonfunctional fragments or weakened versions of the virus that stimulate the immune system to produce the required antibodies but do not invade cells and replicate.


Maybe it would have been helpful to add that a vaccine provides pre
-programming instructions so that the immune system is already prepped and doesn’t have to do it on its own after the real infection occurs.

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Yes – the D614G mutation in the Spike protein.

Not that we know of. It invades cells more easily.

I think I’ve seen one report with evidence for worse outcomes for the mutated version, but most have not seen an effect.

So far, reports are that it shouldn’t.


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