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Comment by actually_a_dog | Hacker News Reader

You make a technically correct, but not very useful statement.

The overall evolutionary path for the virus is most likely to be in the direction of higher infectivity and lower deadliness. Viruses don't tend to replicate in dead hosts, so, a virus that doesn't kill people is fitter evolutionarily than one which does. This means that, while the virus is certainly not going away, the risk eventually will.

This may take a long time, though. It may take decades.

Here is an article from New Scientist that says essentially the same thing, but in more detail: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7825868/

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I just had this thought yesterday: Could the process you described be sped up? If there was a virus variant that spreads faster but is less deadly it would replace the known variants but do less harm. So let's head to the bat cave and build the virus variant we could handle. (what could possibly go wrong?) At least in theory this should be possible, right?

Edit: Fixed typos

It’s not that the more benign virus beats the other one over the head, just that the more deadly strain dies out eventually while the more benign one doesn’t. Adding benign strains can’t speed up this process

o A large part of the mechanism by which ncov kills is the immune system's response. There's no "kill the host" gene that you can simply snip out. It does harm as a second order effect, not as a feature.

o DNA is really complex to work with; designing proteins is harder when you don't have the luxury of being Nature itself and trying it out in vivo.

o You will have a PR problem of hilarious proportions. Virus genetic engineering research labs are a few points short of popular support at the moment.

Those are all valid points but not enough to convince me that it isn't worth trying. Then again I'm not a virologist or anything close so it doesn't matter much what I think. I hope it's something leadership will consider though, and I hope the PR problem, for instance, isn't something they worry much about.

Using "live" virus is a problem. For example there are two versions of the polio vaccine. The injectable uses inactivated ("dead") virus, and the oral uses weakened("live") virus.

Both are safe, but in the oral one the virus can go to another person and cause no problems, and then to another and cause no problems, and after like a year jumping hosts it can mutate and become dangerous. Now most of the the polio cases are caused by virus that mutated from the version of the vaccine. https://en.wikipedia.org/wiki/Polio_vaccine#Vaccine-induced_...

The number is much smaller that the number of cases before the vaccine, but it's concerning anyway. So they are trying to discontinue the use of the vaccine with the inactivated virus, but the other one is better when most of the population is not vaccinated. https://en.wikipedia.org/wiki/Polio_vaccine#Schedule

So ... probably the authorization and test necessaries to use a new vaccine with and attenuated virus are more difficult than a vaccine with an inactivated virus (or a vector virus, of mRNA, that also can't spread).

Very late fix:

* So they are trying to discontinue the use of the vaccine with the weakened virus, but the it's better when most of the population is not vaccinated.

I think this paper describes a similar scenario: for one season in France a rhinovirus successfully delayed the propagation of influenza A in children by virtue of getting there first. https://pubmed.ncbi.nlm.nih.gov/20121829/

SARS2 mutates much more slowly than influenza so the evolutionary path to lower risk will take much longer.

This make me feel that spreading it is better than not spreading it at this point. Luckily it is much more infectious.

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