To make the virus for the vaccine you need to use a different virus that when it replicates it creates copies of the actual virus used in the vaccine.
Think about it as a self extracting archive that creates copies of an uncompressed file (the actual vaccine) the file that it outputs doesn't have the information to reconstruct the self extracting archive itself.
I guess the thought is that a really unlucky evolutionary accident would be when the other virus capable of replicating and the vaccine meet in a body, and by chance transfer some of those instructions across. I presume that's rare or never seen, but I don't know, and (with a safety-engineering mindset on) I'd automatically consider that a "chance" unless it is ruled out by something.
> In extremely rare cases, natural mutations can cause a reversion to virulence. In this case, the virus can revert to wild type or develop into an entirely new strain.
Now, the Oxford vaccine is not an attenuated virus as is usually meant by that term.
On the other hand, it's not the same as an "inactivated virus" vaccine type either, where a virus is broken apart.
It's a different sort which doesn't fall into either of those categories. It's described as a "weaken adenovirus" and "replication-deficient" because of replication genes being deleted, and spike protein coding added. (There's no coronavirus at all, just the spike protein. This is completely different from other vaccines.)
The replication-deficient adenovirus has been studied thoroughly, not just for Covid but earlier as well. There are good reasons they selected it.
I will certainly take that vaccine when it's available, if that counts as any sort of endorsement.
I have high confidence in the people engineering and studying it. (I'm in Oxford, btw ;-) But can you really generalise the observations of inactivated virus vaccines to this relatively new kind? I think no, it has to be studied and monitored with care. Thankfully, I think they are doing exactly that.
Though, sometimes people think vaccines just prevent someone getting a disease. Stop it completely in its tracks. That's true for some, but it's not that simple for others.
Unfortunately a measured immune response does not ensure:
- That the virus can't be transmitted to others
- That you are less likely to catch and replicate the virus
- That you can't get ill from the virus
- That you can't get "long covid" symptoms
- That you can't die from covid
- That the immune response lasts for more than a few months (this is why we keep getting some of the same cold viruses; our immunity to them doesn't last)
- That the R number goes down (if it doesn't prevent transmission)
- That the R number doesn't go up (if people change behaviour in response to knowing they or other are vaccinated)
- That the virus won't evolve a workaround in response, like the rapidly mutating flu viruses
An immune response certainly suggests those things. But we can't be certain from immune response alone. Consequences need to be measured as well. We'll have a real solution when those sorts of things can be demonstrated, but it will take much longer to find out unfortunately. Probably we have to deploy a vaccine on a large scale somewhere before we can even find out how effective it is in the ways that ultimately matter.
Still, if a vaccine combined with uptake and people's behaviour reduces R below 1.0 at scale, that's enough to be a breakthrough. The greater the reduction the better, but 1.0 is the magic number.
Even if there's one good vaccine, having multiple good vaccine types in the world will be better. The virus is less likely to evolve a defence against multiple vaccines than against a single type deployed everywhere.
The fact this vaccine targets the spike protein is also good news, because even if the virus evolves, there's evidence that the spike protein is key to its harmfulness, so any evolved strains that keep it will likely trigger an immune response, and evolved strains that change the spike protein seem likely to be less harmful too.