Heavy emphasis on "candidate". How can you tell if people had a mild case because the virus had deletions or because they mounted an appropriate immune response? It's not clear that the vaccine will be protective.
The real value of finding an attenuated strain (one that causes mild illness in everyone) is that it would be ethical to use it in a challenge trial of a conventional vaccine. The Oxford vaccine group for example are planning a large field trial because they don’t think it is ethical to expose people to the normal dangerous strains. If we found an attenuated strain we could speed things up massively.
You can see this in early and Layer 1/2 posts that go negative while later and Layer 3/4 thread posts that get high amounts of positive upvotes after the initial wave has moved on.
https://www.ncbi.nlm.nih.gov/pubmed/16043204 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7103385/
And as I said, you can't know if the people who had mild infections did so because the virus was deficient or whether their immune response was good. It's not enough to have the antigen, you also need the right adjuvant to mount a response. The last thing you want is to have antibodies that recognize the virus, but do not activate the immune system.
https://en.wikipedia.org/wiki/Antibody-dependent_enhancement...
https://jvi.asm.org/content/94/5/e02015-19
https://www.researchgate.net/publication/340005309_Potential...
The fact that the live attenuated approach worked with polio doesn't mean that it'll work with coronavirus, and if we're not careful we could accidentally worsen the situation.
I agree that this is worthwhile area of pursuit, but one that will take a long time to bear fruit. Maybe you think that studying the variants in the wild will allow us to skip over some animal studies with the live attenuated virus, but I doubt they can be skipped.
I have no background in this whatsoever, so feel free to ignore my comment, but my guess is that finding them in the wild along with a large-enough (and representative-enough) infected population without severe symptoms basically saves the work of trying 5k different possible variant in animals — just skip the the promising candidate directly, no?
However, the PCR-based diagnostic tests that are current being used rely on amplifying only a small part of the virus genome so we are actually blind to how the rest of the virus is changing in the larger population (at least in routine diagnostic tests).
Of course, if this testing infrastructure doesn't already exist, I imagine creating it would be too slow to help with this particular plague.
No, you can't approximate a human immune system with red and white blood cells in a container of liquid. No, adding some other cells in there won't help. If that were effective, we'd be doing it already. You are either overestimating your own ingenuity or underestimating the ingenuity of tens of thousands of scientists, doctors, and engineers.
The answer is no, for somewhat obvious reasons. The human immune system involves many organs and tissues and cells working together in very complex ways.
And I think your charitable interpretation is quite a bit too charitable. OP did not say anything like "why doesn't it work like I think it would".
For the record, my main intention was to get an expert to say something that would gratify my curiosity and that of other readers. I hadn't heard of it before, so I assumed it was likely impractical at the moment, but guessed that technology would eventually get there.
Also, are you an expert in this field? Your sibling comment seems to be saying "yes they are working on it, no it's not practical yet except for HIV" (I presume because HIV infects white blood cells), which is at odds with your second paragraph. (Edit: Though, to be very precise, the examples from the sibling comment are about measuring infectivity and—I guess—the impact of drugs, not immune response.) It would be ironic if a non-expert gave an ignorant dismissal of a question for being ignorant.
there's other approaches to make "organs on a chip" for drug trial screening, since lab models with only one type of cells don't capture the effects of other types, but it's really not fully baked yet.
Your “first level” is something we already do with primary and immortalized cells and it can be a useful model. Your next level would be called co-culture and it also is something we already do. These can be static cultures or connected to flow systems or bioreactors or whatever. These are imperfect models, but they can help to yield useful answers for questions in the model’s scope. The closest fidelity to human immune systems would be animal models, and the closest of these would be Rhesus macaques, and indeed these are used for vaccine development.