"The results of this systematic review indicate that there is an intrinsic relationship between Bifidobacterium and COVID-19. The studies showed that COVID-19 is associated with changes in the gut and nasal microbiome, including a decrease in the abundance of Bifidobacterium. The presence of Bifidobacterium was associated with a reduced risk of severe COVID-19."
Yes, I read the paper. Unless I misread it, it showed that more severe infections lead to lower Bifidobacterium levels.
Obviously, what we really want to know is whether changing them in advance can change the course of illness (and how feasible such changes are, particularly at scale). The paper poses a couple of questions, one is that, and the other is whether changing the gut microbiome (by increasing Bifidobacterium) might influence recovery (perhaps reducing long term effects from infection). It doesn't seek to answer those questions, though.
If I had to guess, I'd guess that making those changes in the gut microbiome of a population would be hard, and that it would make at best marginal changes to the outcome of this (and any other) illnesses. If a part of the intervention meant giving everyone (or large parts of a population) an antibiotic like Azithromycin that would have an obvious risk which would need to be balanced with whatever benefit there might be.
The only solution anybody was allowed to consider was novel vaccines, that's it.
That's not true. Vaccines are the natural thing to look for when you're looking at an infectious disease, and obviously they need to be novel because it's a novel virus. The choice of vaccine platforms was just about timing: you want a vaccine as quickly as possible, and viral vector and mRNA technologies can provide vaccines faster than others. Even if Ivermectin really worked, you don't want to be taking it long term.
Did people look for other things? Most definitely they did. Hence steroids which can reduce the rate of death when used at the right time, changes to treatment (so using less invasive ventilation, proneing, etc.), antivirals like Paxlovid which (if used early enough) can reduce hospitalisation rates by ~85% even when you include vaccinated people. Also a bunch of other things which looked promising but unfortunately seemed not to work out like fluvoxamine. Metformin (against long covid) seems to me to be still on the margin (might help, might not) but people are very much still looking.
What seems most peculiar to me is that in the UK (and some other countries) we're diving headlong into the idea that being infected in childhood is safe and will provide sufficient protection to adults. The theory was raised early that the virus might end up like the other cold-producing coronaviruses and we seem to be assuming it will happen and we should make sure that as many children get infected as often as possible.
I'm not sure why this virus might not instead stay like SARS1 and MERS and just be a (sometimes) very nasty virus (even for children and young, fit adults) that we can (fortunately) vaccinate against.