> It's very unclear to me, as a layman, how this artificial "self amplifying RNA" that incorporates elements from a virus is so very different from an actual virus, given that the SARS-CoV-2 is itself basically RNA surrounded by a coating in a form that can self-replicate.
For one, we can implement protocols to ensure the mrna we are generating contains the instructions we want, at the effect size we want. We could go the non mrna route and grow it as a virus, but that is going to be less accurate, more costly, and take longer. We could also just let people develop natural immunity, which will also work. People will get varying effect sizes, and vary from barely immune to dead. Obviously no vaccine and no virus would be the best outcome. But we don't get that choice.
We could go the non mrna route and grow it as a virus, but that is going to be less accurate, more costly, and take longer.
These are things that concern vaccine makers for understandable commercial reasons, but what you're saying is that there's effectively no difference to the recipient beyond the fact that the artificial self-replicating mRNA might be higher "quality" in some way.
Let's put it like this: given the apparently low probability of being infected (for people my age, in a way that we actually notice, at current prevalence levels etc), most of us actually can choose "no vaccine and no virus". Or put another way we can choose between guaranteed cell damage from vaccines, or the chance of cell damage from virus the exact probability of which is some integral of prevalence, individual risk behavior, how quickly you get treated (e.g. with ivermectin), and how many people around you are vaccinated. To me it looks like a good tradeoff to not take the vaccine, especially when so many other people are: the chance of avoiding cell damage entirely is really quite high, and I like my body spike-free. Stories like the Reuters article this thread is about just reinforce that decision.
That’s how the immmune system works in general, with or without the vaccine.
> what you're saying is that there's effectively no difference to the recipient beyond the fact that the artificial self-replicating mRNA might be higher "quality" in some way
It’s the difference between taking a known dose with quality control or an unknown dose with no quality control.
> Let's put it like this: given the apparently low probability of being infected (for people my age, in a way that we actually notice, at current prevalence levels etc), most of us actually can choose "no vaccine and no virus".
Let’s put it like this. you can take vaccine and have an extremely rare chance if pericarditis, or eventually get the virus (it’s not going away) and have a higher chance of pericarditis.
The assumption that eventually SARS-CoV-2 will infect 100% of the population is a common modelling assumption. When I went looking for validation of it, I couldn't find any.
As for known dosages, as I say above, I couldn't find any information comparing dosages or cell death levels of vaccines vs actual viral infections. That would certainly be helpful to know, assuming such reports were reliable.
It's unlikely you will find validation outside an entry-level text book for virology or epidemiology. From my understanding it's a fundamental assumption that's easy to verify: ALL viruses with a similar transmissibility profile as SARS-Cov-2 (high R0, aerosols) have become endemic, that includes e.g. seasonal influenza and all other human coronaviruses.
That's the reason seasonal influenza is not a big issue most of the time, because we already had it in the past (or a related strain) and our immune system is primed. This happens usually as children and is the reason why both young children and their parents are a lot more ill than the average.
A completely new influenza strain, however, has a similar pandemic potential as SARS-Cov-2, and one hypothesis why the 1918 influenza was so deadly for younger generations is that they likely had not encountered it before, while the older had.
In fact, if SARS-Cov-2 wouldn't go the same route as basically all similar viruses have done before, it would be a big surprise. Try to speak to an expert in the field, preferably a virologist or an epidemiologist.
Somewhat related: it's a common cognitive bias to trust self-generated knowledge more than the knowledge from others.
Absolutely nothing in modern epidemiology is validated against real world data as far as I can tell, and virology isn't concerned with the course of epidemics, so I doubt this very much.
The problem this assumption faces (and it is as you point out, only an assumption) is it quickly runs into definitional and logic issues. That's a very common problem in epidemiology and public health as far as I can tell. Viruses evolve, and so when talking about whether they can eventually infect the whole population you have to very carefully consider:
1. How fast they evolve.
2. How fast they spread.
3. How much evolution is required to make something a "new" virus vs an "old" virus.
4. What those evolutions do to disease which is what everyone actually cares about.
If you don't have a very firm grip on these things (and epidemiology doesn't) then you can get into a situation in which by the time a virus has infected "everyone" it's no longer the same virus at all, and thus cannot be said to have actually infected everyone. All the talk of different COVID variants is pointing in this direction. Taken to an extreme it boils down to "everyone will get infected with a virus at some point" which isn't an interesting statement.
Somewhat related: it's a common cognitive bias to trust self-generated knowledge more than the knowledge from others.
Indeed it is, and scientists are very often guilty of this: they reject any and all negative feedback that comes from people "out of field", even if it's extremely relevant to what they're doing. For example rejecting feedback by computer scientists of the form "your program does not work" because computer science isn't the same thing as epidemiology.
But in this case I actually don't trust self-generated knowledge more than the knowledge from others, because I don't claim to have any superior knowledge of epidemiology. I just know the people who claim to be experts, actually aren't.
By the way, the fact that the body can flush it out doesn't mean it's not a toxin. Alcohol is gone from the body within hours of getting drunk but it's still a toxin, technically speaking.
In contrast, the mRNA vaccine works by getting cells to do things that cause them to be destroyed by the immune system ASAP. Even small amounts are thus (cyto)toxic and the question is how much can the body tolerate.
One of the things that makes me uneasy about the mRNA tech is there seems to be very little discussion or research about dosages, and in particular how cell death levels compare between getting vaccinated and actually being infected with the real thing. This would seem to be fundamental because at some level, the vaccine is actually creating the same problem inside the body that the virus is, the only difference is that the virus can self replicate whereas the mRNA does not (except apparently in the case of so-called "self-amplifying mRNA" vaccines, see below). Thus the question of dosage is critical. If being infected with the virus causes 10x less cell death than the vaccine then I want to take my chances with the virus. If the vaccine causes 10x less cell death than a real viral infection, then it looks better. As ultimately, it's cell death and the fight to destroy those cells that makes people sick.
Such numbers are (nearly?) impossible to find. Vaccine dosages are very different between the different manufacturers. The Moderna vaccine has a dose more than 3x higher than the Pfizer vaccine, for example (100 µg vs 30 µg), which is itself 3x higher than the dose for the Curevac vaccine (12µg).[1] It's a bit unclear how these very different numbers were arrived at or what they're being calibrated against.
W.R.T. the SAM vaccines, also in [1] we find the following text:
"The other type of mRNA vaccines, SAMs, do not only encode the target antigen but also RNA polymerase encoding ‘self-amplifying’ factors derived from Alphavirus ... These are in turn transcribed to many coding mRNA molecules, leading to prolonged and enhanced antigen expression ... The two SAM vaccines in clinical development are nCoVsaRNA by the Imperial College London and ARCT-021 by Arcturus/Duke-NUS (both as mRNA-LNP)."
It's very unclear to me, as a layman, how this artificial "self amplifying RNA" that incorporates elements from a virus is so very different from an actual virus, given that the SARS-CoV-2 is itself basically RNA surrounded by a coating in a form that can self-replicate. Traditional vaccines are virus based but the virus is inert. The new vaccines appear to be ending up at the same end-point but without the whole making it inert part.
It'd got to be higher than that. In Mexico, population 127 mil, excess deaths are about 622k which is 0.49% of the population dead.
The number comes from meta-studies that examine a large range of IFR studies. There is a lot of variance between them - they don't all arrive at the same value, presumably because IFR is inherently difficult to measure. Infected people who don't feel sick enough to report are the dark matter of epidemiology.
However, excess death values are quite tricky to evaluate because they're excess relative to some model of what should have happened in an alternate timeline where the event in question never occurred. For example you can calculate an excess death value for Sweden of zero by making one or two plausible assumptions, or you can calculate a higher value using equally plausible assumptions, and who is to say which is correct? Ultimately you can't know what would have happened otherwise, only extrapolate from the past and try to guess. Some of those extrapolations look suspect on examination (e.g. using fixed averages, or very short timespans), just like everything else around this topic.
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8032477/