[phobosanomaly]

Can you cite specific sentences from the paper that disprove my hypothesis?

I pulled and quoted specific sentences so you didn't have to dig through the paper to see what I'm talking about.

If I'm wrong, and the paper clearly says how I'm wrong, pull the specific sentences and show me. Then I don't have to dig through a research paper trying to guess what you're seeing in there that makes you think I'm wrong. I've outlined a specific mechanism, you can pull things from the papers and refute my mechanism line-by-line if you want. I'm not being vague about anything. I'm spelling it out pretty clearly. If I'm wrong, show me how I'm wrong and then I and everyone reading this will be able to see clearly how I'm wrong.

> "I show you the findings about upper respiratory tract, you then cite "respiratory and stool samples" sentence from the paper as if it somehow disproves what is supported by the paper and the ones it references, that the high viral load in the upper respiratory tract before symptoms and during the first days of symptoms is critical."

I haven't seen any other method of measuring viral load in the upper respiratory tract than PCR. Maybe I've missed something? But in the lower airway they're using lavage in live animals and tissue immunohistochemistry in sacrificed animals to determine actual viral load. So, we don't actually know viral load in the upper respiratory tract from nasal swab PCR specimens (since, as they mentioned in the last paper, PCR from nasal swab doesn't actually correlate with viral load). Do you know of a way that they're measuring upper respiratory tract viral load other than nasal swab PCR?

The point of the bleach anecdote is to highlight what this paper said, which is that you can't estimate viral load based on nasal swab PCR since very high levels of mRNA hang out in the snout for long past the time when infectious viral titers have diminished.

[acqq]

> I haven't seen any other method of measuring viral load in the upper respiratory tract than PCR.

So we came to the truth: you didn't try to read how the researchers perform their research, even if they do publish their methods in the few papers you argue against, but you still claim here you know more than they do.

Of course the researchers can and do establish in their papers how much there's infectious virus in the upper tract. It's just a practical trade-off that, on the mass scale of all the millions of tests daily for clinical purposes, only PCR tests are preformed.

I've given you a single meta-analysis paper instead of linking to all the papers that paper refers to. Whichever detail you'd like to know, the paper links to them. It's mostly a click away. Almost all papers are also open access, meaning that you can read them in full. Moreover, for even those which aren't open access, typically the "appendices" are open access, exactly the parts that describe the methods used in the paper.

So, yes, we do know the actual viral loads of infectious virus good enough (1) to conclude what I wrote. And the conclusions, dumbed down enough, are what I've written before and eventually they can, when we're lucky, even end in the policies in the UK and statements of Pfizer CEO: there's enough research right now to not assume sterilizing immunity, unless the future studies show something else. That's science, it's seldom 100% certainty in 100% of effect.

You can either write about bleach all day or you can try searching in the paper and the references for what you want to know if you really want to learn something. Fishing for single sentences out of the context that support your wrong theories while claiming you know more than the majority of researchers is dishonest and contra-productive, unless you really just want to waste time of everybody (there are actually people paid to do that too, unfortunately).

---

1) Even for a single patient the actual existence of infectious virus can be established and the paper published: https://www.cell.com/cell/fulltext/S0092-8674(20)31456-2 "(SARS-CoV-2) shedding was observed from the upper respiratory tract of a female immunocompromised individual" ... "Shedding of infectious SARS-CoV-2 was observed up to 70 days" Yes, "upper respiratory tract" and "infectious SARS-CoV-2."

[phobosanomaly]

I have been reading the papers, I'm just giving you the benefit of the doubt of having read them and seen something I missed. I read scientific papers in biology all the time over the course of making a living, and I know how difficult they are to actually understand and interpret. I see PhDs and MDs make mistakes in interpreting them all the time. I make mistakes and miss things when reading them all the time. That's why graduate students, and professors, and medical residents, and doctors often read and discuss them in journal clubs, seminars, and conferences. The process is very similar to what we are doing right now.

I just read the paper you cited there. They're not determining titers of infectious virus in the upper respiratory tract with any other method than PCR. So, yeah, I'm right. I had just assumed you had read the papers and seen something I missed. You're making me second-guess myself, but I'm doing a pretty good job of cruising through these papers and understanding what they're actually doing.

Again, from the other paper you sent me, "RNA detection cannot be used to infer infectiousness."

The Pfizer CEO, Albert Bourla is a 'business executive and veterinarian."

Uğur Şahin MD, chief executive of Germany’s BioNTech, and whose main fields of research are cancer and immunology, and whose company actually developed the underlying technology of the mRNA vaccine jointly released with Pfizer had this to say:

'"I'm very confident that transmission between people will be reduced by such a highly effective vaccine - maybe not 90% but maybe 50% - but we should not forget that even that could result in a dramatic reduction of the pandemic spread," he said.'

https://www.bbc.com/news/health-54949799

No sterilizing immunity required.

I'm measuring my interpretation relative to actual scientists. Not just a random CEO who held a press conference. Albert, although he probably doesn't have as deep an understanding of the biology as Uğur, probably knows a hell of a lot more about manufacturing processes, and global distribution networks.

Imagine reducing asymptomatic transmission by 50%! That's insane. That's so awesome! It's going to cut transmission of this virus in half, even by a conservative estimate.

If I was able to sit down with Uğur, (who obviously has a much deeper understanding of the mechanism of action than I do) I'm willing to bet that his mechanism isn't so different than mine. Sounds like he and I agree on a lot!

[acqq]

The papers I've read use virus growth in cells, and even electron microscopy. I don't even know how you managed to claim now that only PCR is used in all the relevant papers.

It's no use for me even trying to discuss with you when your "reading" ends with recognizing that some paper mentions "PCR" and then claiming you're right in general, and all the epidemiologists and virologists aren't.

Anyway, AstraZeneca study just came out, and apparently even when the vaccine efficacy was 90%, the number of asymptomatic cases in the group where that was also measured dropped only 27% percent, which suggest again that the societies can't depend on vaccine providing sterilizing immunity -- it still appears that the vaccinated will be able to transmit the virus, just like the materials that I've referred to suggested.

That's why the UK starts with vaccinating first the most vulnerable, they know it's about protecting from illness, not about making the vaccinated impossible to transmit, as it's covered in many news in the UK -- the expectation is that, at the end, the immunity of population will only be reached once everybody is vaccinated. You can claim that nobody but you gets it, and that your "theory" is better than what's observed in many papers, but it's also a certain symptom.

[phobosanomaly]

Can't measure viral titer with an electron microscope. All the papers are measuring viral titer in the upper airway with PCR.

They may be confirming virus is present with other technologies, but the only way they're measuring viral titer is with PCR.

I don't claim that nobody but me gets it. The head of BioNTech seems to be saying exactly what I'm saying. I don't claim to say anything different from him.

Let's both come together to draft a public health statement that we both would feel comfortable releasing to the public. I'll go first:

Although new vaccine technologies will (1) aid in preventing members of the public from becoming severely ill with COVID-19, (2) will help significantly reduce the number of people contracting the virus in a clinically meaningful sense, and (3) will help to significantly reduce transmission in a community setting, it will be important for members of the public to continue wearing masks and maintaining social distancing until such a significant portion of the population is vaccinated that infection rates as-measured by nasal-swab PCR begin to show significant decreases, and ICU capacity is restored. Based on this, we will incrementally re-open and relax restrictions as deemed appropriate.

Sound ok to you?

[acqq]

I have much more "down to the ground" practical considerations: I don't directly think about some abstract "ICU capacity" or abstract "nasal swabs" meaning too much but:

1) can I or somebody else transmit the virus to somebody I care about and cause them to end on the ICU or die and

2) I know that no country actually measures "infection rates" with PCR but uses that only as a tool to count the "confirmed cases", where a lot of "confirmed cases" are anyway in bad enough state to need hospitalization (meaning it's expected the will need at least something like oxygenation in hospital, if not intubation in the ICU). I also know that there are cases where the CT scan directly shows that somebody is a "case" even if the repeated PCR is negative. So I don't worry too much about the PCR alone, it's just one of the tools.

I also know that some of those who come in contact with the vulnerable which I know will very probably get the vaccine much earlier then I will. I know they will have to behave like they aren't vaccinated, and I know it will be hard for them to accept that, like it was for you to even agree it's a real problem.

I also know that I personally will have to be potentially careful not to think that I can't transmit to somebody who is in worse shape than me, even once I am vaccinated. I know that even if the vaccine has 95% efficacy, it doesn't mean that somebody I care about isn't in the remaining 5%. I also won't know if I am not in the remaining 5% and pre-symptomatic exactly in that moment. And like I've written, it can be it's even worse, and we have to assume that until the studies show otherwise.

And on the higher level, I have to care about everybody actually: as long as the disease spreads, everybody is worse off. The sooner the broad measures don't have to restrict any activity, the better for everybody. I want the real "recovery" as soon as possible.

So what will I do?

a) follow the results of the ongoing studies hoping for some better news, but not assuming everything simply has to be perfect.

b) prepare myself and those I want to remain in contact with that we'll have to be as careful as we are now until there's simply much less prevalence. If I were in Australia now I'd allow myself much more than I will do for some months here where the prevalence (number of people who are new cases every day) is what it is (and it's similar in a big part of the Western world). So I expect that it will be quite hard for everybody for more coming months.

c) try to make as much people as possible understand that the vaccine is almost surely (even with 95% efficacy it's 1 of 20 for whom it's not "working") not something giving them any new "powers." The more are aware of that, there's bigger chance that the prevalence will go down earlier, and that will protect everybody sooner. And it will save some lives, maybe exactly those I know.

In short, it will be very obvious that it's significantly "better" once when the prevalence goes down to something like Australia (7 new cases today among 25 million people, hey! But it's Summer there) and people I care about (including me) are vaccinated. And that "better" won't start at the moment anybody particular has received the vaccine while the prevalence is still much higher. Vaccine simply won't be a magical shield for any single person, as long as the prevalence isn't low. Which is why always more experts now also say that we should do vaccine trials for the children and if needed start vaccinating them too from some point on (once the trials confirm it's safe and the prevalence still exists). I know people who will surely try to be in close contact with their grandchildren before the risk for them is actually low enough.

We will also have to be careful to observe the prevalence in context of how much measures we don't follow at that moment and how big risks we are willing to allow for all we care about. And I consider that all in the local context -- if my city is with much better prevalence than some other, it will be enough.

[phobosanomaly]

Good points, all of them.

Good chat.

Thank you for the conversation.