[phobosanomaly]

My dude, if you review the literature (or just google it) you will find that there is common reference to 'subclinical' and 'asymptomatic' COVID-19. First-page google results for 'asymptomatic COVID-19' include an article in The BMJ from four days ago titled 'Covid-19: Asymptomatic cases may not be infectious, Wuhan study indicates.' I'm not saying I buy the findings in that study, but be conservative with what you claim to be 'common knowledge.'

Again, regarding CT values, continuity of positive nasal swab PCR results can be totally divorced from significantly decreased lower-respiratory-tract viral titers, as the Nature monkey paper you sent me pointed out.

I ask you again: What is the mechanism by which a vaccine takes a person who would normally be symptomatic, and magically makes them asymptomatic, while having zero impact on titers of virus in the body?

I'm not talking about behavior here. I'm talking about direct, biochemical mechanisms inside of the human body.

The vaccine is reducing viral titers. And by reducing viral titers, it is reducing shedding into the lower airway. And by reducing shedding into the lower airway, it is reducing the number of viral particles contained in respiratory droplets expelled from the airway. And by reducing the number of viral particles that exit that airway, it is reducing transmission as it is intended.

Behavior is a separate discussion entirely, but consider the mechanism I have described. It is not only reducing viral titers in those who would normally be symptomatic, it is also reducing viral titers in those who would normally be asymptomatic. Those silent carriers that are walking around among us, well, now they're walking around spreading a hell of a lot less virus. And that is a big deal, especially in places like Oklahoma, Idaho, Arizona, South Dakota, Wyoming, Florida, Tennessee, Georgia, South Carolina, etc, which as I mentioned earlier, have zero state-level requirement for anyone to wear a mask at all.

You are claiming [or at least not refuting svrb's argument] that vaccines have no impact on titers of virus in the body, and yet somehow they magically render people asymptomatic by a mechanism as-yet unknown to biology.

That's just not how it works. And the fact that vaccines knock down the amount of virus being spread around is a big deal, especially in places where there are no mask requirements in place.

Earlier you accused me of spreading false information, and asked me to apologize for spreading beliefs that can put people in danger, but have you come to see that this discussion is not as clear-cut and binary as you originally made it seem?

I promise I'm not the enemy.

[acqq]

The reality is exactly the opposite of what you claim: all the studies of infectiousness of SARS-CoV-2, and even of other respiratory viruses correlate with detection of high virus load in the upper respiratory tract, and don't correlate with the detection of the high virus load in the lower respiratory tract. Here the most recent meta-analysis of the most relevant studies:

https://www.thelancet.com/journals/lanmic/article/PIIS2666-5...

Your reasoning therefore completely doesn't match the results of many different studies across the world, and also doesn't fit with which people are considered infectious in practice, with all the millions of people involved.

So, the study that I've quoted earlier, which detected high viral load in the upper respiratory tract of non-human primate animal model therefore suggests exactly what I've already mentioned that it suggests, namely, that we can not assume that vaccine provides sterilizing immunity unless the later studies with humans show otherwise. And that is exactly how the UK is going to proceed with their vaccination policy, as I've already documented, and also matches the statement of Pfizer's CEO.

(I also note that you again try to insinuate that my claims are something that I've never even mentioned, hoping to change the topic. Please don't.)

[phobosanomaly]

Dude. This paper you're sending me is saying exactly what I'm saying. My reasoning matches all of the papers you've sent me so far:

You're saying:

> "all the studies of infectiousness of SARS-CoV-2, and even of other respiratory viruses correlate with detection of high virus load in the upper respiratory tract"

But, RNA fragments detected by PCR in nasal swabs != live, infectious virus.

The paper you linked is saying, instead:

"Our study shows that despite evidence of prolonged SARS-CoV-2 RNA shedding in respiratory and stool samples, viable virus appears to be short-lived. Therefore, RNA detection cannot be used to infer infectiousness."

"Our findings suggest that, although patients with SARS-CoV-2 infection might have prolonged RNA shedding of up to 83 days in upper respiratory tract infection, no live virus was isolated from culture beyond day 9 of symptoms despite persistently high viral RNA loads."

Residual RNA from lysed cells is sticking around and getting picked up on nasal swabs even when actual, infectious, titers of virus in the body are plummeting, and patients are no longer infectious. I used to work with RNA in a research lab! The shit is everywhere. Our experiments used to get contaminated with RNA from the lab next door all the time. I used to have to spray my bench with a bleach solution every day, sanitize my pipettes, and work at night so my RT-PCR experiments didn't get contaminated. That's in the air. Imagine how long it hangs out in the moist, snotty environment of the nasal cavity.

"Nevertheless, most studies demonstrate faster viral clearance among asymptomatic individuals than those who are symptomatic."

"This finding is in keeping with viral kinetics observed with other respiratory viruses such as influenza and MERS-CoV, in which people with asymptomatic infection have a shorter duration of viral shedding than symptomatic individuals."

Giving these people a vaccine will help them clear the infection even faster, which will help reduce community transmission, especially in places where they're now wandering around without masks on, in full compliance with state law.

I'm happy that the UK is prepared to make aggressive and forward-thinking health policy. Good for the UK, but this ain't the UK. There are a lot of countries like the US where I live, as well as my neighbor Mexico that don't have an NHS, and don't live on a small island with a well-functioning government. These vaccines will help to reduce community transmission in places where the scenes from urban hospitals can best be described as nightmarish.

"No part of the world has been as devastated by the pandemic as Latin America. Mexico, Brazil, Peru and other Latin American countries — hobbled by weak health systems, severe inequality and government indifference — have several of the highest deaths per capita from the virus in the world.

And unlike in Europe, the United States and many other regions, the outbreak in Latin American has not struck in waves. It hit furiously in the spring and has continued for months, with few of the respites savored elsewhere, however briefly, around the world. By the first week of September, the 10 countries with the highest deaths per capita were all in Latin America or the Caribbean."

https://www.nytimes.com/2020/09/23/world/americas/mexico-cor...

Again, shift your frame of reference. The rest of the world does not look like the UK and Europe. Enjoy living somewhere that isn't a charnel house. The vaccines reduce community transmission, and I can say that confidently because I have outlined a pretty clear mechanism for it and there is zero data you have presented that points in the other direction, despite the fact that you keep saying it. Celebrate that fact that we now have this tool in our arsenal.

I promise I'm not the enemy. I promise I'm not conjuring things out of thin air. I'm reading all of the papers you're sending me, and I'm drawing valid scientific insights from them that are applicable to the broader world-at-large, not just the UK with the NHS at the helm, which is able to take steps that for much of the rest of the world is an unrealistic luxury.

[acqq]

The paper, and the papers it references, disproves your wrong theory that you repeated many times in more messages on this page about "lower respiratory tract" being more relevant for virus transmission, which is still wrong, as in, completely the opposite of what is reported in the scientific papers.

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.

You cherry pick the sentence about the "viable virus" not being present "beyond day 9 of symptoms" (meaning day > 9) but that doesn't disprove what is claimed in the studies: that the transmission occurs even before symptoms (days -2 -1 and 0) and during the first few days of symptoms, that is, before the host's immune system has the time to fight the virus infection.

https://academic.oup.com/view-large/figure/210823252/ciaa144...

from

https://doi.org/10.1093/cid/ciaa1442

The scientific facts aren't less true in the US than in the UK and Europe. Your claim that you "used bleach solution" in the lab also doesn't make your wrong theory and your other wrong claims less wrong. Of course PCR tests detect RNA longer than the infectious virus is present, but all studies I've cited haven't ignored that fact.

[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!