Will you Please Wear A Mask Now

I'm a bit skeptical of this rebreathing stuff. It seems to make sense but it's unconfirmed. What bothers me is that the concept ignores the fact that an infected person already has billions of viral copies and I frankly doubt that breathing out a tine fraction of them decreases viral load in any significant way. There is the argument that rebreathing might spread the virus to other areas of the lungs that are not yet colonized... frankly, with replication going on everywhere, there is blood-born spread anyway, and it is probably much more important than whatever new seeding might occur through rebreathing. Confirming this would be difficult in terms of ethical concerns if we were studying a population by risking making them worse, or risking unmasking a control group and thus increasing transmission to healthy subjects including the researchers. We'd have to randomize a large number of patients and have a group masked and a group unmasked, measure viral loads and severity. I just don't see a study being done with a design like that, given the "do no harm" mandate from Institutional Review Boards. Your first link sounds like a paid ad for people who are trying to make these one-way masks. I'm not saying that it is excluded that this rebreathing might be a factor; but color me unconvinced; at the very least I'd expect it to be just a minor factor.

As for the "it doesn't matter" idea, yes, of course the evidence does point in the opposite direction. For those who are not very much in tune with Science (not your case; I'm just saying it for the benefit of others here), it's sufficient to look at the steep decline in transmission in the 15 Kansas counties that have adopted mask mandates, as opposed to the 90 that did not. Transmission decreased in all 15 "masked" counties, no exceptions, and remained the same (at high levels) in all 90 "unmasked" counties, no exceptions.

 

Are you offering that correlation is causation?

 

No, I'm aware that it is a correlation but it is a suggestive one given that the 15 counties with mask mandates are actually more urban and more densely populated and rely more on public transportation so conditions there if you look at intervening factors are actually more favorable to transmission than in the other 90 counties. And do pay attention to this part of the post you've just quoted: "for those who are not very much in tune with Science." For those who are, I mentioned elsewhere, instead, the 29 studies with coronaviruses (SARS-1, MERS, and SARS-CoV-2) pointing to a steep reduction in relative risk by mask wearing, both N95s and regular facemasks, and both in healthcare settings and community settings. I've posted here both the link to a meta-analysis and its full PDF, and tables showing the reduction in relative risk. Most people have no clue on how to read and interpret these studies (which do control for intervening factors therefore are more demonstrative of causation than correlation) so FOR THOSE it is more convincing to look at this Kansas correlation, especially one that is so complete (no exceptions in both groups of counties; the ones with reduction being the least likely to post a reduction before this one intervention).

It's always cute to see someone questioning a post, by selective leaving out an essential phrase that indicates the poster's intention. It's there. You quoted it. No excuse for not having read it.

 

The leading disease experts around the world are not the US government.

 

It is even more cute to watch a self-described scientist attempt to rationalize mistakes by way of sophistry.

 

Exactly. It always amazes me how people reduce this to some sort of domestic political strife, ignoring what PAN in a PANdemic means, with about 215 countries in the world, pretty much all facing issues with this virus to lesser or bigger degree, and 214 out of these 215 not having the domestic political issues of the US of A. Sure, they have their own, but most places couldn't care less for our domestic politics, even as influencing as we are. So there are many scientists researching and publishing everywhere who do not do this out of any relationship with the American government's agendas and lies.

 

Now that is a profound statement!!!

It has been well demonstrated that leading disease experts, like the ones in England who offered such a grossly wrong model regarding covid, are mere mortals like us. And that many of them will write and say whatever on earth they are paid to write and say.

What are you actually curious always about?

 

Yeah, whatever. My professional association, board, the universities that granted me my degrees, my decades-long professional activity and publications, and my employer might disagree with your "self-described" claim. Congratulations on your cute response; it doesn't erase that I had ALREADY pre-emptied it by dosing my contribution to the level of knowledge and capacity for understanding of the readers, even saying it in all words. If I had not done that BEFORE your cute response you'd have had a point. I insisted for weeks with the scientific side of this; I authored a number of posts on correlation and causation (notoriously one in which I used the ice-cream sales and shark attacks correlation); but I've learned that most people here don't really get it if we keep it strictly scientific, so I adapt. But feel free to think whatever you want about me. I'm not about to lose any sleep because some Internet warrior who read a book thinks that I'm "self-described." Have a nice day.

 

I finally put that guy on ignore. He's not a serious person. I don't have time for that.

 

When a well-packaged web of lies has been sold to the masses over generations, the truth will seem utterly preposterous and its speaker a raving lunatic.

 

From a mathematical perspective we are dealing with something like the law of diminishing returns in economics. At infection, and for a time (undetermined) after initial infection, the concentration of virons in airways/respiratory tract is important. At the point the immune system is overwhelmed it’s no longer relevant. What that curve of diminishing returns looks like we will likely never know. But if initial infectious dose matters I think it’s illogical to assume more virus moving into the lower respiratory tract isn’t worse than less.

I don’t believe blood born spread is relevant in the early stage where rebreathing would be relevant. Everything I’ve read shows virus can’t usually be found in blood until a couple days after symptoms and sometimes isn’t in blood at all in asymptomatic individuals. We know viral shedding occurs before onset of symptoms so any damage done by rebreathing would occur long before spread through blood. So actually the argument could be made that rebreathing may actually lead to blood infection. If you have newer, better information on timing of blood infection vs. shedding in respiratory tract I’m incorrect. But this is my understanding.

There is an issue with false negative PCR tests early in infection period that plays into this as well, but I’ve been up for 30 hours and can’t articulate it now. I’ll add more later.

Agree mostly on controlled studies. Not practical. But if I was in charge I’d sure be compiling survey data on infected individuals. That would tell us a lot.

That sounds good. Transmission is our target now, not necessarily outcomes of individuals. Rebreathing (if significant) only affects the individual so will likely not be research much. On the Kansas stats, did anyone check when the surges in “mask counties” began and ended and the same for non masking? It’s important to not mistake mask usage for decreases in infection rates if rates were already on the downhill of 6-8 week surges we see in populations regardless of behavior modifications. I’m not saying the rates in Kansas aren’t being affected by masks, just pointing out the correlation/causation thing. It seems most places don’t get serious about masks until already peaking in infections and starting to see upticks in mortality.

 

No one wants to believe they've been lied to, manipulated or used.

No one want's to believe that truths they have held for all their lives, are not truths at all.

'But if X number of people say it must be true, then it must be true'

 

Like I said, I don't discard that it might be a small factor (so nothing illogical in what I'm saying); I just doubt it is significant. We'd have to see those curves of timing of blood infection vs. shedding through the respiratory tract and rebreathing. And given that it's been known that the main mechanism of even the lung damage for COVID-19, is endothelial lesions rather than direct lesions to alveoli cells, I'm not that convinced that the blood part of it is not more significant than the respiratory part of it. You know, this thing seems to be fast. In 4 to 7 days after contagion people are already having high fever, generalized muscle aches, etc.; sometimes before they're even coughing. The respiratory symptoms are very variable. Have you noticed how symptoms from other organs got added more and more? Some cases even present initially with GI symptoms, not with respiratory symptoms.

If I have new information? I don't. I can't find anything in scientific papers. Maybe it's there but I'm not finding it right now or not looking hard enough. In any case, I found some related lay press articles - not specifically about rebreathing, but FWIW:

https://apnews.com/afs:Content:8949990001

They do say that masks don't trap the virus and "Breathing out the virus is not going to appreciably change the amount that is there.” Which is precisely my claim.

This source doesn't even talk about rebreathing of viruses as one of the risks:

https://www.bbc.com/news/53108405

Same here:

https://www.statesman.com/news/2020...-about-effectiveness-of-masks-for-coronavirus

 

Your links are interesting even though they don’t address the topic specifically. I had not even heard the claim masks activate dormant retroviruses. LOL. Stress would be the only mechanism I know that could link the two and surely wearing a mask isn’t that stressful.

I don’t think the myths debunked in your links have any validity based on known science or logic. That’s why they are easily debunked. Brain infection was another good one I hadn’t heard. And brain infection was the context of the pull quote, not rebreathing and further infecting the lower respiratory tract.


I do think there is support for rebreathing being potentially harmful from both perspectives. I would think if solid evidence to the contrary existed it would appear in the list of debunked myths with these others.

As far as viral spread by blood....did you ever get to watch the interview of Dr. Marik you posted a couple weeks ago? He did a good job breaking down the difference between the infection and the out of control immune response in certain individuals. The data shows both asymptomatic and critically ill patients do quite well at eradicating the infection. It appears most damage to heart, lungs, clotting, etc. is caused by the immune system and occurs mainly after the actual viral infection is over. To determine whether blood infection is a player or not should be relatively easy by determining if viable virons exist in blood after being eradicated from areas like the upper respiratory tract etc. Of course you would have to test whether the virons isolated from blood and saliva have ability to infect using in vitro cell lines or something. Just using PCR to detect viral RNA would not suffice. I’m not sure why there is still confusion about the difference between detectable viral RNA and actual virons with the ability to infect cells, but I still see the two conflated regularly.

Anyway, as far as damage to different organs in individuals it looks to me like the evidence points to autoimmune dysfunction as the cause, not actual viral infection. I could be missing something, but if most damage is occurring after infection is mostly over and caused by cytokines etc., I don’t think we can blame blood viral spread on it’s own.

On to PCR testing and what it means in relation to re-inhalation of virus a bit of background on PCR. The whole point of PCR testing is to be able to detect very small amounts of genetic material (DNA or RNA) by isolating minute amounts and “replicating” it until we have enough to detect and identify. We have been using this technology to link criminals to crime scenes for decades now.

Here’s where it gets interesting to me. Until eight days after infection with SARS-CoV-2, nasopharyngeal swabs are unable to recover enough viral RNA to avoid high rates of false negative results. This mirrors information we have on varying times to symptom onset in individuals. In short, either virus is replicating much faster in certain individuals or this is dependent on initial infectious dose being larger in the group having earliest symptom onset and being able to test positive by PCR early.

So my argument is this. In certain individuals, viral replication seems to be a relatively slow progression. This could be caused by low initial infectious dose, a strong immune system, or a combination of the two. Some of these individuals would be right on the borderline of the virus outpacing ability of the immune system to deal with it. These would be the individuals affected by rebreathing virons. Individuals going from infection to symptoms in 2 days would fit in a group you described where billions of virons already exist early on and rebreathing is mathematically insignificant.

That’s what makes this virus so odd. So much variation in individuals in respect to progression, symptoms, and outcomes.

In respect to progression and contagiousness, I learned today some polymorphic enveloped viruses produce elongated virons early in the infection but more spherical ones as the disease progresses. Incidentally, the elongated virons are much more likely to infect cells. So even before viral shedding decreases, infectiousness decreases as disease progresses. Since SARS-CoV-2 is a polymorphic enveloped virus I’m wondering if this has been observed in C19.

Just another clarification. I’m not attempting to cast mask wearing in a bad light. I’m just looking for answers to questions nobody asks and answers to the question of why nobody asks the question.

 

Excellent points, but do realize that I did say that my quotes were not ideal and weren't directly addressing it but they were what I could find at the time, with limited time to search.

No, I haven't had the time to watch the interview yet. I had planned to do it last weekend, but I've been busier lately. This weekend I'll have to do some work from home as I'm falling behind with some paperwork (I do have remote access to our electronic medical records). And I have a long report to produce. Anyway, if I have some time I will but it's looking like it will be next weekend.

But no, there is a strong hypothesis that the endothelial cell damage may be caused by direct infection by the virus itself, as in, infecting the cells and destroying them. This is an older article so it's still saying it's unknown if the virus does play a direct role, but it's strongly hypothesized:

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30937-5/fulltext

Even in the lungs, in this other article:

https://www.nejm.org/doi/full/10.1056/NEJMoa2015432

And this one here, more recent, does affirm more categorically that direct lesion of the cells by the virus itself is responsible by 3 of the 5 mechanisms for the damage (EC here stands for Endothelial Cells); the first two are obviously direct without further explanation, and the 3rd one also derives from the presence of the virus inside the cells, because it's infected cells that get killed by recruited activated neutrophils (cytotoxic T-cells); only the 4th and 5th mechanisms are systemic and can act regardless of the cells themselves being infected:

https://www.nature.com/articles/s41577-020-0343-0

The above makes it very clear that blood-born spread is real. Hard to say which one predominates, but hey, it's 3 out of 5 mechanisms. So yes, viruses do spread blood-born, and yes, they do infect and damage the endothelial cells everywhere.

So, sorry, but I continue to think that rebreathing is not a significant mechanism to worsen the infection.

The fact that it was not debunked in the lay press articles I found, in my opinion only proves that it wasn't yet on their radar. Comparatively, I've heard this concern much less often. So you are right about "questions nobody ask."

 

Yep, I understand. It’s often hard to find specific information. It can eat up a lot of time. I’ve spent a lot of time looking for information on this subject and there just isn’t much. Even confirmation that high initial dose leads to more severe outcomes is just now emerging. I’ll admit there isn’t enough information to come to a definitive conclusion, but what we do have certainly doesn’t conflict with what I’ve proposed.

Paperwork. The worst part of every occupation. I’d tell you to be careful and take care of your immune system but it would be a hypocrite preaching to the choir. LOL

I’m not disputing that blood infection can occur. Im saying it isn’t in play when rebreathing would be an issue. I’m addressing this statement.

The billions of viral copies I’ve addressed by showing early in the infection/incubation period there are not as many virons in play as we imagine. Not enough to detect with PCR that has the ability to amplify minute amounts of RNA. Early on I maintain each newly infected cell matters, exponentially—just like with the initial dose. I don’t see any evidence to the contrary.

On the issue of blood spread, it is not possible for it to be a factor at the time rebreathing would be in play. Blood infection only occurs after severe damage has been done to the lungs, many days on average after the period of time I’m talking about with rebreathing. The current theory is that coughing (a symptom) may sever blood vessels in the lungs allowing blood to become infected. The time period rebreathing would have impact is pre-symptomatic. Blood infection is post symptomatic.

As far as the mechanisms of damage to endothelial cells, certainly there is a case for some damage being caused directly by infection. Your links were informative and I learned several new things from them. I’m hesitant to attribute a majority of damage to direct infection for a couple reasons. First, treatments that are effective slow down and regulate the immune system. The effectiveness of the MATH+ protocol you introduced to the forum bears this out in my opinion. Second, the references to cell lysis concerns me. Enveloped viruses do not lyse cells, they bud from them, leaving the cell alive for a matter of time until the phospholipid bilayer of the cell wall is depleted. Lysis of cells with an enveloped virus must be caused by Pyroptosis which is a function of the immune system inflammation response which is already out of control at the point of endothelial cell infection. Maybe I’m picking nits, but I’m not convinced there would be as much damage to EC’s (infected or otherwise) anywhere in the body in late stages of infection if an overactive immune response wasn’t happening. One point I base that on is the feedback loop of lysed cells triggering even more immune response than if budding infected cells died less violently.

That’s fair but I’ve yet to see any evidence it is not. Only that it may be.

If there isn’t an answer in the negative, and I think I’ve presented a pretty good case there isn’t, why not keep asking the question until there is?

 

Wow, huge day of work from home... Only finished now and it's not over (I mean, only stopped now, will have to continue tomorrow).
Anyway, you again make good points. I'd still question the idea that pulmonary symptoms always precede blood-born spread, given that some patients present first with non-respiratory symptoms, even GI symptoms. But I know what's going on. I'm being uncharacteristically stubborn in discounting this possibility and being kind of narrow-minded about it which is kind of not typical of me, I hope. What is happening, I have to confess, is that I'm fighting tooth and nail against what you are saying not because you are not making good points, but because I shudder when I think that less informed people may read this and run rampant with it, yelling "see? masks are detrimental! Don't wear them!" Which would do a lot more harm than good.

Think of it... if in the very early phases masks might increase viral load and pulmonary seeding to some degree (which I still think might be minor), their benefits in preventing the infection to start with, seem to me to outweigh these possible, unproven, maybe minor risks. But yes, I have to acknowledge that this is a possibility... but one that I am not eager to highlight, LOL, similar to how I rarely talk about ADE regarding vaccines...

We have enough misinformation making masks and vaccines unappealing... if we add to them, real concerns but not that likely and not that frequent concerns, we'll be doing more harm than good to public health.

How many worsened viral loads we'll have as compared to the thousands of prevented infections with masks?
How many ADEs we'll have as compared to the millions of prevented infections with vaccines?

See my point?

But it's not the most honest way of debating a point, I acknowledge. Sorry...

I guess I mean well.

Like Fauci when he spoke against masks...

But hey, I did get mad at Fauci for that, so it's justified if you get mad at me for this.

Cheers.

 

I understand your position. I’m too stubborn to stop pursuit of information that may benefit individuals over the collective. Or just too stubborn to not pursue knowledge for knowledge’s sake. LOL

I’ve tried to be clear to the forum I’m not anti mask and am not pushing this issue to influence someone not to wear a mask. In fact, I’ve spent considerable time researching and advocating for wearing masks at home where asymptomatic and pre-symptomatic transmission is more likely to occur than in public. I well understand the challenges of getting people to base their decisions on evidence as opposed to public opinion or instruction from authority not based on science. As far as I know, I’m the only member here who isn’t anti mask to some degree. Many here who claim to be pro mask are vehement anti maskers in reality.

I know my position is confusing to many because I’m not authoritarian. It’s hard for many to wrap their head around the idea someone can base positions on evidence, advocate for those positions, care about people, and still not wish to force anyone to behave a certain way.

Your points on individual and public protection of uninflected mask wearers outweighing individual potential harm to early infection mask wearers are valid. If we had a way to know exactly when infection occurred in the individual and could tailor behavior from that point on to benefit both the individual and the public, this would all be meaningless debate. Alas, we haven’t the tools no to know when infections occur so we have to do the best we can. That’s what you are doing in good faith. There’s no reason to be upset about that.

 

I have nothing against your position and I share the non-authoritarian approach. I've always said, it's best to inform and educate, allowing the person to make an autonomous decision, than to try to force one.

"As far as I know, I’m the only member here who isn’t anti mask to some degree." Hey, I'm here too... (It makes me think of Kamala Harris' response to Joe Biden when he said there is only one woman of color in Congress, LOL).

You know, this issue, may a mask slightly increase the viral load in the very beginning and spread pulmonary seeding, versus the good it does in preventing the infection in the first place, is really hard to know with certainty (you and I have agreed that a large trial to look into this is not likely to occur - and to the reasons I've already suggested, I'd add, I think researchers would be wary of starting one, the issue getting to the lay press ahead of conclusions, resulting in a high number of people abandoning mask use, with the contagion then ballooning). It is ultimately similar to the early debate about ACE inhibitors and ARBs *theoretically* increasing the susceptibility to COVID-19, versus the good they do in keeping blood pressure under control, given that hypertension is one of the risk factors for severe disease course in COVID-19. How do we compare the risks and benefits?

Ultimately the debate was settled in favor of continuing ACE inhibitors and ARBs for patients who are already on them. This conclusion came out of a large case-control study, very well-matched, that showed no association between these drugs and severity of disease.

https://www.nejm.org/doi/full/10.1056/nejmoa2006923

Again, this is not an RCT, for the same ethical reasons. You can't simply double-blindly give ACEis and ARBs versus placebo to randomized healthy people with no hypertension and expose both groups to the virus because we are not supposed to give to someone a medication that is not needed or indicated, which carries risks of side effects; and this design wouldn't answer the question about the good that these drugs do versus the risk because they wouldn't be doing any good (they would just make people have hypotensive episodes (some of them might get dangerous; think of falls and broken bones or car crashes). The only way to really get to a very final answer would be to get two randomized similar groups of patients with hypertension who are already on ACEis and ARBs and then let one group continue the medication while the other group would have their active medications replaced with placebos, and then expose them both to the virus. This could be done blindly: all patients in both groups would have their regular home medication replaced with study tablets, half of which would be placebos and the other half real ACEis and ARBs. But again, that's quite dangerous to do. The patients for whom we'd be withdrawing effective treatments that they need and on which they did well, would be exposed to a severe risk of rebound hypertension, strokes, and heart attacks. So, no can do.

Similarly, the only remedy for masks would be a large case-control observational, retrospective study - and you and I know that the answer these provide is imperfect. For one thing, there would be a HUGE intervening factor: the viral load for the unmasked group might get higher because they'd be breathing in more virus from the environment, not benefiting from the partial filtration provided by the masks. The study's conclusion might be hopelessly flawed; viral loads in the masked ones might get slightly higher due to rebreathing but masks would be considered harmless when compared to a group with... even higher viral loads, although in reality the masks might have indeed slightly increased viral load, so, not 100% harmless as the study would indicate.

Anyway, have you thought of it this way? Say, a high filtration mask used the right way (say, an ASTM level 3 mask with enhanced seal from the use of rubber bands to keep it tighter, delivering according to studies, a filtration of 0.1micron particles at a rate of 98%) would still get a patient infected with the SARS-CoV-2 from walking into a cloud of particulates expelled by an infected person. However that patient would absorb only 2% of that cloud and get a tiny viral load. But then through rebreathing, let's say that viral load would go up by 25%. That would put that person at a load of virus of 2.5%. Compare this with the unmasked person who would breathe it all in with not filtration, resulting in... 100%. What would you prefer? A viral load of 2.5% of what it could have been, or a viral load of 100% of what could get in?

It's interesting to think that for the individual, N95s with exhalation valves are the perfect solution... high filtration from the outside to the inside, and no trapping and rebreathing because it all goes out through the exhalation valve. It doesn't protect public health, though.

I actually have adopted a hybrid solution for myself. I wear an N95 with an exhalation valve enhanced with a neoprene rubber brace. That's extremely good seal. Nothing comes in that doesn't travel through the mask's filters. But donning and doffing an N95 and installing the rubber brace on top of it is time consuming and complicated and needs a mirror to perfectly position the brace. So it's not the easiest thing to do on the fly. So if I'm out shopping for example and need to go in and out of multiple stores, what I do is that I don everything in advance inside my car, using the vanity mirror. Then I keep an ASTM level 3 facemask in my pocket. While I walk from the parking to the store, I'm benefiting from the exhalation valve which keeps it all cool and comfortable (as you know, outdoors under the sun and wind, I'm really not putting anybody at risk). When I approach the store I don the ASTM level 3 mask on top of the exhalation valve so that I protect other customers. I shop, and when I come out of the store and while I walk to a neighboring store, I doff the ASTM mask and get things cool and comfortable again and get better O2-CO2 exchange.

This initial paper of yours, about the attempt to make one-way masks that would prevent the trapping of the virus for the already infected person, is kind of crazy. Ultimately it is the same as an N95 mask with an exhalation valve. But what is the point? Again, the person is already infected... so the one-way mask or the one with the exhalation valve would still allow that person to shed the virus into the environment... defeating the purpose of wearing a mask to protect others... while doing little for the patient because the patient is already infected... so it would make more sense to just not wear a mask at all... (except in a really highly contaminated environment where that patient would be breathing in more viruses expelled by others) but then, what does that do to the healthcare workers interacting with the patient or family members if the patient is at home?

So, I think, ultimately this whole thing is a bit off. Maybe there is a small increase in viral load through rebreathing in very initial phases of the disease, but this is probably counteracted by the smaller initial viral load that gets in through the mask's filtration to start with, making the whole point ultimately moot, and making of mask use an advantageous strategy anyway.

 

Good analysis of the pros and cons. I agree, that’s why I said the only way to protect both the wearer and others is to know exactly when infection occurs and modify mask wearing behavior on that knowledge. Otherwise you are just playing odds that do favor continuous usage.

Of course there are other ways to deal with the conundrum, like wearing a mask very short periods of time when you MUST be around others and seriously social distancing the majority of the time without a mask. But that isn’t “convenient” so it’s off the table.

I’ll repeat here what I try to convey when I advocate for mask usage in places besides public venues. I’m not trying to tell anyone what to do. I don’t even know anyone’s circumstances to know what’s best for them. I want people to think about why they are doing things a certain way and to consider they could likely come up with better personal protocols to protect themselves and others than what is recommended by bureaucracies. One size fits all recommendations or mandates aren’t necessarily best for you, your family, or community. Wearing a mask just in public places doesn’t mean you can do anything you want and go everywhere that pleases you and still be personally safe and protective of others. They aren’t talismans. They are tools that used properly have an important function. Think about how to leverage their usefulness beyond the generic “masks in public” recommendations.

Perhaps rebreathing virus isn’t consequential. You’ve pointed out the roadblocks to determining if it’s significant or not. But regardless of whether we ever get a definitive answer, I think there is value in examining the issue. Looking at things from every angle helps us apply critical thought and leads to us making correct decisions on things like masks even if someone like Fauci is being less than honest with us in the future. We as a country are supposed to be citizens who are informed and capable of making wise decisions on our own. We are not supposed to be (or have to be) told what we must do.

I believe you had a thread on antigen tests a while back. If something like that could inform us in real time when infections occur the rebreathing thing may be more relevant. For now I’m content to just keep learning about the underlying science.

Oh, on the “I’m the only member here who isn’t anti mask to some degree” I guess I’m not sure of a few people’s position. I just discovered some of the members most insistent on masks in public are vehemently opposed to their use in private. I’m glad to have you on board!

 

I'll wear a mask when prostitutes are required to use condoms, Fair is fair.

 

Good post. Nothing to comment on it, given that I agree with everything you're saying. Thanks.

 

thank you for posting this and confirming the elitist mentality

Please go to Australia where they masked up, locked down, tanked the economy, yet are now in lockdown 2.0 because masking up and locking down does jack ship

virus gonna do what virus gonna do

herd immunity is needed

 

Trust in the scientific process is now considered elitist.

There it is. Your new campaign slogan. Vote Team Red - we promise to ignore science!!!