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Most of us Lyme people know that modern medicine has failed us. In general, you know what I mean. The people telling us the science are wrong (IDSA). I feel this is a similar situation. Little or nothing they have said so far has worked or IMO, been correct. Rebreathed air is the problem with COVID, it is not influenza. If you want to stop spit and coughs, wear a mask and you can do that. SARS-Cov-2 goes through a mask like it isn't even there. I was looking at a standard medical mask under my microscope the other day and I hate to tell you, it's a very open weave. I would bet it stopped less than 50% of airborne viral particles. Some will argue that 50% is better than nothing, I say it is not. How long you stay in the rebreathed air and how concentrated the CO2 level are more important. If it does bind CA like all indications point to, then your increase in CA activity due to increased CO2 from wearing a mask would be much more important than a 50% drop in circulating viral laden droplets. I want to stop this virus and I will do whatever I can to do it, but mask wearing won't stop it. To stop it, you have to ventilate indoor areas and keep CO2 levels down.

GH said...
An older study I read showed that TB could not grow in oxygen, it required CO2 to grow. This may also apply to SARS-COv-2...

I’m hesitant but I have to ask... Why are you looking for similarities between sars-cov-2 and the bacteria that cause TB?

GH said...
...the way it see it is that the virus enters the cell at the ACE2 receptor but there are things that can bind the inside of the ACE2 receptor and prevent entry into the cell. Carbonic anhydrase is such an item. With high oxygen levels and little CO2 to deal with, CA stays attached and prevents entry. With inadequate cellular buffering capacity, zinc and/or Vitamin D are in lower concentrations and CA doesn't stay attached to ACE2. This allows the viral replication process to occur after the virus enters the cell.

So sars-cov-2 is binding ACE2 and CA is just in its way preventing it from entering the cell (until blood CO2 rises and CA needs to leave)?

What makes you think CA would be able to block entry in this way?

It seems this process would not lead to RBC damage in covid-19 as RBCs do not express ACE2.

Post Edited (potsnpans) : 12/24/2020 7:55:51 AM (GMT-7)

I am pretty adept at cross referencing health related topics. Some of my searches show no results, some show many. The CO2 TB connection just came from a lot of reading. CA inhibitors like acetazolamide have an inhibitory effect on Pseudomonas and CA is linked directly to disease progression in malaria (and I assumed other) diseases. We know that antibiotics and at least one pathogen bind CA inside the cell. There are 16 known CA and I focused in on CA II and CA IV. One inside the cell, one outside the cell. There are multiple references now that refer to CA and it's role in COVID. They are looking for answers like I am but we are on the same page. Back in March, I stated I thought the terminal protein on SARs-Cov-2 was 32 kDa and haven't seen anything to change that opinion. CA is bound to ACE2 inside the cell but is released to move around. Zn and Vitamin D levels play a role in this I am certain. When more CO2 is present, CA is released to do what it does. Does that open up the ACE2 receptor for easier viral entry? I believe we need less CO2 in our system to lessen viral load.

When I looked into "What would happen if SARs-Cov-2 bound CA?" is when I came up with my hypothesis. The progression of disease for COVID-19 directly parallels the inconsistent activity of CA. It's a intracellular acid-base problem that must be rectified at any cost. Sometimes that cost leads to one's death.

Astro - my store with an 8 ft ceiling and small square footage is the one we have CO2 issues with. It also has more employees and more foot traffic. Trajectory doesn't play a big role in COVID as the particles can linger for hours. Scientists pulled the virus out of the air 16 feet from a bed ridden patient. SARs-Cov-2 is not influenza. I agree with the ceiling height, building volume plays a big role because of the air circulation.

GH said...
When more CO2 is present, CA is released to do what it does. Does that open up the ACE2 receptor for easier viral entry?

Well that's what I'm asking about.. is it physically possible for CA to block entry in the first place, and why should we believe that it does? Seems to be the crux of your argument around the amount of breathed CO2 increasing viral load.. I thought you would have more insight here.

GH said...
When I looked into "What would happen if SARs-Cov-2 bound CA?" is when I came up with my hypothesis.

Why would a virus evolve to bind an enzyme that prevents it from replicating?

Georgia Hunter said...
Number one, this virus didn't evolve.

Are you now suggesting that the virus was genetically engineered/modified to bind CA? Please go on...

I think it's much more likely that sars-cov-2 originated in nature. Just how many leaps of faith am I going to have to make here to find support for your hypothesis?

I still would like to know if it's even physically possible for CA to block viral entry into cells w/ ACE-2.. regardless of whether the virus was engineered to bind CA or not.

Georgia Hunter said...
Number two, survival of the fittest. Sicker, less healthier people would be more vulnerable to such a virus or pathogen.

So it's selecting for hosts that it would be more likely to kill? ... doesn't really add up.

Maybe I'm misunderstanding you, but "survival of the fittest" means virus vs virus with a random mutation.. not virus vs host. For a feature like binding CA to win out, it needs to somehow have a net positive effect on replication.. or maybe something to do with transmission. Evolution is not always so straight forward of course, and if you're saying that the virus was genetically modified, then I guess it's possible that this wouldn't apply at all.

Post Edited (potsnpans) : 12/25/2020 9:17:05 PM (GMT-7)

Hard to keep up will all the questions, here is a quote:

"Viruses cannot attack cells that do not bear the appropriate receptors, but they will attempt to infect cells that do, even if those cells are not suitable for viral propagation. If the receptor-expressing cell cannot support replication of the virus, then the virus will spend itself fruitlessly in an attempt to infect it. This idea can be advantageously applied by using selective expression of viral receptors to redirect virus to nonproductive cells, thus protecting susceptible tissues. We propose that erythrocytes are the ideal instrument for this strategy, because these cells are present in vast numbers, permeate every organ, are easily manipulated, are relatively disposable, and cannot serve as hosts for viral replication.

Erythrocytes are simultaneously the most numerous and the simplest cells in the body. In their mature form, they lack the nuclei and organelles required to replicate nucleic acids and elaborate proteins. Because viruses depend on the use of the host cell machinery to replicate, erythrocytes are invulnerable to viral infection. The redirection of virus to erythrocytes has the potential to attenuate infection by leading virions to a dead end, leaving fewer infectious particles free to invade susceptible tissues."

This is one way the body tries to reduce viral load but at the same time, it is reducing oxygen carrying capacity by the virus binding heme oxygenase II. At some point, the viral load overcomes the strategy.

As for experiments with CA Inhibitors, yes, they have been done. In low doses early in the disease process, they were beneficial. At a point later in disease progression, they become extremely detrimental. This follows my thinking.

I don't agree with your statement on selecting hosts it would more likely kill. A virus's goal is to spread and the ultimate outcome of the host is irrelevant if it spreads. Pathogens have always done this, it is nothing new. The only issue is with E bola which kills the host so fast if doesn't have time to spread. SARS-COv-2 doesn't have that problem.

I believe the virus was made in a lab (by Americans) and either got out accidentally in Wuhan or was intentionally released. The North Carolina professor didn't get arrested for making cookies and it has been hush-hush since then.

As far CA, it is bound inside the ACE2 receptor in a complex. There are a couple of natural isoforms of the ACE2 receptor in humans, an open form and a closed form. The intracellular components bound to that receptor can alter the isoform. I have not found that anywhere in the literature for ACE2 but that is the basis of my hypothesis. Internal molecules often determine the exterior configuration of a membrane bound molecule. That is just common molecular biology. As carbonic anhydrase is released from the complex, it opens the ACE2 receptor. That the basis of my thoughts in a nutshell. The more CO2 inside the cell, the more CA is released. This allows viral entry and once inside, it binds CA or it could possibly bind the inside of the ACE2 and prohibit CA reattachment to the ACE2. Either way, there is a reduction in CA activity. I believe this is absolutely zinc related in some way. Since CA is pH dependent, it fails to work at some point which leads to massive ROS and oxidative stress. Early on during the pandemic, they didn't give supplemental oxygen for fear of disseminating the virus. Now, O2 is standard therapy and the survival rates have gone way up.

Vitamin D binds CA. People with high Vitamin D don't have issues with COVID-19. Since supplementing with higher doses of Vitamin D, the survival rates have gone up. Both O2 and Vitamin D increasing survival goes along with my hypothesis. Limiting CO2 would be another and it was shown to be true with TB patients. That is how I came across the literature. The Pseudomonas reference came from a CA study which would theoretically support my hypothesis as well. Please don't go into bacteria, viruses, and protozoans being different. I am aware of the differences. The fact that CA is already known to be bound by pathogens is the point I was trying to make.

Pillin said...
So boring the mask discussion.

Why does poeple makes it a political philosophical or religious issue?

Simply a nonsense. If you could ask those who died because of not wearing the mask, you would change your mind.

Merry Christmas to all!

I know multiple people who have died and got COVID while wearing a mask. Early on, I advocated that everyone should wear a mask. If you read what I read, you would change your mind. It has nothing to do with politics. If you don't have anything positive to add to this thread, please refrain from making statements about politics.

I'm just going to give up because you do not understand what I am trying to say. You do not have to believe what I am saying, that is fine. Until they find out what is going on, I am sticking with my statements. Everything I find is supporting it.

I mentioned CD147 in one post and how it binds CA IV but that is extracellular. That is different. I think CD147 comes into play as things start going south because of the pyruvate and lactate.

One more time, my opinion is that if CA II is attached to ACE2, the virus can't enter. If more CO2 is present, then less CA II will be bound to ACE2 and the virus can enter and replicate. The virus binds unattached CA II and prevents it from attaching back to ACE2. CO2 is broken down into HCO3 and water raising pH until CO2 eventually builds up which lowers pH inside the cell. No one knows exactly what is going on and I won't speculate any further, there are just too many things that could go wrong.

Yes, I said CA binds ACE2 like it was not in question. It is not a question because it is a fact. I have 53 references saved on my home computer about COVID. I own 11 computers. I have 5 times that number of scientific references saved on my other computers. I am basing my opinion on what I am finding and using TB or malaria to track a parallel path is not a far stretch. I've looked at many more pathogens but they did not fit the progression of disease I was finding. TB can't grow in oxygen and the more CO2 present, the more infectious it is. An article came out this week that Horowitz posted and it said that scientists believe that removing more trees from the earth would increase more viral infections. Our air goes up about 2 ppm of CO2 per year. That just coincides with what I have been saying. Fewer trees, more CO2 and more viruses.

I said that the virus was entering through our eyes and many scoffed at that. I saw an article this week that said that people who wear glasses have a lesser chance of getting COVID than people who don't wear glasses. The numbers were about 6% of the people who wore glasses got COVID where 31% of that population had glasses.

I don't understand your obsession with RBC's. They have nothing to do with viral replication but the virus can bind the CA II inside them along with heme oxygenase II and prevent the cell from carrying as much oxygen. This is what ultimately causes breathing difficulty.

As for articles on CA inhibitors and COVID, the first search I looked at showed 1780 references. On the first page 5 articles were directly related to it. I didn't look any farther.

Please search acetazolamide and COVID. You are acting like there has been no use of CA Inhibitors in COVID patients.

Think a little for me, if SARS-Cov-2 binds CD147, and CD147 binds CA, then is it possible for SARS-Cov-2 to bind CA? I said in March that SARS-Cov-2 had a 32 kDa terminal end protein but haven't seen any literature to get closer to that hypothesis. The science isn't there yet.

I stand my my statement of the virus binding CA increases viral load. You can say that it is not true but nothing has been shown to prove it is not true. Combined with the other things I've found about the virus, I stand by the statement. I may be proven wrong next week but that is science. That is why it is called a hypothesis.

What is the reason you brought up CD147?

CD147 is certainly involved in the process, it's one of several things that "go wrong." IMO, the cellular dysfunction that occurs is because of a cellular pH issue. One of the things that CD147 does is facilitate the transport of lactate and pyruvate through the cell membrane. Altering that function could certainly cause pH issues and may play a big factor in the progression of the disease. I see it as not being a first stage problem but occurring after having CA issues. The main cellular buffering agent is CA making HCO3 and that is why I focused on it. Add in that other pathogens are known to alter its level and that is why I went in that direction. I have no agenda and will focus elsewhere when and if turns out to be a dead end. I have only found things to strengthen my argument, not weaken it.

This article basically explains what I say happens in COVID patients. Just replace endometriosis with COVID and for the most part, everything fits as far as progression of disease. COVID is much more severe and causes the RBC's to no longer carry as much oxygen.

https://www.sciencedirect.com/science/article/abs/pii/s1472648314000728