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CV19: New York 21% infection rate + 40% Existing T-Cell immunity = 61% = Herd Immunity ?

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3 hours ago, specinho said:

Mistakes or changes occurring inside of a cell will generally provoke an immune response called programmed cell death....... Signals will be sent out. Autolysis would be initiated, or T killer and macrophage would be called upon to action.

Programmed cell death has a name: apoptosis. It is the method by which all organisms die and is highly related to the length of the telomeres, the little aglets that cover the end of the chromosomes. 

On the other hand, genetic mistakes are handled by a DNA repair mechanism, which consists of a packet of enzymes. Imagine a little railroad car running along the double-stranded DNA--the double helix. This thing constantly measures stoichiometry of fit: how many angstroms apart the two strands are. A genetic mistake will throw the "fit" out of kilter and the railroad car will stop, whereupon a cleavage enzyme will remove that genetic mistake as a cluster of nucleic acids--oligonucleotides. Another set of enzymes selects the appropriate nucleic acids to provide for complementarity and stoichiometry of fit. 

Every cell contains a genomic repair packet. They vary in how well they function. If a cell endures a small amount of say UV radiation, its repair mechanism can usually handle it. If it receives a lot of radiation, the damage incurred may overwhelm the repair mechanism. The horseshoe bat in which SARS and Covid-19 reside has an incredible repair mechanism--the only bat to fly, it creates zillions of free radicals. Humans lose their repair mechanisms as free radicals accumulate, their telomeres shorten and their repair packets age. 

That's the reason we're more apt to develop cancer as we age, and also become more vulnerable to infections of all types. Since one out of every million cell replications creates a genetic accident (most die but some become cancer cells), there's always something for T-cells to do and also for DNA repair mechanisms to do. In the case of Covid-19, if you can't muster a good T-cell response, you're not going to do well. That's usually: aged, diabetic, hypertensive, obese, those with high levels of von Willebrand Factor. Going into the hospital with Covid-19 and an A1C-Hgb >7 predicts a dismal prognosis, probably as bad as a low lymphocyte count. 

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On 7/15/2020 at 1:00 PM, Gerry Maddoux said:

Programmed cell death has a name: apoptosis. It is the method by which all organisms die and is highly related to the length of the telomeres, the little aglets that cover the end of the chromosomes. 

On the other hand, genetic mistakes are handled by a DNA repair mechanism, which consists of a packet of enzymes. Imagine a little railroad car running along the double-stranded DNA--the double helix. This thing constantly measures stoichiometry of fit: how many angstroms apart the two strands are. A genetic mistake will throw the "fit" out of kilter and the railroad car will stop, whereupon a cleavage enzyme will remove that genetic mistake as a cluster of nucleic acids--oligonucleotides. Another set of enzymes selects the appropriate nucleic acids to provide for complementarity and stoichiometry of fit. 

Every cell contains a genomic repair packet. They vary in how well they function. If a cell endures a small amount of say UV radiation, its repair mechanism can usually handle it. If it receives a lot of radiation, the damage incurred may overwhelm the repair mechanism. The horseshoe bat in which SARS and Covid-19 reside has an incredible repair mechanism--the only bat to fly, it creates zillions of free radicals. Humans lose their repair mechanisms as free radicals accumulate, their telomeres shorten and their repair packets age. 

That's the reason we're more apt to develop cancer as we age, and also become more vulnerable to infections of all types. Since one out of every million cell replications creates a genetic accident (most die but some become cancer cells), there's always something for T-cells to do and also for DNA repair mechanisms to do. In the case of Covid-19, if you can't muster a good T-cell response, you're not going to do well. That's usually: aged, diabetic, hypertensive, obese, those with high levels of von Willebrand Factor. Going into the hospital with Covid-19 and an A1C-Hgb >7 predicts a dismal prognosis, probably as bad as a low lymphocyte count. 

In 1983/84 a cancer specialist explained the primary cause of cancer to me, along the way he took the time to explain T-cells function in the body. Or perhaps better said how they react to the body...as to why they failed was a mystery he just looked at me said that is how life comes and goes...I find it incredible it has taken so many yrs to understand their beginnings and how we are preprogrammed from the very beginning...It seems Science and i use that word loosely is caught in analysis/paralysis...It makes one wonder what a few stem cells and a fat old thymus gland would produce...But then there would to yrs of study....grants...careers reputations....business interests to consider...What has science become?

 

Edited by Eyes Wide Open
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Lots of good science out there, especially in immunology and T-cell function, as well as DNA repair mechanisms. We're just not seeing much of it right now, as that sort of thing takes time.

The Wuhan Institute of Virology has had since 2002 to study and engineer the old SARS virus. I'm willing to say that they were engineering it for gain of function, and that it escaped the lab before they had a vaccine. It should be noted that SARS escaped labs in Taiwan, Singapore and Beijing before they finally moved it to Wuhan BSL-4.  

Suddenly, this very sophisticated virus got away. Only then was it discovered by Americans that it has the potential to damage heart muscle, the endothelium of blood vessels, use its "can-opener" to claw its way into the cell via ACE2 and furin-cleavage, and to replicate primarily--and silently--in the cells of the upper respiratory tract before dumping the whole load into the alveoli, setting the stage for the fabled cytokine storm. Any treatment has been discovered on the fly.  

It's hard enough to study a novel chimeric virus under controlled conditions but doing so under these wartime conditions is especially tough. Combine that with the fact that the whole thing has been politicized, coming during an election year, and you've got a real rodeo. Not only that but the phylogeny of the virus has to be tracked on a daily basis--otherwise, it could mutate and create a whole new chimera (which I strongly suspect it has done). The virus studied at St. Petersburg seems to cause thrombosis especially in those with high levels of Von Willibrand Factor. Whether that occurs in Florida and Texas is another question. Here in the U.S., the thing seems prone to go for the heart muscle (myocarditis).

What a mess! We are desperately in need of a convincing, young, articulate physician to keep the public appraised of the situation in a totally apolitical way. They are plentiful, but also without the means to move up the ladder and take up the gauntlet.  

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(edited)

Looks like a vaccine race between Oxford and Moderna Pharma.  Both starting their phase 3 before end of the month.

Oxford leaked very promising data data . Great immune response with both antibodies + T- cells.  Oxford working with U.S. pharma Astra Zenaca. 

A paper on Oxford results published in the Lancet this coming Monday. 

https://www.theguardian.com/science/2020/jul/16/covid-19-vaccine-what-have-we-learned-from-oxford-phase-one-trial

Study on T- cell efficacy 

https://www.sciencemag.org/news/2020/05/t-cells-found-covid-19-patients-bode-well-long-term-immunity

Edited by BLA
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16 hours ago, Gerry Maddoux said:

Programmed cell death has a name: apoptosis. It is the method by which all organisms die and is highly related to the length of the telomeres, the little aglets that cover the end of the chromosomes. 

On the other hand, genetic mistakes are handled by a DNA repair mechanism, which consists of a packet of enzymes. Imagine a little railroad car running along the double-stranded DNA--the double helix. This thing constantly measures stoichiometry of fit: how many angstroms apart the two strands are. A genetic mistake will throw the "fit" out of kilter and the railroad car will stop, whereupon a cleavage enzyme will remove that genetic mistake as a cluster of nucleic acids--oligonucleotides. Another set of enzymes selects the appropriate nucleic acids to provide for complementarity and stoichiometry of fit. 

Every cell contains a genomic repair packet. They vary in how well they function. If a cell endures a small amount of say UV radiation, its repair mechanism can usually handle it. If it receives a lot of radiation, the damage incurred may overwhelm the repair mechanism. The horseshoe bat in which SARS and Covid-19 reside has an incredible repair mechanism--the only bat to fly, it creates zillions of free radicals. Humans lose their repair mechanisms as free radicals accumulate, their telomeres shorten and their repair packets age. 

That's the reason we're more apt to develop cancer as we age, and also become more vulnerable to infections of all types. Since one out of every million cell replications creates a genetic accident (most die but some become cancer cells), there's always something for T-cells to do and also for DNA repair mechanisms to do. In the case of Covid-19, if you can't muster a good T-cell response, you're not going to do well. That's usually: aged, diabetic, hypertensive, obese, those with high levels of von Willebrand Factor. Going into the hospital with Covid-19 and an A1C-Hgb >7 predicts a dismal prognosis, probably as bad as a low lymphocyte count. 

Flu season will be less than 3 months away.  What do you think will happen when a person catches BOTH Covid19 and the flu?

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One or the other would activate the immune system, which would hopefully prevent a concomitant infection. However, if that occurred, it would likely spell disaster. 

I suspect there will be a bigger audience for the flu vaccine. And certainly for Covid-19, if one is obtained. 

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17 hours ago, Gerry Maddoux said:

Programmed cell death has a name: apoptosis. It is the method by which all organisms die and is highly related to the length of the telomeres, the little aglets that cover the end of the chromosomes. 

On the other hand, genetic mistakes are handled by a DNA repair mechanism, which consists of a packet of enzymes. Imagine a little railroad car running along the double-stranded DNA--the double helix. This thing constantly measures stoichiometry of fit: how many angstroms apart the two strands are. A genetic mistake will throw the "fit" out of kilter and the railroad car will stop, whereupon a cleavage enzyme will remove that genetic mistake as a cluster of nucleic acids--oligonucleotides. Another set of enzymes selects the appropriate nucleic acids to provide for complementarity and stoichiometry of fit. 

Every cell contains a genomic repair packet. They vary in how well they function. If a cell endures a small amount of say UV radiation, its repair mechanism can usually handle it. If it receives a lot of radiation, the damage incurred may overwhelm the repair mechanism. The horseshoe bat in which SARS and Covid-19 reside has an incredible repair mechanism--the only bat to fly, it creates zillions of free radicals. Humans lose their repair mechanisms as free radicals accumulate, their telomeres shorten and their repair packets age. 

That's the reason we're more apt to develop cancer as we age, and also become more vulnerable to infections of all types. Since one out of every million cell replications creates a genetic accident (most die but some become cancer cells), there's always something for T-cells to do and also for DNA repair mechanisms to do. In the case of Covid-19, if you can't muster a good T-cell response, you're not going to do well. That's usually: aged, diabetic, hypertensive, obese, those with high levels of von Willebrand Factor. Going into the hospital with Covid-19 and an A1C-Hgb >7 predicts a dismal prognosis, probably as bad as a low lymphocyte count. 

To expand on this quality post the UV light "bends the rails" by two neighbouring T's dimerizing.

tt cancer.png

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11 hours ago, Gerry Maddoux said:

We are desperately in need of a convincing, young, articulate physician to keep the public appraised of the situation in a totally apolitical way.

We have one in Alberta.  Very calm and articulate, and holds peoples attention.

 

 

dr hinshaw.png

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6 hours ago, Enthalpic said:

To expand on this quality post the UV light "bends the rails" by two neighbouring T's dimerizing.

tt cancer.png

Believe it or not, I did the original research on cyclobutane moities of pyrimidine dimers created in Reovirus, a double-stranded RNA virus way back in 1966-'68. It is very interesting to see how far the research has come in this area. Back then we labeled using tritiated thymidine and then measured oligonucleotides that were excised in an attempt at repair. In those oligonucleotides was, of course, tritiated cyclobutane moities, and the more the better the repair mechanism. 

The betacoronaviruses and influenza are single-stranded RNA viruses and therefore don't contain "repair mechanisms," per se, because all the known repair trains work on stoichiometry of fit (1.54 A units, as I recall). But single-stranded RNA viruses don't make many mistakes either.

It would be something evil and altogether frightening if a chimera were to be formed by recombinant genomes between the influenza and the covid-19. I think this would be in short-segment fragments. However, whoever would have thought it possible that the genomic sequences between coronaviruses in the Malaysian pangolin and the Chinese horseshoe bat would be so similar? And that they would combine resources to develop the "can-opener" having to do with the ACE2 and the furin-cleavage?

To me the likelihood of this accidental bumping up against nature--using betacoronaviruses from a flying mammal (the horseshoe bat) and a land-locked animal (the Malaysian pangolin)--coinciding so naturally, despite being so widely separated in geographic existence, is almost a theoretical impossibility. Of course, the wet market has been blamed, but it is now my understanding that not only would no self-respecting Chinese eat the pangolin, but that it has been illegal to sell pangolins for food at Chinese wet markets for some time. 

This poses an interesting conumdrum for the CCP to explain away. It makes it so much more likely that the WIV was using gain of function to make the virus worse in order to make the vaccine better . . . and the virus got away from them. These things are very, very, very hard to keep in the laboratory, just like the slippery Reovirus.  

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(edited)

On 7/16/2020 at 4:00 AM, Gerry Maddoux said:

Programmed cell death has a name: apoptosis.

On the other hand, genetic mistakes are handled by a DNA repair mechanism,

In the case of Covid-19, if you can't muster a good T-cell response, you're not going to do well. That's usually: aged, diabetic, hypertensive, obese, those with high levels of von Willebrand Factor. Going into the hospital with Covid-19 and an A1C-Hgb >7 predicts a dismal prognosis, probably as bad as a low lymphocyte count. 

Thank you for the info shared.

I'm not certain. They are under specific response which means T cells could not provide a response until a distress signal is received and they know what they are targeting at...... My guess is this virus might be too small and well disguised as direct target for T cells.

My another guess is high metabolic rate during viral replication in cells increases the body temperature. The accidental binding of pathogen to pathogen-associated molecular pattern could also trigger it. Fever triggers immune response. There is a viral and cancer targeting immune cells called Natural Killer Cells (neither T nor B cells)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4786079/

https://en.wikipedia.org/wiki/Lymphocyte

I'm not sure if this is correct but......... Diabetes might provide slow healing to cut or injury but not necessarily low immunity.... Oxidation of sugar reduces sensitivity of cells to detect cut, the ability of cells to repair or call out for help in case of infection. But it might just mean the immune cells are not alerted, not necessarily not functioning. Shall the sugar is reduced, you might see the immune cells activity is normal. Application of antibiotic could heal diabetic wound. This observation adds to the deduction that the immune system is working just not vigilant because the injured cells are not aware enough.....??

Edited by specinho

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On 7/16/2020 at 2:09 AM, Enthalpic said:

I would read your post if it wasn't written in crayon.

It hurts my eyes and makes me think you are a moron.

So you read and reply.......

image.png.dbce8b35b9a624bb5233f7f4ec64fa4a.png

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^

So true. I had a friend who finally yielded to his wife's nagging. They were registered via a tablet at a mobile testing park. After a 2-hour wait, with another 1-hour wait ahead of him, he pulled out of line and went home. Four days later they learned that they'd both . . . tested positive. 

😂

You just can't make these things up!

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15 hours ago, Gerry Maddoux said:

^

So true. I had a friend who finally yielded to his wife's nagging. They were registered via a tablet at a mobile testing park. After a 2-hour wait, with another 1-hour wait ahead of him, he pulled out of line and went home. Four days later they learned that they'd both . . . tested positive. 

😂

You just can't make these things up!

I guess that's what you call the 2nd Blue wave of Covid-19!  And I'm supposed to trust mail in votes?  KMA!!!

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On 7/17/2020 at 4:26 AM, Gerry Maddoux said:

Believe it or not, I did the original research on cyclobutane moities of pyrimidine dimers created in Reovirus, a double-stranded RNA virus way back in 1966-'68. It is very interesting to see how far the research has come in this area. Back then we labeled using tritiated thymidine and then measured oligonucleotides that were excised in an attempt at repair. In those oligonucleotides was, of course, tritiated cyclobutane moities, and the more the better the repair mechanism. 

The betacoronaviruses and influenza are single-stranded RNA viruses and therefore don't contain "repair mechanisms," per se, because all the known repair trains work on stoichiometry of fit (1.54 A units, as I recall). But single-stranded RNA viruses don't make many mistakes either.

It would be something evil and altogether frightening if a chimera were to be formed by recombinant genomes between the influenza and the covid-19. I think this would be in short-segment fragments. However, whoever would have thought it possible that the genomic sequences between coronaviruses in the Malaysian pangolin and the Chinese horseshoe bat would be so similar? And that they would combine resources to develop the "can-opener" having to do with the ACE2 and the furin-cleavage?

To me the likelihood of this accidental bumping up against nature--using betacoronaviruses from a flying mammal (the horseshoe bat) and a land-locked animal (the Malaysian pangolin)--coinciding so naturally, despite being so widely separated in geographic existence, is almost a theoretical impossibility. Of course, the wet market has been blamed, but it is now my understanding that not only would no self-respecting Chinese eat the pangolin, but that it has been illegal to sell pangolins for food at Chinese wet markets for some time. 

This poses an interesting conumdrum for the CCP to explain away. It makes it so much more likely that the WIV was using gain of function to make the virus worse in order to make the vaccine better . . . and the virus got away from them. These things are very, very, very hard to keep in the laboratory, just like the slippery Reovirus.  

Seems like there has always been a very active trade in pangolins

https://www.sciencedirect.com/science/article/pii/S2351989415300342

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On 7/15/2020 at 2:05 PM, Enthalpic said:

BS.  While it's been maybe 3 years since my last flu shot, before that I got them every year for at least a decade and almost never catch colds.

Colds can be cured / prevented with zinc.

Navy study. solid stats.

You have 45-50% probability of a cold in a season but 95-100% after a flu shot. Which is why they recommend that Navy personnel get a flu shot if the flu poses a specific health risk to them, but not as a general practice. Your personal circumstances may have a separate cause.

I used to get 4-8 colds a year, now I use colloidal silver to control a MRSA infection and have not had one with symptoms lasting for more than a few hours after the next dose.

.

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(edited)

On 7/19/2020 at 1:48 AM, 0R0 said:

Navy study. solid stats.

You have 45-50% probability of a cold in a season but 95-100% after a flu shot. Which is why they recommend that Navy personnel get a flu shot if the flu poses a specific health risk to them, but not as a general practice. Your personal circumstances may have a separate cause.

I used to get 4-8 colds a year, now I use colloidal silver to control a MRSA infection and have not had one with symptoms lasting for more than a few hours after the next dose.

.

Do you have a reference?  I did a few journal searches and didn't find a ton of stuff.  Flu vaccination decreased other URTIs in children but made no difference in health care workers. Couple pointed out that the immune responses overlap (not surprising) so I could entertain a small possibility that the vaccine stress makes you slightly more susceptible to colds for a short time.

 

Where is you MRSA infection, and how do you use the Ag?

 

Edited by Enthalpic

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3 hours ago, Enthalpic said:

Do you have a reference?  I did a few journal searches and didn't find a ton of stuff.  Flu vaccination decreased other URTIs in children but made no difference in health care workers. Couple pointed out that the immune responses overlap (not surprising) so I could entertain a small possibility that the vaccine stress makes you slightly more susceptible to colds for a short time.

 

Where is you MRSA infection, and how do you use the Ag?

 

Posted it on oilprice before. It isn't a stress issue but an overconsumption of your immune system capacity with production of the antibodies and filling up your T cells with antigen impressions of the flu viruses, Best explanation I found so far. The vaccine goals are incompatible with your health unless you need its specific protection at the cost or suppressing your other immune responses.. Not unusual for a vaccine.

If you want to learn more of the colloidal silver us the PM function here. I don't want to just put it here without a full explanation and interaction.

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3 hours ago, Enthalpic said:

But are you a patriot?

It's patriotism that filters the virus! #Science

 

 

trump mask patriot.png

 

IMG-20200720-WA0030.jpg

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On 7/19/2020 at 12:56 AM, 0R0 said:

More grist for our mill

Masks don't protect much

WHO are thick as a brick

https://www.cidrap.umn.edu/news-perspective/2020/04/commentary-masks-all-covid-19-not-based-sound-data

Quote

we continue to conclude that cloth masks and face coverings are likely to have limited impact on lowering COVID-19 transmission, because they have minimal ability to prevent the emission of small particles, offer limited personal protection with respect to small particle inhalation, and should not be recommended as a replacement for physical distancing or reducing time in enclosed spaces with many potentially infectious people. We are very concerned about messaging that suggests cloth masks or face coverings can replace physical distancing. We also worry that the public doesn't understand the limitations of cloth masks and face coverings when we observe how many people wear their mask under their nose or even under their mouth, remove their masks when talking to someone nearby, or fail to practice physical distancing when wearing a mask.

 

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