Rough past few weeks. The past 10 days alone I experienced things breaking in my house (a faucet that was hard to fix, a burst pipe that is UNFIXABLE because the house is so old... its a rental btw, another leakage). My modem was basically fried, so 2 days and change without internet.
The reason for delays. I hope my September is better or I will be entering a major villain arc.
Wish you all a great weekend.
Related to this subject, it is far longer and more complex than this, but it is something I am interested in and believe it has a lot of importance for the future.
This goes along with the latest US braggarts, crowing about their universal vaccine progress and the $500 million they received in order to play God -- again. I think many have been sickened in their brains. Zero common sense and no regard for life.
Sorry to hear of your trials... but at least you don't have COVID again!!! ;)
Really interesting piece you wrote here, I had missed the mTOR connection for instance, congrats!
I have a minor quibble with a small detail, the idea that the HIV homologies were introduced when Spike was engineered, because the three short peptides homologous to gp120 all come from the hypervariable regions of gp120, and from different strains of HIV. Since gp120 functionality must come from its conserved regions, there is no way for short hypervariable segments to reconstitute that functionality in the context of Spike. Of course, an homology with HIV is striking, but if you extend the search from only virus sequences to all available sequences, you will find the exact same peptides in other organisms. The computation of the likelihood of finding these homologies in Spike (or in these other organisms carrying them) is of course a very low number, but these computations are based on the incorrect assumption that any sequence can be formed with equal probability. In both gp120 and Spike, these three peptides simply play a structural role, linking the functional domains in each protein, and because they are solvent exposed, have constrains on the type of amino acids present in this linkers. Unlike HIV that infect only CD4+ cells (and very rarely CD8+ cells, a small fraction of which are CD4low in the circulation), SARS-CoV-2 infect both CD4+ and CD8+ cells, and infection of the later is more problematic as you noted. The infection of these cells is not productive of new virions, but it is the anergy or death that is induced in T cells that causes some of the symptoms of Spike/SARS-CoV-2. So in all probability, these homologies are simply fortuitous. My 2 cents.
Been looking at lymphocytes subset results of a number of people here in China, notably several with quite severe long covid. As well as several abnormalities there are some very, very low CD4/CD8 ratios, I’m talking as low at 0.6 in some cases. I’m personally right at the other end at 2.6 which isn’t a great place to be but has been where I’ve been from 2022 to now and it’s hasn’t really moved after either of my Covid infections. I know they aren’t as easy or cheap to get everywhere but I would recommend a lymphocyte subset twst to everybody vaccinated or infected and also anybody with concerns of autoimmune disease
It has been my recommendation for the best part of the last 3 years for anyone able to. To get a lymphocyte panel and if possible with a subset measurement, the problem is that in most of the West you must convince your healthcare provider and especially your doctor to prescribe you the test.
They need significant convincing and arguments on how and why you "need such a test".
Interesting you are at the opposite end 🤔 better than the low trust me lol.
"Omicron’s origins are still shrouded in mystery, but it was first discovered in South Africa, precisely in Botswana, a country with the world’s most severe HIV epidemic in the world. Some HIV patients have SARS-CoV-2 infections lasting over 300 days, and many of the virus mutations are exactly what you see in Omicron and newer variants."
"SARS-CoV-2 origins are shrouded in mystery, despite the enormous number of hypotheses and ideas thrown out there. The reasons I named the complex effects of the Spike Protein as “PAID” (Paradoxically Acquired Immune Dysfunction) are many, but the main one is the paradoxical effects the virus and its chimeric Spike Protein possess in the body."
"This aligns with a crazy idea from a few years ago…"
Your so close, if it were a snake you'd be bitten.
"I care more about data" The truth is out there, dig and ye shall find.
It's like going to Lost Wages...
What happens IN decades of vaccine trials? - Stays IN vaccine trials?
The data that is. I nudged you on HMGB1 - now this.
You say that SARS can reactivate latent reservoirs in HIV through mTOR, but there’s another simpler explanation at hand. SARS2 directly infects LFA-1 receptors on lymphocytes and CD4 cells that directly release Human Endogenous Retroviruses which activate HMGB1 and RAGE through mTOR. The human genome has 8% retroviruses and over a million Alu-elements that all cause immune inflammation and cause give false positives for HIV. Human endogenous viruses are non replicating and HERV-K is interchangeable and indistinguishable from HIV, especially the viral envelope. You are catching your own bait and calling it fish? See PMC3457174/PMC3272926
HERV-K specifically is structurally similar, but it is distinct from HIV, and not only at that, but modern tech can easily distinguish between the two.
But to your point of false positives, the specificity of sequencing technology, and sensitivity of most used techs (such as Ilumina) are NOT enough to distinguish even between HERV-K's from different healthy donors. So that is a bit inaccurate.
SARS-CoV-2 will also use CCR5 to infect lymphocytes, something I literally predicted in March 2020. In fact, to this day I am surprised by the absurd number of receptors the virus can use to infect different cells, it just "prefers" ACE2 because of the FCS.
In the context of general, systemic inflammation HMGB1->RAGE activation of mTOR will happen, but here the authors found DIRECT interaction of the Spike Protein with the mTOR protein itself. This is a primary activation method, not secondary, prone to multiple post-translational processes. Galectin-3, inside a cell, will sense Endotoxin and activate mTOR. The list goes on.
HERV-K itself has been found to interact and sometimes hinder HIV's life cycle too.
I have written about HERV's and how they play an extensive and overlooked role in regards to SARS-CoV-2, correlating each new variant infection wave with coming disease outbreaks and cycles, thus I am aware of their importance.
Rough past few weeks. The past 10 days alone I experienced things breaking in my house (a faucet that was hard to fix, a burst pipe that is UNFIXABLE because the house is so old... its a rental btw, another leakage). My modem was basically fried, so 2 days and change without internet.
The reason for delays. I hope my September is better or I will be entering a major villain arc.
Wish you all a great weekend.
Related to this subject, it is far longer and more complex than this, but it is something I am interested in and believe it has a lot of importance for the future.
Hmmm... sounds like the goblins aren't waiting until Halloween to haunt you. ;) Feels like the whole world is in a villain arc.
GOOD LUCK FREIND
Mercury was retro. It was brutal for some reason this time around. I had similar experiences
I am sorry to hear that, I hope things improve for you too. It has been tiresome 😆
Certainly improving. I hope for you as well. Hang in
This goes along with the latest US braggarts, crowing about their universal vaccine progress and the $500 million they received in order to play God -- again. I think many have been sickened in their brains. Zero common sense and no regard for life.
Sorry to hear of your trials... but at least you don't have COVID again!!! ;)
Really interesting piece you wrote here, I had missed the mTOR connection for instance, congrats!
I have a minor quibble with a small detail, the idea that the HIV homologies were introduced when Spike was engineered, because the three short peptides homologous to gp120 all come from the hypervariable regions of gp120, and from different strains of HIV. Since gp120 functionality must come from its conserved regions, there is no way for short hypervariable segments to reconstitute that functionality in the context of Spike. Of course, an homology with HIV is striking, but if you extend the search from only virus sequences to all available sequences, you will find the exact same peptides in other organisms. The computation of the likelihood of finding these homologies in Spike (or in these other organisms carrying them) is of course a very low number, but these computations are based on the incorrect assumption that any sequence can be formed with equal probability. In both gp120 and Spike, these three peptides simply play a structural role, linking the functional domains in each protein, and because they are solvent exposed, have constrains on the type of amino acids present in this linkers. Unlike HIV that infect only CD4+ cells (and very rarely CD8+ cells, a small fraction of which are CD4low in the circulation), SARS-CoV-2 infect both CD4+ and CD8+ cells, and infection of the later is more problematic as you noted. The infection of these cells is not productive of new virions, but it is the anergy or death that is induced in T cells that causes some of the symptoms of Spike/SARS-CoV-2. So in all probability, these homologies are simply fortuitous. My 2 cents.
ALL IN ALL THIS WAS PURE EVIL BY EVIL
Been looking at lymphocytes subset results of a number of people here in China, notably several with quite severe long covid. As well as several abnormalities there are some very, very low CD4/CD8 ratios, I’m talking as low at 0.6 in some cases. I’m personally right at the other end at 2.6 which isn’t a great place to be but has been where I’ve been from 2022 to now and it’s hasn’t really moved after either of my Covid infections. I know they aren’t as easy or cheap to get everywhere but I would recommend a lymphocyte subset twst to everybody vaccinated or infected and also anybody with concerns of autoimmune disease
It has been my recommendation for the best part of the last 3 years for anyone able to. To get a lymphocyte panel and if possible with a subset measurement, the problem is that in most of the West you must convince your healthcare provider and especially your doctor to prescribe you the test.
They need significant convincing and arguments on how and why you "need such a test".
Interesting you are at the opposite end 🤔 better than the low trust me lol.
Professor - Simply brillant.
"Omicron’s origins are still shrouded in mystery, but it was first discovered in South Africa, precisely in Botswana, a country with the world’s most severe HIV epidemic in the world. Some HIV patients have SARS-CoV-2 infections lasting over 300 days, and many of the virus mutations are exactly what you see in Omicron and newer variants."
"SARS-CoV-2 origins are shrouded in mystery, despite the enormous number of hypotheses and ideas thrown out there. The reasons I named the complex effects of the Spike Protein as “PAID” (Paradoxically Acquired Immune Dysfunction) are many, but the main one is the paradoxical effects the virus and its chimeric Spike Protein possess in the body."
"This aligns with a crazy idea from a few years ago…"
Your so close, if it were a snake you'd be bitten.
"I care more about data" The truth is out there, dig and ye shall find.
It's like going to Lost Wages...
What happens IN decades of vaccine trials? - Stays IN vaccine trials?
The data that is. I nudged you on HMGB1 - now this.
The answer is in the question Mr Mulder.
You say that SARS can reactivate latent reservoirs in HIV through mTOR, but there’s another simpler explanation at hand. SARS2 directly infects LFA-1 receptors on lymphocytes and CD4 cells that directly release Human Endogenous Retroviruses which activate HMGB1 and RAGE through mTOR. The human genome has 8% retroviruses and over a million Alu-elements that all cause immune inflammation and cause give false positives for HIV. Human endogenous viruses are non replicating and HERV-K is interchangeable and indistinguishable from HIV, especially the viral envelope. You are catching your own bait and calling it fish? See PMC3457174/PMC3272926
HERV-K specifically is structurally similar, but it is distinct from HIV, and not only at that, but modern tech can easily distinguish between the two.
But to your point of false positives, the specificity of sequencing technology, and sensitivity of most used techs (such as Ilumina) are NOT enough to distinguish even between HERV-K's from different healthy donors. So that is a bit inaccurate.
SARS-CoV-2 will also use CCR5 to infect lymphocytes, something I literally predicted in March 2020. In fact, to this day I am surprised by the absurd number of receptors the virus can use to infect different cells, it just "prefers" ACE2 because of the FCS.
In the context of general, systemic inflammation HMGB1->RAGE activation of mTOR will happen, but here the authors found DIRECT interaction of the Spike Protein with the mTOR protein itself. This is a primary activation method, not secondary, prone to multiple post-translational processes. Galectin-3, inside a cell, will sense Endotoxin and activate mTOR. The list goes on.
HERV-K itself has been found to interact and sometimes hinder HIV's life cycle too.
I have written about HERV's and how they play an extensive and overlooked role in regards to SARS-CoV-2, correlating each new variant infection wave with coming disease outbreaks and cycles, thus I am aware of their importance.
I appreciate the above discussion.