June 10, 2020
My Hypothesis of Pathogenic Disease Behavior Associated with COVID-19
BY JOANN PERALTA
Though no doubt obvious to the medical community but whereas myself, a lay-person, interjecting my hopeful analysis of much research I find myself having to embarrass myself with an introduction with commonplace biological analysis prior to my entering into specifics of my findings. So with many apologies to the scientific and/or medical community at large, I shall endeavor to proceed with my research analysis of the COVID-19’s pathway to destruction in the human body and the prospects that my humble efforts may, with God’s help, lead to even an inkling of deeper understanding which may be further investigated by people of a higher learnedness in these fields of study and research than myself.
This research was done over ten weeks, and the discovery of the protein link to COVID-19 disease pathway was on May 12, 2020.
Beginning with the information I received at the first, that COVID-19 is said to be a protein cell structure and not a bacteria-driven cell structure, and therefore possess precise sequence of amino acids, also known as enzymes, and do not have cellular walls, and is not organelle or nucleus organized, I laid the groundwork study of this devastating virus.
Whereby enzymatic function relies on the release of chemical-reactions traveling extremely fast to enable the cells to discard or receive information to either grow and build, or take-apart within the items as needed, I tried to locate where this virus first would’ve entered the body and then hi-jack many of its bodily systems, with variation and degree of severity. It was clear the invading virus was riding through the body quickly with many people reporting that “once specific symptoms were noticed”, often it didn’t take long before many serious conditions followed and began to be reported.
Since COVID-19 was first reported months ago as a virus-protein cell structure, that would mean it initially began as an enzymatic function of combined amino acids but eventually after entrance into the body, is now deemed an epitope. An epitope also known as the ANTIGEN-DETERMINANT, is part of the antigen to which antibodies bind. Of importance to note is that while the antigen evokes the antibody response in the host chain link, the antibody does not bind to the entire protein chain, BUT ONLY TO THAT SEGMENT CALLED THE EPITOPE. So, as it invades the body, it becomes part of the stringing together of between 100 to 1,000 AMINO ACIDS, in very sequential and specific order. Again, amino acids commonly referred to as enzymes, are proteins in the body.
If it entered via mucosa tissue it could very well have gained quick entrance to LANGERHANS CELLS (LC), WHICH ARE PRESENT IN ALL LAYERS OF THE EPIDERMIS (SKIN) SUCH AS STRATUM SPINOSUM. BUT ALSO OCCUR IN PAPILLARY DERMIS, MOST ESPECIALLY AROUND BLOOD VESSELS, AND MUCOSA OF THE MOUTH, AS WELL AS FORESKIN (MALE), AND VAGINAL EPITHELIUM (FEMALE). LANGERHANS CELLS ARE FOUND IN OTHER TISSUES AS WELL SUCH AS LYMPH NODES, AND SPECIFICALLY ASSOCIATED WITH A CONDITION CALLED, LANGERHANS CELL HISTIOCYTOSIS (LCH).
** IMPORTANT TO NOTE IS THAT LANGERHANS CELL HISTIOCYTOSIS (LCH) WHICH IS A RARE DISORDER, DISPLAYS THE TRAVEL RECORD OF THE PATHOGENETIC ANTIGEN PROVIDING A TEMPLATE FOR SCIENTISTS AND MICROBIOLOGISTS TO VIEW THE SPREAD OF COVID-19 IN THE IMMUNE SYSTEM AND DISPLAY ITS SEVERE EFFECTS THROUGH DENDRITIC CELLS WHICH ARE A FORM OF HISTIOCYTE (WHITE BLOOD CELL). THESE HISTIOCYTES CAN BE FOUND IN THE SKIN, LUNGS, STOMACH, BONE, EYES, AND INTESTINES: THE VERY PLACES THAT ARE BEING AFFECTED BY THE COVID-19 ANTIGEN.
THE FACT THE IMMUNE RESPONSE IS THE MODE, OR GROUND ZERO, OF THIS MUTATIVE, EXPRESSIVE PATHOGEN IS A VERY SIGNIFICANT DISCOVERY.
The inflammatory-like behavior is indicative of the reactionary state associated with this virulent pathway and its overtaking of the Immunological System as well as Adipose Tissue System, which are comprised of Adipose Tissues and Endothelium layers. This is all accomplished via macromolecules, which vary in their make-up and contributing functions in cellular design and are present in four basic components of lipids, proteins, carbohydrates, and nucleic acids.
I will explain more as to how I derived at these conclusions as we proceed.
One can see if the Immunological system which is comprised of special organs, such as the liver; cells (histiocytes for eg.); and chemicals that fight infection called, microbes, were to report dysfunction from their abilities to ward off the antigens invading the body, it would be as we have it now; a pandemic.
Important to note are other parts of the Immune System which are affected as well consisting of white blood cells, antibodies, the complement system, the lymphatic system, the thymus, spleen, and bone marrow.
The B-cells and dendrites are formed in the lymph nodes, which is part of loose connective tissues found in the bone marrow.
The dendritic cells migrate into the circulatory system before they assume tissue locations as immature dendrite cells. These location areas are skin tissue, GI tract, and airways. Surface bound signaling occurs also from infection or damage, as dendrites present T-cell proliferation in guiding appropriate immune responses which adequately target the areas.
** I believe T-cell response contaminates on the B-cells, (T cell-derived Protein S, Pro s1, TAM signaling in dendritic cells), engages with special aggregation occurring at the BBB when the antigen reached this locale presenting mutations of reactions with regard to response mechanisms and signaling.
This also involves fibronectin coating, or fibral adhesion capabilities in relation to attractants which bind on the surface of the cells which has interfered with correct T cell proliferation signaling. Such as phagocytosis and opsonin-related responses (described in greater detail to follow later).
FIBRONECTIN, also known as a protein dimer, is comprised of two nearly identical polypeptide chains linked by a pair of C-terminal DISULFIDE BONDS. Disulfide bond is a sulfide containing two atoms of sulfur in its molecule or empirical formula. An organic compound containing the group S-S-bonded to other groups. Or, the covalent bond between sulfur atoms that bind two peptide chains or different parts of one peptide chain and is a structural determinant in many protein molecules. In other words, half a chain looking for a connection or bonding to its structural determinant other.
This can cause major problems if a recombination with negative effects is produced such as in the hydrogen peroxide bond.
**The enzyme protein’s chain “very specific sequence” then fold into a unique shape once it has derived at the sequence desired, such as a salt, disulfide bond quaternary structure found in plasma.
The virus which was once disassociated has now become associated and made to appear organized, yet is covert. The “new protein” made in response to an antigen, that can combine with that antigen, is referred to as an ANTIBODY RESPONSE. And it has now infected the immunological system of the body and formed very specific shaped multicellular organisms.
The quaternary structure of the Hemoglobin (Heme group) is both Fibrous, and Globular, which is specific to this structure….sequence determines structure, structure determines function.
In Hemoglobin, each polypeptide chain, ( a, a2 , B1, and B2) of which there are four are named; primary structure, secondary structure, tertiary structure, and quaternary structure. This Hemoglobin protein, whereby all four are deemed polypeptide chains, and therefore makeup a series of combined amino acid chain links are attached together by a porphyrin ring, which is an organic ring-like compound attached to an iron atom. The Hemoglobin carries oxygenated blood to the cells. It transports both oxygen and carbon dioxide, through its unique globular shaping. If any of the peptide chain protein links has a defect on it, it will multiply that same defect throughout the chains. So, the same goes for any corrections. Any corrected structures will multiply the corrected state.
SYMPTOMATIC ASSOCIATED-BEHAVIOR TO ANTIGEN’s PRESENCE
Now that the antibody-response enzymes, which have shown themselves to be “hi-jacked” due to the fact the enzymes no longer function in the capacity to which enzymatic function is reserved for (which is the storage and release of energy throughout the body), it is important to trace what these corrupted functions look like, one by one and address each in how that take-over in the body is playing itself out, aside from its initial immunological takeover.
This will involve the process of defining the symptomatic relationship related to the invasion of the COVID-19 Virus and how it is “corrupting the files” in vivo, and also how one might treat the symptoms associated with it.
Thereafter however, once many of these symptoms are noted, it is my desire to look for the main focus in my research, which is to find the cause and ability COVID-19 has in vitro on its path of destruction and instead utterly destroy this demon antigen, cutting it off at the head rather than the tail. This is my hope and prayer.
Upon initial knowledge that these protein-enzymes are present mostly in PLASMA as well as TISSUE fluid, once it arrived, how it interfered with normal body functions I have tried to log as many as I could ascertain.
Important reminders are that the enzymes are like small, chemical-reaction machines whose purpose is to allow the cell to carry-out chemical reactions very fast. Those reactions allow or enable the cell to discard or receive and therefore build or take-apart things as needed. This is the process of cellular growth and how it reproduces too. The cell is therefore like a box of chemical reactions all made possible because of enzymes.
This epitope, anti-body response enzyme, requires a host to enable it to thrive and survive. Though it has successfully tied itself to the antibodies of the organized protein-amino acid chain, it needs a host to continue to live.
**The HOST of the COVID-19 virus, in my opinion became the Macrophage and Mast cells of the Adipose Tissues, (which store the fats to be used throughout the body for energy to all cells which comprise the Adipose Tissues); as well as the Endothelium, which are cells that contain fats that line the interior surface of blood vessels; and lastly, the Lymphatic vessels, and are flat, along the lining mostly of the arterial and vascular systems (blood vessel arteries and veins leading to and away from the heart as well as throughout the vascular system by way of capillaries). This enabled the passage into the connective tissues and mast cells with respect to Langerhans Cells pathway prior to entrance to the BBB and cellular tissues of the Adipose and Endothelium, uptake and downward movement in relation to the CNS and stem cell proliferation.
The reason, I suspected the epitope chose these regions were due to the symptoms involved with each of these areas. The Adipose Tissue, as well as the Endothelium, and Lymphatic vessels, as being the enzymatic cellular “hosts”, were because the trail of symptoms appeared to hi-jack the normal function of these bodily systems based upon the many chronic and often deadly examples being outlined almost daily in the news as well as through the government task force briefings.
This protein virus-driven enzyme, requires fat to secure the cellular wall, or membrane, since the virus protein-enzyme is without one, as it appeared it was without at the first. Therefore, I would say it began as a prokaryote, which it seemed to be described as such, but later news conferences started saying otherwise and I found as it secured a host it morphed into a eukaryote. But more on this as this paper unfolds.
FAT DEPOSITS REQUIRED TO KEEP ANTIGEN ALIVE AND EVADE DETECTION
Not only do both the Adipose Tissue and the Endothelium contain the majority of fat deposits, (known as the Adipose Depots in the Adipose Tissue), and which have the fat to nourish the enzyme-protein to maintain and uphold their weak-cellular wall structure, but the cells within these regions are also susceptible to virus and antigen/bacteria. This is due to the attempts and in some cases, advantage the prokaryote has in trying to elude the antibodies and macrophage cellular first responders, such as mast cells, from being taken over by the antibodies or phagocytes sent to kill them by invading a host cell. The antibodies cannot bind to antigens that have already entered a host cell which provides the antigen some security at the first.
As the Macrophage cells become inflamed because over-ridden with toxins in the Adipose Tissue and as the Macrophage is now inflamed with antigen offenders, noted due to its lack of ability to fight the offending agent, showing it to be more than viral in nature, and it won’t calm down through the normal means of homeostasis at the cellular level, then the Macrophage become aggressive and mutate into EXCESSIVELY AGGRESSIVE PROTEIN CELL STRUCTURES, (which in turn recruit monocytes). These macrophage which normally maintain HOMEOSTASIS in healthy Adipose Tissue, if they become overloaded with lipids (fats; or fatty acids), they move outside of remaining in a state of homeostatic behavior and become metabolically activated PHENOTYPES.
** Recent information has demonstrated that several intracellular bacteria have abilities to induce an M1-Phenotype upon Macrophage infection, thereby creating pro-inflammatory responses within the macrophage, as well as interrupt the M-2 Phenotype of Macrophage which are anti-inflammatory and beneficial responses to infection and homeostasis in the body. There are many diverse fields of study involving Macrophage variations and I hope to uncover one or more in this research analysis of the COVID-19 trail of destruction. But this is what led me to wonder if bacterial invaders were also at play.
EARLY DETECTION NEEDED
In my opinion, if the antigen was caught with early detection prior to it invading fat tissues, or host cells via macrophage or mast cells, then antibiotics such as erythromycin would be beneficial in taking it out. However, if not caught early, then it would evade antibiotic treatment if the pathogenic behavior escalated to more extreme symptoms, and/or disease associated symptoms with respect to COVID-19.
There are however, multiple combinations of treatments with respect to where it is on its pathway. Preventative and early detection are the most preventive and treatable measures to be taken with COVID-19. I have personally witnessed what appear to be symptoms of early-onset COVID-19 caught within the earliest signs and used home remedy therapeutics outlined via a YouTube doctor as well as my own analysis of measures that can be taken. It stopped after two days with only nominal signs of tiredness. They were completely well after three days and I continued to monitor them and encouraged rest and drinking fluids along with multi-vitamin to continue strengthening the body’s internal health.
Another follow-up series of therapeutic treatments one day later, such as garlic, lysine (an amino acid), Schweppes Tonic Water which contains quinine (careful of sugar content if diabetic), vitamin C and zinc, with Tylenol if needed, and as directed on the bottles, or via YouTube doctor dose recommendation for zinc and Tonic water, and this person I knew felt 100% better. Their red-eyes, pressure feeling in their head, and low-grade temperature as well as hot bodily feeling, was gone. It has not returned and its been over two months. I also highly recommend sitting in warm-hot outdoor indirect solar energy, or if need to kill germs only in direct sun at minimal amounts of time, if extremely hot. But, always seek the advice of your doctor first, and especially if hydrochloroquine is readily available and administered by your doctor if you test positive for the COVID-19. But, let there be no mistake, early detection leads to better prognosis for available treatments, and always under doctors advice first.
I had mentioned one treatment on my Facebook site but I have to warn that be careful with garlic use, which contains quercetin and is extremely beneficial to keeping bodily inflammation down. The danger being, it may do such a good job helping with inflammation in vivo that blood pressure may regulate so much if you have high-blood pressure, that it may drop it too low if you are already on blood-pressure medications. My own mother had to cut her dose of high-blood pressure meds in half, and the doctor wanted to keep her on it, not because of the now gone high-blood pressure, but because of the treatment the medicine contains in keeping her kidney’s functioning properly. Her doctor also continued to advise her to stay on the garlic as well. My mother may need kidney dialysis without the high-blood pressure medication she was told. I will have to check into this at a later time.
For now, back to my research findings.
THE SIDE-CHAIN BACTERIUM DISGUISED
The bacterium-antigen went unnoticed prior to its entrance as it side-chained with the invading virus via enzymes, which are amino acid chains known as proteins and was allowed into the macrophage as a protein chain, but with the activation process of inflammation triggering it’s release, the once dormant bacterial-antigen is now awake to interfere with Immunological functions.
The now metabolically-activated macrophages cannot keep up with maintaining evenly distributed ant-inflammatory phenotypes (their normal function) and have now transformed the tissues to which they are living amongst into obese-Adipose Tissue. These now obese-Adipose Tissue Macrophages accumulate in so-called, “Crown-Like” Structures around dead adipocytes because the normal function involving phagocytosis, has been disrupted.
I believe the display of the crown-like features is demonstrative of their engulfment either by antigen and/or a type of flag waving that they contain a now disguised prokaryote which is become a eukaryote invader antigen, and therefore the macrophage are now non-functioning as a macrophage.
Instead, it is a toxic macrophage which recruits monocytes such as leukocytes, and myeloid lineage dendritic cells.
The toxic macrophage will not calm down with normal cellular homeostasis function (ATP to ADP), and is no longer a normal functioning macrophage. I would like to do more research in this area as it pertains to type I & ll diabetes which I believe there is a connection to but I have not yet found evidence whether both my suspicions are valid yet, or if it is any theory at all and simply the imaginations of my mind. But I will return to the papers research concerning the lucid activity and path of COVID’s destruction, in my opinion.
Now the phagocyte works in conjunction with the macrophage to engulf antigens and after disposing of it, send the debris to the top of the cells which are eaten up by the phagocytes. However, if the signaling is “off “ via the messages sent from macrophage to phagocyte then the debris will be sent with no engulfment by the phagocyte to eat up the dead adipocytes which are there through various other reasons as the bodies system is in a constant state of cellular regeneration.
The macrophage-phenotype HAS BECOME A GENE-EXPRESSIVE PHENOTYPE. Gene expression involves shared characteristics of proteins, but are not limited to this function alone. This display of a metabolically activated Phenotype, which is an organism that shares both genetics and environment (Gene Expression), is made it all the more dangerous in its mutative state.
Whether the gene-expressive type phenotype, which began as a bacterium, was purposefully connected to the protein enzyme is unknown. I suspect unsanitary conditions may have been in play, or where the research scientist to which this all began may have been sick with bacterial induced illness which compromised the research causing contamination unbeknownst to themselves. I say the latter due to the information released at the first from media reports that (patient-zero) researcher, had also come down with the COVID-19 illness and succumbed to its conditions. But, that is not for me to determine specifically, only that in my view of said virus, it remains possible that fowl play was not involved due to evidentiary results of patient-zero contracting the virulent disease. That coupled with the fact China did not shut down the information which was at first de-classified and then they sealed the information afterward. At least that seemed to be the time line scenario the media reported as it happened in real-time and seemed to be verified in my watching as events unfolded within months. Thank you to the media for the constant updates!
But now back to the research involving COVID-19 with respect to my analysis and findings:
These now, mutated-Macrophage which have become metabolically-activated Phenotype (shown with Crown-like Structures), form multiple, intracellular, lipid-droplet-protein (HILPDA) in the adipose tissues, and are eventually expressed in several various tissues in conjunction with distinct transcriptional profiles and the involvement of LIPOLYSIS. This denotes a new pathway of destructive behavior in vivo.
The feature of HILPDA expression is indicative of an attempt by Macrophage to buffer excess lipids, which is adaptive in the leaner state, but become maladaptive in obese-Adipose Tissue.
Normally, Lipolysis, which is the process whereby fats are broken down in the human body through enzymes and water (hydrolysis), have now become dysfunctional Lipolysis, in which the facilitation of the breakdown of fats, such as triglycerides into fatty acids and glycerol, throughout the bloodstream and then repurposed for fuel in plasma and cells, begin to disrupt how the production and subsequent distribution of these energy-release determinants travel. This is due to the release of HILPDA’s disposition in lipolysis.
This would account for COVID-19’s symptoms by patients suffering severe fatigue, which I surmise is due to the misappropriation of the breakdown of triglycerides and fat which are the proliferators of providing fuel for energy in the body.
The reason HILPDA is released in more abundance, I theorize, due to COVID-19 VIRUS is in conjunction to the B-cells with T Helper Cells becoming oxidatively reactionary after antigen-binding with regard to antibody generation, which was compromised when transmitter signaling of ions was interfered with thereby stimulating release of HILPDA in lipolysis.
Entrance into the BBB (Blood Brain Barrier) by the antigen has compromised Immunological antibodies in the involvement of connective, myeloid, and other tissues and the endothelial membrane which is all part of the Adipose Tissue System. The now tainted cellular structures are giving compromised or elucidative signaling via the B-cell receptors (BCR) of ion transport chains as well as involvement via ligand gateways with regard to dendrite polar cells, as discussed earlier in the paper.
The ligand gateways are openings whereby helical twists involve the passage of macromolecules and ions via polarization signaling into these gateways involving dendrite cells.
Ligand-gated ion channels (LIC’s, or LGIC’s), also known as ionotropic receptors, are transmembrane (TM), ion-channel proteins, which open to allow certain ion configurations to pass such as Na+, K+, Ca2+, and/or Cl- to pass through the membrane. This is in response to the binding of a chemical messenger, (i.e. a ligand), such as a neurotransmitter, which are also activities connected to dendrite cellular expressions leading to capillaries of the lungs.
Interesting to add, in a prior study, endothelial cell marker Tie2-Cre driven deletion of HILPDA was found to DECREASE fatty acid, and oxLDL-driven lipid droplet formation in macrophages, and helped reduce lesion formation and progression of atherosclerosis in Apo E-1-mice. These studies involved Tie2-Cre transgene mice identified by genomic PCR and Southern blot. This was to study the function of genes in Endothelial Cells using Cre-lox P System. **I would cite the source but can’t find right now. I will do so later when I find it.
All this to say that HILPDA is not only an inhibitory reaction or disposition of Lipolysis but its decrease has been found to reduce destructive fatty acids and oxLDL, which contribute to the cause of atherosclerosis and cholesterol building plaque in arteries, and with regard to lesion formation.
There is knowledge as well that the consequences of HILPDA has been presented that it also directly binds and inhibits (ATGL) ADIPOSE TRIGLYCERIDE LIPASE, which is required for healthy cellular function in Adipose Tissues and the release of toxins from the cells.
This is consistent with HILPDA’s abilities to inhibit lipolysis. Lipolysis, as stated, is required for the breakdown of fats, or lipids by HYDROLYSIS, which release fatty acids, and not build up as atherosclerotic plaques.
**My hypothesis. The expression of HILPDA, is induced by a number of different stimuli including hypoxia, beta-adrenergic activation, and PPAR, which I theorize has a lot to do with the chemical exchanges involved when ions deliver incorrect signaling. In my hypothesis, it may be evident but if a PPAR-alpha translates the lesion expression of the gene of the HILPDA induced macrophage via transcriptional profiles of lesions at the ligand gate this may adapt to a protein lesion at this gate and enter through with this anomaly, which would not be a good thing. Especially if it were to cross paths via signaling with a different protein. I would think adherence proteins may cause a negative mal-adaptive reaction whereby this would be possible, or via class-switching.
This Peroxisome Proliferator-Activated Receptor (PPARa)-Alpha, is a ligand-activated transcriptional factor, belonging to the family of nuclear receptors. PPAR-alpha regulates the expression of genes involved in fatty-acid Beta-oxidation and is also a major regulator of energy and homeostasis. Other names for gene expressive regulators of PPAR are gamma(PPAR-y); gamma (PPARG); or Glitazone Receptor.
HILPDA also promotes lipid disposition in hepatocytes (liver cells), adipocytes (cells that store fats in CONNECTIVE TISSUE), and MACROPHAGES.
Lipid disposition is where a phase of transition in which gas transforms into solid, without passing through the liquid phase as the intermediary stage . This “skipping over one of the phases of Hydrolysis in Lipolysis” is super critical in the lack of release, or speeding up, of the lipid-liquid-phase (which I would like to personally name, and summarize with the acronym, LL-Phase). I believe part of the toxic associations attributed to the possible speeding up of the phase from stage 1 to 3 has also intervened with the time-lapse required for correct ion signaling to transport the triglycerides, which may have instead become a different construct. Sequence determines the function and shape…
**In my estimation, and another theory/Hypothesis, the increased time involved with the passing over of the LL-Phase has created a by-passing of the liquid state of the lipolysis process which initiates Hydrolysis and turns the much needed liquid oxygen molecule from being able to be turned from a compound of Hydrogen + Oxygen + triglycerides, into a grounded liquid-oxygen, where the grounding molecule is now looking for a compound element to bind and may have found it in the reformation of the third stage of lipolysis-Hydrolysis thereby creating a succinctly different final profile of the solid stage. One which initiates serious mal-consequences and may even interfere with correct Ligand-gating, and/or Transmembrane (TM) passage of proteins.
Lipolysis takes place in the Adipose Tissue and uses storehouses in the adipose to save energy to be released when needed such as when fasting, or exercise and enables energy from lipids and triglycerides to be delivered to various regions of the body for use in cellular activation and distribution. It is the metabolic path for the transformation of lipid triglycerides into glycerol and three fatty acids via hydrolization methods found in the second into the third and final stages of lipolysis.
This hydrolization method is hydrolysis and it involves the breakdown of these components with water because at this first stage lipid triglycerides are in a gas form and become involved with the second stages where oxygen-hydrogen molecules and the lipid esters enable it to be broken down into component parts with water involved in the second stage of lipolysis, and prior to it becoming a hydrolyzed solid form in the final stage. Lipolysis is induced by hormonal activity which includes, glucagon, epinephrine, norepinephrine, growth hormone, atrial natriuretic peptide, brain natriuretic peptide, and cortisol.
Therefore in my theory regarding the inhibiting factors associated with the release of HILPDA corresponding with overladen macrophage and its disposition of lipolysis I suggest that the oxygen molecule was transferred straight from the gas state into a solid state, via the skipping of the LL-Phase, and became a solid form of mutated energy fat, not as easily broken down for cellular energy than if it had experienced the second stage correctly.
If my analysis is correct, chemical equations involving the chemical changes through reactions whereby if an atom or molecule is lost or displaced, doesn’t make it go away, but it finds itself in a different reaction or change. Sorry to the scientific community but I did not do well in my chemistry class in high school but I understand its concepts.
Therefore, if the molecule not used, is looking for a new compound element to bind to, prior to it becoming a solid, whereby it normally would have been in the fatty-liquid-state, in order for the molecule to become a liquid molecule it needs to become grounded.
My suspicions are that the hydrogen molecule is looking for a metal to bind with as it is needing a solid state to assume its molecular structure as such. The state of metals in the body will turn the hydrogen seeking molecule into a compound in its quest to become a state of solid.
Hydrogenation, whereby the hydrogen molecule has been added and whereby a catalyst is required to stabilize its activity, which is normally a metal, is my suggestion about what may be happening with the LL-Phase being passed by due to the release of HILPDA in lipolysis.
**If what I’ve suggested is true, then it may be responsible for iron being borrowed from the iron rich plasma in the body to finish the molecular binding operation, which would account for lack of energy in vivo, and in more scenarios than that which involve COVID-19.
**What is interesting to note is that the Hydrogen-Oxygen state of liquid is a hydrogen-peroxide construct, and therefore the absence of this stage could be theorized that replacement of similar molecular compositional properties back in vivo, could be useful in closing the gap and reconstructing the lost process of the LL-Phase which could be of benefit in more areas than just COVID-19. I surmise the compositional content of ACETYLCHOLINE MAY CONTAIN THE SAME COMPOSITION IF COMBINED WITH AN ESTER GROUP, (if it doesn’t already have one), TO FORM THE MISSING STAGE but this is not proven and I would need verification on this.
Also, for non-scientists and non-medical personnel, it is not advised that one drink hydrogen peroxide because this is not the same as the covalent bonding I am referring to in this regard.
As far as the continued hypothesis I have about the consequences of a different composition of the final product of lipolysis when HILPDA induced changes occurred, are that ionic polarization molecules to hinder, obstruct, or open correct ligand-gated activities and passage of particular necessary molecules have been compromised. The possibility also erupts that an mRNA expression on the host cells, and involve Y-1 and Y-2 Receptor, as well as reverse transcription-polymerase chain reaction (RT-PCR) is occurring due to the evidence of Chemotaxis being interfered with. I think I said the same thing but just used different nomenclature, so please forgive me.
Chemotaxis being the movement of cells or organisms in response to chemicals being disrupted in their normal functioning and affects the gradient of a diffusible substance making it less or more diffusible. Fibronectin re-modeling which cause a coating of soluble or insoluble cellular fibronectin involves the extracellular matrix of the Adipose Tissues, Endothelium, and Plasma membranes.
An example is found in leukocyte chemotaxis where the leukocytes form in response to products formed in the immunologic reactions of the body to antigens, or pathogens. Leukocytes are attracted to the site of the chemical response reaction to the antigen or pathogen, based upon the inflammation response of the Phagocytes. But if there is not a proper response by the Phagocytes to the invader then Chemotaxis is interfered with intracellularly. Otherwise, the antigen/pathogen would have been eliminated.
In this case, the possibility is that the supposed bacteria may have the ability, as some bacteria do, to elude the Phagocytes by coating its bacterial surface with FIBRONECTIN, which is produced naturally by the body and is vital in its role to wound healing. Or that the antigen was bound to the surface of the B-Cells which have fibronectin coating which is an adhering viscosity.
FIBRONECTIN, also known as a PROTEIN DIMER, is comprised of two nearly identical polypeptide chains linked by a pair of C-terminal disulfide bonds. Each Fibronectin serves as a cell adhesion molecule by anchoring cells to collagen or proteoglycan substrates.
In the beginnings of the virus/pathogen, and its entrance into the host cells, which I believe were initially macrophage cells sent to stop the virus in the tissues of its entry, but instead were deceived as the amino acid enzyme had a side-chained virus invader that took the macrophage as a host cell. I believe the virus then became captured or integrated into the fibronectin cellular adhesive top-layer and became undetected by phagocytes. Fibronectin, which contain glycoproteins binds also to other extracellular matrix proteins such as collagen, fibrin, and heparin sulfate proteoglycan (such as syndecans).
**A very possible mal-protein enzyme invader, such as Streptococcus Pneumonaie (S. Pneumoniae) which may be one of the antigen/bacterial invaders due to its polysaccharide capsule’s imitating fibronectin, when it goes undetected, is the most important virulent factor into Macrophage, and its abilities to hinder OPSONIN-related ingestion. This is what led me to be encouraged that my hypothesis of Macrphage becoming a host cell to the invader, as well as a bacterium side-chained in vivo was not too impossible to consider.
Now, Mitochondria which are the organelles of the Macrophage-turned Phenotype cellular structure and are used in response to bacterial pathogens, act as metabolic depots and signal reactions within the cell. They can either become friend or foe depending on the status of the organelle environment within the Macrophage. The Phenotype which is an aggressive display and response within the Macrophage which is now maladaptive due to COVID-19 will trigger modifications of the host metabolism that will lead to changes in immunological function. This is not good as plasma antibodies are the body’s antibodies, called Immunoglobulins, which are those agents which fight infections.
BLOOD TRANSFUSIONS THREATENED
This also poses a serious threat to blood transfusion and/or transplants for organ directed recipients in that if an antigen not normally present because it never began in the persons body but was only received as a donor of plasma, the person’s immune response system recognizes the plasma as foreign and a threat. The averse reactions can be quite serious, and involve activation of intravascular incompatibility to red blood cells.
What this means is if patient is not already positive to COVID-19, and they receive plasma with an antigen not normally present, the person’s immune system recognizes it as foreign.
Now, if the antigen were bacterial in origin, possibly transferred to the laboratory if the person in Wuhan, China, had become ill with Streptococcus Pneumonaie, in their bloodstream and lungs, while ill began to do experiments involving animal streptococci aureus or otherwise, which went horribly wrong, this could result in cross-contamination. It would fit the obvious antigen symptoms related to more than one streptococcus germ, thereby causing variant symptoms of virulent nature. But the case is of no concern to me how it happened but that it became what it did.
What is of concern is the presence of mutated functions in the bodily systems which have become maladaptive.
This is what must be addressed to fight this COVID-19 virus.
The reason I submit the possibility that it was a bacterial-virus such as STREPTOCCUS PNEUMONAIE is because the definition of the symptoms fit much of the criteria for it to have been one of the enzymatic causes of COVID-19. As well as the knowledge that many of the patients that tested positive for the COVID-19 DID COME DOWN WITH PNEUMONIA.
For example, the Streptococcus Pneumonaie PRODUCE PROTEINS, SUCH AS M-PROTEIN in the body, AND FIMBRIAL PROTEINS, which show to be higher than normal in the blood as blood proteins and are also shown to be at high levels as the body fights an infection or some other inflammation.
The M-protein, which stands for MONOCLONAL-PROTEIN, is an abnormal protein; and the Fimbrial proteins, considered a mal-protein, stop or inhibit the phagocytic engulfment by the antigen or bacteria. These mal-protein invaders hinder OPSONIN-related ingestion. This usurping of the phagocytosis process has all the earmarks of the attachment of the bacteria to the surface of the cell. Both pathogenic bacteria and fungi display on the cell surface, and polysaccharide capsules (virulent), mentioned in the form of Streptococcus Pneumoniae, but also in specific molecular moieties, put hindrances to both opsonin-dependent and opsonin-independent ingestions. It is also noted in research studies that the pathogens may secrete substances which undermine phagocytic work as well in its functioning to signal the need for phagocytosis, or exert a broad cytotoxic effect on hemocytes (blood cells).
It is important to note that hemocytes are mainly in cellular components of the blood in invertebrates, but also are noted as included in the presence or absence of blood cells in mammalian species, most notably human species.
Therefore I suspect that as fibronectin secretes glycoproteins of the cellular matrix in relation to membrane receptor proteins called, integrins, it undermines correct signaling data via the correct cellular response.
All this interference with the functioning of Phagocytes in regard to the expression of phagocytosis is indicative of immune suppression related to inhibition of phagocytosis where these symptoms occur; exhaustion, recurrent infection; and digestive problems.
The recurrent infections or the return of COVID-19 once it has seemingly been recovered from in the body involves the interference with the phagocytosis function. As known to scientists and doctors, phagocytes are crucial to fight invading infections as well as maintaining healthy tissues by removing dying and dead cells (Opsonin), that have reached their lifespan of productivity.
The phagocytes protect the body by their reactions to ingest damaging particles, bacteria, and dead, or soon-to-be dead cells.
All pro-functioning phagocytes have “receptors” which are molecules that are on the phagocyte surface which detect the harmful, invading objects, such as (but not limited to) bacteria antigens.
During infection, signals attract the phagocytes to those places where the pathogens have invaded the body. Chemical signaling from the phagocytes due to the bacteria or from other phagocytes already present, which attract more phagocytes to the infected area is called, CHEMOTAXIS.
When the phagocytes come into contact with the bacteria, the RECEPTORS, ON THE PHAGOCYTES’ surface will bind to them.
This BINDING-ACTIVATION will lead to dissemination of the bacteria by the phagocyte. It does so by releasing a chemical reaction upon the bacteria which is comprised of oxidants and Nitric Oxide (NO). This is part of the process of Phagocytosis.
Once this process is finished the phagocyte moves the particles of the non-dangerous leftovers from the antigen “debris” back to the outside, top of the phagocyte cell and the entire phagocyte itself moves TOWARDS THE BODY’S LYMPH NODES.
The non-damaging, pathogenic debris material is displayed to the other cells in the immunological system (IMMUNE SYSTEM), as well as the Lymph Nodes. The Lymph Nodes constitute what contain white blood cells, known as Lymphocytes. This is the process which is mandatory for building immunities to the invading antigen.
HOWEVER, THE DANGER TO THE BODY IS WHEN THE PATHOGENS, OR ANTIGENS, HAVE EVOLVED METHODS OF COUNTERING THE ATTACKS BY THE PHAGOCYTES, AND WHICH INHIBIT OR DELAY, OR STOP ENTIRELY, THE RELEASE OF THE DEBRIS TO THE LYMPH NODES. OR ANOTHER DANGER, WHERE THE ANTIGEN WAS CARRIED TO THE LYMPH NODES VIA THIS PROCESS INVOLVING SUBVERTING, OR MASKING THE ANTIGEN.
There are many ways bacteria, and/or antigens, avoid contact with phagocytic watchers in that they can grow in sites phagocytes cannot enter, or the invaders can also evade by by-passing the inflammatory response required to notify the phagocytes, or certain species of bacteria can inhibit the ability of Phagocytes to travel to the infected bacterial, or antigen site by interfering with CHEMOTAXIS.
Chemotaxis, again, is an important cellular response where a signal given, initiated by G-protein-coupled receptors, (GPCRs), on the cell surface bind with specific chemoattractants. These receptors share important structural similarities with other G protein-coupled receptors, including rhodopsin.
The chemoattractant “ligands” found in chemotaxis receptors exhibit a broad variety of sizes and chemical properties. They range from small at the molecular level, and peptides, to protein ligands, such as Langerin.
All this moves the cells toward transmembrane (TM), signaling where depending on the arrangement of the transmembrane, helices have been proposed in vivo as having the ability to use forms of ‘dimers’, which can be dim-formations that play a pivotal role in transmembrane signaling. Studies of genetic mutations have occurred to find out just how to identify and find if ligand-binding, receptor activation, and transmembrane signaling have been influenced through bacterial pathogens, which bring about interruptions in normal transmissions such as interference with normal chemotaxis performances. I believe I addressed one in a previous theory regarding macrophage.
Important to note is how compromised, negative-chemotaxis can contribute to many factors involving diseases. If the right signaling of receptors are interfered with, then the process involving chemotaxis can send the wrong signals, and/or not signal at all. These unregulated chemotaxis of immune cells can lead to inflammatory diseases, such as asthma and arthritis.
Asthma-like conditions and inflammation in branchial regions of the lungs, where increase are found in the symptoms associated with COVID-19 should be suspect in regard to negative-chemotaxis function.
** I am looking into Acetylcholine as a polar neuro-transmitter to bind with an ester, such as nicotinic or muscarinic, which are part of ester functional groups to possibly bring back the polar balance for right signaling but not sure if this is the right neuro-transmitting one. It may need to remain all on its own, simply Acetylcholine, which has an ester functional group already, and therefore can bind to a receptor protein, which is also called a LIGAND. But more on this theory at the ending of this paper.
Getting back to a previous comment/analysis, of some bacteria that elude phagocytes, by coating its bacterial surface, with FIBRONECTIN, which is produced in the body naturally, a research find states;
…the possibility that the modification of bacterial cell surface by treatment with Proteinase K affects in vivo, phagocytosis (since in a research analysis, the brightness of FITC-labeled bacteria results reduced both, in Escherichia coli (E.Coli) and another specimen, the ability of phagocytosis), therefore, yes, Proteinase K can negatively affect phagocytosis. (Source not given, but was performed Aug. 22, 2019).
However, I have since found alternative research involving the positive results involving this enzyme so I will have to defer to more research at a later time. But I do find it suspect that no name was attached to the negative effects of Protinease-K on phagocytosis in the aforementioned research. (Protinease-K May have considerations involving disease control and cancer).
**But, since writing this paper I’ve gone back and did more research and found that Proteinase K is used for the isolation of native high molecular genomic nucleic acids, as those found in certain bacteria in the cell.
A protease, also called a peptidase, or proteinase, is an enzyme that catalyzes (increases the rate of) proteolysis which is the breakdown of proteins into smaller polypeptides or single amino acids. This is accomplished by cleaving the peptide bonds within the proteins by hydrolysis. Hydrolysis is a reaction where water breaks bonds. Proteases are involved in many biological functions, including digestion of ingested proteins (not easily broken down in a normal situations), protein catabolism (the breakdown of old proteins), and cell signaling.
Proteinase-K is used for the destruction of proteins in cell lysates (tissue, cell culture cells) and for the release of nucleic acids since it very effectively inactivates DNases and RNases, (both part of the cell which compromise healthy DNacids-DNA and RNacids-RNA).
Therefore, I would highly consider Proteinase-K being used for the destruction of certain bacterium enzymes such as Streptococci, or E.Coli bacterium; but this is only to be certified by biologists and under safe conditions because I have not found a non-commercial grade yet.
Continuing on, I surmise that the antigen-pathogen virus, were first a product found in E. Coli ; as well as in Streptococci, which produce M-protein as mentioned earlier, and the Fimbral Proteins which block phagocytic engulfment by the antigen, or bacteria, due to the fact these mal-protein invaders hinder OPSONIN-related ingestions as they invade the host cell, and in my research, the B-cell. It is also why antibiotics do not effectively work, I surmise.
Whereas, STAPHYLOCOCCUS AUREUS produces Protein A, which has the ability to bind immunoglobulins, in order to block the antibody receptors (chemotaxis), which would otherwise have helped in the effectiveness of opsonins.
S. Aureus produces these numerous molecules that have the capacity to evade the immune system and this includes the Protein-A (SpA), which is an immunoglobulin (Ig)-binding protein present on the bacterial surface and freely secreted into the extracellular environment. SpA binds the Fc region of the antibody and the Fab regions of the B-cell receptor, processes that are known to block phagocytosis-opsonin whereby B-cell death occurs.
The fact that SpA subsequently promotes S. Aureus immunological evasion and antibiotic resistance, as well as methicillin-resistant S. Aureus (MRSA), has made it very enticing for me to view SpA as being suspect in that it has similar entrance capabilities present in pathogenic species of the genus Yersinia which bind with the use of the disease, or poison factor YopH, to receptors of phagocytes from which they influence the cells capability to exert correct response phagocytosis, or lack thereof.
Therefore, it has genetic expressions consistent with symptoms of genus Yersinia. All this may mean, or point to, PPAR gamma (Peroxisome Proliferator Activated Receptor) involvement. PPARy (gamma) being a key factor in cellular Adipose Tissue differentiation and therefore may be linked to Protein A (SpA) pathway and its significance whereby the antigen attaches to the protein and travels in vitro the same migratory signaling pathway as the genetic expressive bacteria normally routes. If any genetic expressive gene is hi-jacked by an antigen I suppose it will also interfere with moderating signaling pathways at dendritic links and subvert Adipogenesis.
It is here where I would like to invest time in the area of study with respect to bio-information in regard to activation pathways, transcription pathways and hemocyte function found in Plasma and Immunoglobulin. The hi-jacking by pathogenic antigens of the cells in Adipose Tissue, which includes the Endothelium, perhaps as mentioned via PPARy (gamma), will also be highlighted with its post-effects due to passageways via capillaries into the vascular, and endothelial cells.
The Vascular, and Endothelial Cells, which are the lining of the entire CIRCULATORY SYSTEM, and which function throughout the body’s transport system by way of blood vessels and capillaries, were in my opinion the naturally targeted region as proposed earlier, due to the allure of the rich fat deposits therein known as lipids, which are metabolized and controlled by the Endothelium.
** The Endothelium is the gateway that prevents the penetration of circulating lipoproteins into the arterial wall which can otherwise cause arterial sclerosis and other circulatory defects.
Furthering my investigative work, it became obvious the macrophage, hepatocytes, and adipocytes, all which promote lipid disposition throughout the body, which comprise the plasma and connective tissues of the body are being unwilling participants in this virus takeover.
For example, the macrophage, which are immunity cells, and are a type of white blood cell (leukocyte), respond to the foreign invader, such as infectious organisms and ingest the foreign material. They are found in the liver, spleen, and connective tissues of the body. Their job in the Adipose Tissue immune program is to keep the healthy cells calm and in a state of HOMEOSTASIS.
However, as suggested that the macrophage have become over-laden with excess lipids (fat) in ingesting the foreign particles that had become virus-driven, bacterial protein-enzymes, with lipid-enriched wall membranes adapted by the virus, and/or as a result of the effects of its entrance into the connective tissues of the body via mucosa, are now in a state of oxidative maladaptation.
These negative functioning macrophage have become metabolically activated phenotypes, which under normal states of homeostasis keep the macrophage calm, are now releasing enhanced oxidative stress and therefore the secretion of cytokines and chemokine. The release of Cytokine and Chemokine cause more LDL/remnant oxidation, Endothelial cell activation, and monocyte recruitment. Such an activation may be what triggered erythrocytes to incite pro inflammatory responses near the endothelial lining.
Erythrocytes travel close to the lining of the endothelium and therefore capillaries.
This aggressive protein monocyte (single-celled) recruitment can suck into its cell any protein cell structures such as the adherence proteins (VCAM-1, ICAM-1, and P-selectin), among others.
My studies have established a clear link between these aggressive adherence proteins, which I believe have been the causal effect of the misinterpreting of chemoattractant signaling within the cells surface, such as the B-cell, and also involve dendritic malfunction accessibility from both the lipid and cytoplasmic side of the transmembrane (TM).
These Endothelial cell activations in Macrophage/Phenotype leads to increased production of reactive oxygen species (ROS) that can cause oxidative modification of apopB-containing-lipoproteins.
Besides mechanical stimuli, Endothelial cell activation is increased by various molecular stimuli, including, oxidized LDL and cytokines, as well as advanced glycosylation end products (AGE’s), and pathogen-associated molecules.
In contrast, an ARTERIAL PROTECTIVE function of HDL (high-density lipoproteins) is to prevent endothelial activation and enhance Nitric Oxide (NO) production to maintain barrier integrity within the endothelium and its proliferation of mal-dendritic cellular activity via capillaries. Oxidative stress in these macrophage cells, which leads to oxidation of lipoproteins, and in particular of low-density lipoproteins (LDL), is a negative reaction to the synthesis of developmental atherosclerotic plaque brought on by the presence of these.
**These oxidized lipoproteins cause atherosclerosis by the inhibition of the right breakdown of lipids, which otherwise control arterial clogging plaque; as well as the pro-inflammatory receptors such as toll-like receptor 2, (TLR2), and cytokines (MCP-1 and IL-8, and GM-CSF)
(I want to invest more time into studying of these specific receptors, MOST ESPECIALLY GM-CSF, but I leave it for now for the end of this paper. However, suffice it to say no research is needed to know that when these nuclear receptors are affected and inhibition of correct lipid breakdown the results are misguided interpretations which release pro inflammatory responses such as these).
Nitric Oxide (NO) has the ability to bind with free-radicals, which helps to prevent against good cells dying prematurely. This is accomplished as NO keep free-radicals “busy, or occupied” and therefore NO inhibits free-radicals from killing good, healthy cells. This is even one of the foundations of research against aging prematurely.
HOWEVER, IMPORTANT TO NOTE IS THAT EVEN THOUGH (NO) IS USUALLY LACKING IN OUR BODIES, OVER ABUNDANCE OF (NO) CAN HAVE NEGATIVE CONSEQUENCES OF WHICH SHOULD BE LOOKED INTO BUT NOT FOR PURPOSES OF THIS STUDY/RESEARCH AS INVARIABLY (NO) IS REDUCED IN THE BODY DUE TO PRO-INFLAMMATORY RECEPTORS, DURING COVID-19 VIRUS IN-VITRO.
Oxidation of lipoproteins does not unfortunately result in the generation of a single, defined molecular species; BUT OF A VARIETY OF OXIDATION-SPECIFIC EPITOPES (OSE), such as oxidized phospholipids and malondialdehyde epitopes. These oxidized-Phospholipids are one of the core suspects in the redefining of correct functioning of cellular activity involving surface of the cells and their polar or non-polar receptor bonds. At least this is my understanding involving COVID-19’s overtaking of correct Immunological cellular responses.
Unique monoclonal antibodies have been developed to bind these well-defined epitopes, and have been used in-vitro assays to detect them on circulating lipoproteins present in plasma. Much of this involves research to prevent atherosclerosis.
In plasma, the antibody, also known as Immunoglobulins, are Y-shaped proteins produced by the immune system to help stop “intruders” and are attracted to the invading virus, bacteria, pathogen, or other chemicals and becomes attached to it. This is known as an ANTIBODY RESPONSE. The antibody, acting as nature’s chivalrous “dance partner”, pairs with the antigen along the peptide chain to occupy it, and keep it incapacitated.
For example, IgG (Immunoglobulins), are the most common antibody present and predominantly found in the blood and tissue fluids but also in other regions of the body in lesser mass quantities with respect to overall mass percentage. There are five types of Immunoglobulins in Plasma.
IgA is one such example of where it is found in the mucous membrane which line the respiratory and G.I. Tracts (gastrointestinal tracts).
There are however exposed parts to which this organized coupling of antibody to antigen along that poly-peptide chain (epitopes), found in regions of the blood and tissue fluids, may cause the exposed, (non-epitope binding) site to become the source of the invading antigen’s negative effect upon the various systemic functions of the body.
There are two forms of Antibodies. The soluble form and the membrane form. And since we know most antibodies are found in the Immunoglobulin, I shall first begin with observances of antigen COVID-19 attacking the systems managed by the five Immunoglobulin
However, since the “walls” are weak and are made up of a sequence of amino acids (proteins) that inadvertently bind to other molecules which are selected in order to maintain their active molecular structure, the virus maintains its integrity, by using selective reasoning. It mutates to stay alive, after it is not overcome by the antibodies’ function. The antigen/virus, or compromised-protein cell, continues its move and looks for options to keep it stable, to stay alive, for it is structurally unstable without cellular “walls” or membrane, so it takes advantage of healthy Adipose Tissue, present throughout the body, in skin (subcutaneous fat, especially the brown tissue, and around internal organs/visceral fat), and bone marrow (yellow), Inter-muscular (muscular system) and breast tissue. It does so by “eating up” the fat which give it the wall it needs to protect itself, and become stable.
I believe the entrance of the virus and into the human body was through the Sinusoidal, or Discontinuous, capillary pore openings of the sinus (nostril), and mouth cavity. These capillaries contained in these regions have large open pores which allow a blood cell through. The virus traveling through the Sinusoidal capillaries are able to facilitate the transport and exchange of fluids, gasses, and nutrients throughout the body’s systems. The capillaries are where the exchange of certain processes take place which then transport the products of the fluids, gasses, and nutrients throughout the body’s arteries and arterioles. These transports are carried into Adipose Tissue, and Plasma.
As stated earlier, the virus, attaching itself into the enzymatic function of a string of amino acids which form the protein enzyme, go into the wet or moist cells of the mucosa found in the lining of the nasal and mouth and are transported throughout the capillaries into the Adipose Tissue and Plasma of the body.
Symptoms of the antigen-enzyme entering the mucosa, initially may be evident by the nose being dry, as well as the throat, due to the virus attaching itself to the cellular host-tissue matrix, which gives it stability in the body and protection, but then enter the Macrophage cells, as well as other bodily systems which are trying to destroy the entrance of the antigen.
However, it is my suspicion that the antigen, which became an epitope, not only acts like a normal virus, where the antibodies are rushing to help fight the infection and gave it the epitope status, but also like a pathogen, whereby the IgA (Immunoglobulin A) antibodies which are found mostly in the nose, airway passages (lungs), digestive tract, ears, eyes, and saliva, have become derelict in their ability to carry out the job they were created to do. Also, as referenced earlier, antibodies cannot bind to pathogens that have already entered a Host Cell.
In fact, some viruses that act as pathogens (HIV and HSV for example), are dormant inside the cell for long periods of time. This may be why when some people have gotten better, or seem to be past the COVID-19, then it returns again. I also have other theories about why it returns but I will address that later in this paper.
As the capillaries are used to transport the virus via macromolecules into the plasma, as well the fat deposits of the Adipose Tissues, which surround the internal organs, where the visceral fat is comprised, as well as the skin (subcutaneous layers of fat deposits), and inter muscular regions as well, it is obvious by the symptoms (extreme lack of overall energy) that it has compromised this region’s abilities to defend itself. One of the signs of fatigue being the non-delivery of triglycerides and other fatty lipids which comprise the functioning of the Adipose Tissue system.
THE ADIPOSE TISSUE
The Adipose Tissue tries to defend compromising agents by releasing Macrophage cells, which are immune cells important for maintaining homeostasis in healthy Adipose Tissue. Homeostasis is crucial for maintenance of bodily insulin sensitivity. It releases the insulin by the breakdown of the lipids as stored energy that gets sent to all parts of the body via Macrophage, along with hepatocytes (liver cells), and adipocytes (found in connective tissue), all which promote lipid dispersion throughout the body because they are fat-laden (enriched with fat), which have now become engaged in warfare or defense, and disposition. The Macrophage also become overloaded as they try to ward off the antigen invader. Homeostasis is disturbed, altering the production of several inflammatory cytokines and adipokines. The increase of these now inflammatory cytokines and adipokines can disrupt normal insulin signaling (and contribute to obesity-associated insulin resistance). Again, one of the symptoms of COVID-19, where diabetics are more susceptible to its interruption of insulin signaling, which they’re already having to deal with. It exacerbates this arena of finding insulin balance. Interesting to note, is in lean persons, the Adipose Tissue macrophages predominantly show anti-inflammatory phenotypes and are distributed EVENLY throughout the Adipose Tissue.
In contrast, obese Adipose Tissue display macrophages accumulated in so-called, “Crown-like structures” around dead adipocytes and display a METABOLICALLY-ACTIVATED PHENOTYPE.
A PHENOTYPE being an organism that shares BOTH GENETICS AND ENVIRONMENT. I have learned that COVID-19 displays such features which, IF ITS TRUE, means the macrophage of patients with the pathogen have now entered a stage where the cellular makeup has become a maladaptive cell and the macrophage are no longer defenders but pathogenic cellular carriers of the antigen/pathogen.
In Plasma it appears all antibodies have become corrupted and/or engaged in epitope binding, therefore new red blood cells are fighting with newly birthed antibodies to thwart, or regain control over the invaders. This is where healthier bodies, or people under a certain age are having advantages in regard to stronger immunological rebuilding, or replenishment of Immunoglobulin Isotypes. In one of my suspicions I believe particular attention should be paid to the Quaternary Structure of the polypeptide chains due to the fact the Quaternary is both Globular, and Fibrous, due to its lack of ability to hold the shape of the protein which may indicate it takes on various “personalities” depending on the mutation of the action, and therefore, biological polymers are at play.
Amino acid enzymes, coupled with protein lipids such as Protein-A (SpA) may be involved which became aggressive and mutated. The polynomer receptors and covalent bonding mechanism needs to be broken in the chain to bring to a state of homeostasis. In Protein-A, antibody dimers and Cu metals are attracted to positive and negative ions. Zinc, a transitional metal can break a bond of CH-CH. Which if Protein-A (SpA) has become a covalent bond with a antigen enzyme in vivo, the zinc would have important benefits to break the bond, and maintain homeostatic behavior.
Important to note is how the corruption of plasma may have transpired. I believe a new answer was given me by the latest symptoms being reported, at the time of this particular writing.
Today, new symptoms have been reported by the medical community that patients with COVID-19 are experiencing unprecedented blood clotting. Immediately my mind went to Heparin. (news reports will verify what day this transpired).
Heparin is made by the liver, lungs, and other tissues in the body, but can also be made in laboratories. Heparin is used to break up blood clots or to prevent blood-clotting. It is a type of anticoagulant.
In my previous research I had found that the MAST CELL, also known as a mastocyte or labrocyte, is a migrant cell of CONNECTIVE TISSUE, that contains many granules rich in HISTAMINE and HEPARIN.
Mast Cells are found close to small blood vessels in loose connective tissue. Specifically, it is a type of granulocyte derived from the myeloid stem cell that is part of the immune and neuron-immune systems.
The Mast Cells are known for their role in ALLERGY and ANAPHYLAXIS and contain large secretory granules of HEPARIN PROTEOGLYCAN, which is a weak anticoagulant. Therefore, in my analysis of the events unfolding today via information related to COVID-19 patients experiencing an increase of blood-clotting in the body, it helped add one more piece of the puzzle in ascertaining where the initial invasion of the virus arrived and where it had thrown the body into confusion.
The reports of these symptoms tell me that if blood-clotting is happening throughout the body then the MAST CELLS ability to release HEPARIN PROTEOGLYCAN has been stopped. Since we know Mast Cells play an important protective role as well as being intimately involved in wound healing via, angiogenesis (development of new blood vessels); immune intolerance (ability to give immunity); defense against pathogens, as well as the maintenance of the BBB (Blood-Brain Barrier) Function, then this Mast Cell system has been hi-jacked, or corrupted.
In the Immunological function of the IgE, (specific antibody found in plasma), antibodies reside in LUNGS, SKIN, AND MUCOUS MEMBRANES. When the IgE is active, the antibody triggers an allergic reaction called a hyper-sensitive reaction. This hypersensitive reaction causes the allergen to bind to the Immunoglobulin on SPECIFIC IMMUNE CELLS, called BASOPHILS and MAST CELLS.
This binding results in the release of chemicals that cause inflammation in the body such as, HISTAMINE, SEROTONIN, PROTEASES, BRADYKININ GENERATING FACTOR, CHEMOTACTIC FACTORS from various immune cells, LEUKOTRIENES, PROSTAGLANDINS, and THROMBOXANE, all which can happen within 30 minutes of exposure once the IgE is active and the release of chemicals which cause these reactions.
These chemical “mediators” just mentioned can also cause allergy symptoms, such as urticaria (hives), runny nose, watery eyes, sneezing, wheezing and itching, NOT AS A RESULT of the COVID-19 VIRUS itself, but more as being the results of the chemicals released due to the pathogens binding on these immune cells. In other words, these symptoms are being triggered as trait-effects of IgE being activated as binding to specific cells, but not due to the cause of the pathogen directly.
COVID-19 Virus is the entrance of a protein-side-chain-bacterium, entering through the nose, ears, eyes, and saliva, which send the Virus/Pathogen, (possibly enteropathogenic species of the genus Yersinia, Escherichia coli, or Staphylococcus Aureus) throughout the body via the Mucous Immunoglobulin A (IgA) antibodies. The IgA antibody CAN ALSO BIND TO THE MICROBES IN THE MUCOUS, which in turn neutralize toxins by binding with them.
However, if the pathogen or bacteria has by-passed the IgA antibodies by way of using fat cells, or lipids, of the mucosa as the “host cell”, it can thereby evade the initial binding response by the antibodies.
Once it has maneuvered past the IgA antibodies, inside the host of lipids which include, fatty acids, glycerolipids, glycerophospholipids, glycolipids, sterols, polyketides (produced by fungi), and prenol lipids, participate in organizing of membranes to keep it alive as they continually “eat up” the lipids, in order for the new invading pathogen/bacteria Host to maintain structure.
These entry mechanisms of using the cell membrane lipids as host to the bacteria, or fungi, were essential to the life preservation activities required for the continuation of the microbes in vivo.
The invasion of the bacteria, or antigen/COVID-19 inside these lipid hosts can also dupe the inflammatory response. And since, as stated, antibodies cannot enter a host cell (as this virus/pathogen has become a eukaryote), then the normal response of the release of chemicals that cause inflammatory response at the first release: histamine, serotonin, proteases, leukotrienes, etc, within 30 minutes of exposure, are all but non-existent at the first, due to the evasion of the signaling receptors on macrophage via phagocytosis being interfered with.
This is the more universal reaction to COVID-19 which shows the nose to not exert mucous, i.e. runny noses as the first site response due to the antibody response mechanisms being subverted, but not to say it won’t happen eventually.
BODY TEMPERATURE RISES
The cytosol is the liquid inside a cell and it also comprises the cytosol cellular matrix involving organelles. When the bacterial pathogen/antigen first arrived as a prokaryote virus, it needed fat to stay alive and construct a “membrane”. The fatty deposits are not a long-lived solution, and its burning them up in the action taking place of thermogenesis, which causes body temperature to rise (another symptom of COVID-19 in the earlier stages, of endothermic reactions).
In the Adipose Tissues where the host cell antibodies have mutated to form a new cellular description, is now traveling throughout the tissues and thereby affecting the cellular structures involved in the care and release of homeostasis in the cells surrounding all the internal organs. These areas of the internal organs include subcutaneous, brown tissue region of the underlying skin, where the most lipid deposits are. Inflammatory active sites involving Lupus related reactions were taken care of with the malaria drug, Hydroxychloroquine, a treatment used for Lupus sufferers. It gained positive results for treatment associated with COVID-19.
The heat activated reaction of thermogenesis is caused by oxidative stress (which is a well-known etiology factor in the development of cardiovascular disease as well) by the macrophage reaction to the toxins surrounding the pathogenic cellular invader. It reacts with foam cells as well, which is indicative of overladen macrophage mostly on blood vessel walls. Patients with COVID-19 had reported feeling hot whether there was a high temperature or not, as I recall, which I believe was attributed to the heat activation of oxidative stress and can be also found in the Endothelial lining of the cellular matrix which involves the BBB with transport proteins which go through Endothelial Cell Activation. This in turn leads to increased production of Reactive Oxygen Species (ROS) that can cause oxidative modification of apolipoprotein B (apo B-containing lipoproteins, and therefore oxidative cell activation.
In the Adipose Tissue, in the fatty cell structures where the oxidation is taking place, producing oxidation of lipoproteins which does not result in the generation of a single, defined molecular species, but rather of a variety of oxidized specific epitopes, such as oxidized phospholipids and malondialdehyde-lysine epitopes; unique monoclonal antibodies have been developed to bind with these well-defined epitopes, and have been detected via circulating lipoproteins present in plasma, under normal conditions and to which the body is able to perform. However, in this instance and under the conditions to which this pandemic is illustrating I believe the antibodies have not been able to bind to these epitopes.
There are TWO MAIN BIFURCATION POINTS which I theorize have become reasons why various symptoms have arose regarding COVID-19, and they are : Adipose Tissue System (Adipose tissue, and Endothelium layers), and Plasma, to which I will now put my attention toward the mutation in vivo involving the Immunological System being hi-jacked, which affects the Plasma, but also, results in the fat tissues via the Adipose Tissue System becoming inflammatory which releases oxidative meal-adaptive measures and thrusts the COVID-19 throughout the body.
The Endothelial Cells that prevent SOLUTES in the circulating blood from non-selectively crossing into the extracellular fluid of the CNS (Central Nervous System) where neurons reside, are handled through the BBB (Blood-Brain Barrier) function.
The BBB is formed by Endothelial Cells of the capillary wall, astrocyte end-feet ensheathing the capillary, and pericytes embedded in the CAPILLARY BASEMENT MEMBRANE.
This system (BBB) allows the passage of some molecules via PASSIVE DIFFUSION, as well as the selective transport of various nutrients, ions, organic anions, and macromolecules; such as glucose, water, and amino acids (crucial to neural function).
The BBB restricts the passage of pathogens, the diffusion of solutes in the blood, and large hydrophilic molecules into the cerebrospinal fluid, while allowing the diffusion of hydrophobic molecules (O2, CO2, and hormones), as well as small polar molecules. Cells of the BBB actively transport metabolic products such as glucose across the barrier using specific transport proteins.
If this passive diffusion transport of various macromolecules such as glucose, water, and amino acids, that are crucial to neural function has been compromised via normal passive entry turned pressurized, intercellular matrix thrust into the brain by way of hydrophobic or hydrophilic macromolecules being compromised, this needs to now be addressed.
An enzyme acting as a catalyst can carry a damaged protein cell structure, piggy-back in a string of sequential amino acids (proteins) through an exothermic reaction (body temperature rising, due to ADP not being released from the cells) and this can result in an activation energy. Entropic is the change from a state of order to a state of disorder. Of course, if the entropic can be stabilized to look like order, then the virus is more dangerous or deadly. This could be the transporting of the pathogen at the microbe cellular level as it goes through the passive diffusion through the BBB.
For example, if substances with high, lipid solubility move across the BBB via simple diffusion, this would create the scenario of the bacteria invading at the microscopic cellular level which would enter most body areas involving not only regions that involve plasma, but also tissue regions that involve bodily organs.
However, blockage caused at the BBB, recognized by symptoms which include COVID-19, where patients feeling pressure and hallucinatory states with severe pain is indicative of blockage at the site. This may be caused by inflammation which would restrict blood flow and cause pressures of the brain due to restrictions on passive diffusion, or inflammatory cell states of the B-cell. The possibility of the antigen-binding-soluble antibodies being released into the tissue and blood, as well as secretions, surveying for invading microorganisms are being hindered or stopped altogether due to the occupied Memory B-cells with Helper T-Cells which are no longer functioning in the capacity to which they were designed. This would be the concern for any cellular activity, such as T cell derived Protein S (Pro s1, which engages TAM-signaling in dendritic cells to control myeloid lineage dendrite cells, if it would be compromised; which I surmise it has.
The surveying antibodies of the IgD plasma super family called, GLYCOPROTEINS, constitute most of the gamma globulin fraction of the Blood Proteins. They are typically made of basic structural units, each with two large Heavy Chains, and two small Light Chains.
There are several types of antibody Heavy Chains that define the five different types of crystal-like fragments (Fc’s) that may be attached to the antigen-binding fragments. In other words, these glycoproteins are not functioning in the capacity they were also designed to do and are incapacitated.
The solution is to free these super-family of Immunoglobulin proteins such as the glycoproteins to function again and release the antibody chains to function as antigen-binding agents once again. This has to start with the BCR, found only on the SURFACE OF THE B-CELLS, and facilitate the activation of antibodies into the needed form (Soluble or Membrane Form) to contain, or overcome the antigen/pathogen. The “antibody factories” known as PLASMA CELLS and the Memory B-Cells, work together to first eliminate the virus, antigen, or pathogen, throughout the body’s plasma and tissue regions, but then the memory B-cells remember the same antigen, pathogen, bacteria, or chemical, and respond faster for any future invasions, with the ability to mobilize the Plasma cells again, but with faster response time.
It is at the Crystal-like Fragments (Fc) which comprise the five different types of antibody HEAVY CHAINS, which attach by way of these Crystal-like Fragments to the antigen-binding fragments along the chain. IT IS AT THESE Fc REGIONS THAT A PARTICULAR ANTIBODY ISOTYPE IS ABLE TO BIND TO ITS SPECIFIC Fc Receptor along that chain. It is the small region (of 5 to 10 amino acids) of the antibody’s Fc region , which is part of the fragment antigen-binding Fab (alpha-beta) region, that contains parts of the antibody’s Heavy and Light Chains.
The five different types of Fc Regions which allow antibodies to be grouped are comprised of FIVE (Antibody) ISOTYPES; Immunoglobulin family of: IgG, IgA, IgE, IgM, and IgD. These antibodies comprise a large portion of blood/plasma makeup.
Each Fc Region of a particular antibody isotope is able to bind to its specific Fc Receptor (FcR), except for IgD, which is essentially the BCR (B-cell receptor). It is on that surface that the B-Cells are found and facilitate the activation into EITHER THE BLOOD OR TISSUE FLUIDS.
They, The Antibodies, are either sent through in one of two ways: One is a Soluble Form, and the other, a Membrane Bound/Receptive Form, where the Soluble Form is secreted from the cell to be free in the blood plasma and coated with immunoglobulin G (IgG), antibodies which signal other cells to destroy the bacteria on the surface, and the Membrane Form that is attached to the surface of a B-cell, referred to as the B-cell receptor (BCR).
However, since in the case of COVID-19, which I surmise, the antibodies have coated the bacteria cell with the Receptor coating such as the COMPLEMENT PROTEINS (C3b and C4b, and other opsonin-type attaching antigens to phagocytes), the cell becomes an Opsonin via its chemical receptor output and disguises itself so that it is not eliminated as the other antigens usually are.
In this specific case, with COVID-19, the bacteria-pathogen gained access to the cellular host, (possibly a macrophage-phagocyte) and the antigen-bacteria protein enzyme tricked the cell to gain access and what it needed to replicate.
I make the theory that the bacterial-pathogens first line of attack had to be at the IgM ISOTYPE due to the fact IT IS THE FIRST ANTIBODY TO BE MADE BY THE BODY TO FIGHT NEW INFECTION, but once it was duped, as the virus entered the Host Cell Structure bypassing the antibody to create a new cell structure, it stopped using IgG and IgA immune defense system because the Phagocyte became an opsonin, and disguised itself. Therefore, in my opinion testing for COVID-19 using a system whereby IgM antibody was used to test for invasion of the antigen would return a negative result even if the antigen were present in the body because it is disguised.
Therefore, with the knowledge that the IgM is found mainly in the blood and lymph fluid, I surmise that once this infectious antigen-pathogen began it’s entrance into the mucosa via the nose, eyes, mouth, and possibly ears, the invasion took over the blood and lymph fluid via capillaries which held dendritic end-cells, and emptied the virus-pathogen-protein enzyme through specific transport proteins throughout the bodily systems beginning with the mast cell in the connective tissues and traveling to the B-cell and affecting the BCR. This is the primary source which has infected the antibodies of the immunoglobulin as well as red blood cellular activities in plasma governing mast cell proliferation.
These now virulent transport proteins, have corrupted the various Mast cells, lymphocytes, platelets, basophils, macrophage, opsonin, and phagocytic defense teams to make them mal-efficient conductors where they’re either inhibited or acting in non-functioning states and have created new problems for the organisms they were meant to protect.
The undefended organs which include; heart, lungs, liver, kidney, stomach, and skin, are now left unattended by their defense-mechanisms. So, the science community watches helplessly as the doctors can only provide cures to offset the SYMPTOMS of these attacks, and hope the body’s defense system will re-boot once the organs are treated to enable them to recover.
Recovery is via the fact the body is continually making new blood plasma cells which carry new antibodies (immunoglobulins) to fight the invading pathogen as well as the fact that treating the symptoms pertaining to the specific organ, or vascular-related decline (because of the corruption of the body’s defense system), gives the body time to regenerate and re-boot with respect to fighting the offending virus-pathogen. And this is possible if there is any break in the chain of activity of the antigen. However, the worst case scenario is if the corruption into the virulent pathway has led to replicating various disease related protein entryways via Transmembrane or tainted cellular membrane functions which find their way through stem cell uptake and down take, or into the vascular and tissue systems, or connective tissue which govern the new blood line. But, as I believe, there is still always hope, and hope does not make us ashamed. So, with treatments related to the various symptoms associated with certain diseases and cancers brought on my COVID-19, I still believe either treatment of the disease itself is a viable solution, in combination with breaking of the chain of virulent activity at any spot along the way of various known symptoms of COVID-19. This includes options that involve therapeutics which are effectively known to break certain bonds, such as the case with Zinc, and Vitamin C (which is an ester that strengthens the efficacy of zinc). Also, must be tested by scientists for its heath related effects and how to administer it, but also Protinease-K, and/or Lactoferrin, which is a glycoprotein that binds easily to iron; and helps boost immune response. The claim from Lactoferrin proponents is that by capturing the iron present around an infection, Lactoferrin deprives pathogens of their nourishment and thus their proliferation. N-Acetyl Cysteine would also have to be looked into for its properties to which I have not yet investigated but have heard good things. Lastly, collagen, found in bone broth or via therapeutic-collagen, which contain bone building food to strengthen the site where the most serious impact of COVID-19 first began, with regard to mast cells, in my analysis. I still defer to Hydrochloroquine and its positive outcome for many COVID-19 victims, turned survivors. Also, erythromycin in some earlier cases involving, I surmise, bacterial infection where the mast cell or macrophage host had not yet been entered.
And not to dismiss my preventative theory that by keeping the body’s internal systems in a constant state of homeostasis, and therefore inflammation down, quercetin’s properties mostly found in garlic and onions, are natural effective measures. But watch out if you are on high-blood pressure medications, as stated earlier. And to non-scientists, and non-doctor related personnel, always check with your doctor first to avoid any drug interactions, especially if you’re on pre-existing medications related to pre-existing conditions.
So, early response to the COVID-19 is detrimental in stopping an increase of the severity of symptoms, and its progression, and to stop the pathway activation of a more serious outcome later, I believe. And these cures have already been successful via the ones reported by the White House; with the possible exception of the blood plasma being used for transfusion which is a very unstable method unless ways have been discovered to check for COVID-19 antibodies not related to IgM, IgA, or IgE Immunological antibody checks.
***. I would also like to make a suggestion about a possible effective way to check for the presence of COVID-19 using what is normally used to test for Lupus, CHROMATIN ANTIBODY RESPONSE, via use of A-ChrVariant to check for antibody in response of COVID-19 being present in connective tissue, which is where I stated was the first line of invasion via tissue membrane and subsequent mast cells, and/or macrophage cells. This would be consistent with the presence of high-mannose N-linked oligosaccharides on A-Chr subunits that are present on the endoplasmic reticulum (ER), and/or in the Golgi, via presence of COVID-19.
Now, with respect to the cause of the invasion and stopping it from continuing its path of destruction, I revisit the site of the pathogen’s ability to enter into the body’s internal systems (in vivo).
In order for it to bypass the BBB’s (Brain-blood Barrier) well-designed protections against antigens, as well as allow passage of healthy cells, which the BBB is having trouble doing, the antigen had to evade the defense systems specific to the BBB, and as stated previously.
Therefore, in one of my hypothesis, the bacteria enters the mucosa cavities of the nasal, and sinus passageways (indications of pink-eye) then it implants directly into the adipose tissues, blood-plasma, and Lymphatic regions of the body, via enzymatic protein chains, with side chain bacterium. Initially this prokaryote, which began as a single-celled organism which had neither a distinct nucleus or membrane, nor any other specialized organelles, which is by definition, bacteria or Cyanobacteria, found a host cell to become a Prokaryote turned Eukaryote.
In the plasma this now paratope, I surmise, in which the antigen-paratope became tightly bound to four polypeptide chains to join the Heme Group (IgG) of antibodies in the plasma have caused the blood antibodies to become corrupted.
I derived at this by all the definitions which fit the obvious results that the initial experiment in Wuhan, China involved gene expression experiment with regard to E. Coli, or some type of Group A-Streptococcus bacteria, which are known to produce proteins such as (Myeloma)-Mal-protein M (M protein), and Fimbrial Proteins (which block phagocytic engulfment and interfere with phagocytosis). M proteins hinder the work of opsonins which ingest the debris of the antigen/pathogen and aid Immunoglobulins.
In my opinion and in order for the evasion to be effective in the course of this devastation of by-passing the immune system, then one of these strains of bacteria has to be in play which mediates the by-pass of antibodies influence.
GROUP A- STREPTOCOCCUS (or GAS), ALSO KNOWN AS STREPTOCOCCUS PYOGENES, is important to note that while a pathogen in humans (showing toxic shock-like syndrome, rheumatic fever, and necrotizing fasciitis), its encoding marks it as a eukaryotic-like signaling enzyme. Therefore it may have began as a prokaryote and like stated, became a eukaryote once it entered a host cell such as macrophage, or mast cells.
So, assuming this group A bacteria is one of the antigens which has compromised the body’s defense systems, this gene-expression would express M-protein. This bacteria would have a DNA structure organelle system and can replicate the functionality of RNA with non-protein coding genes such as transfer RNA (+RNA), or small nuclear RNA (snRNA) to give it its processing control.
Gene Expression as defined, is the process by which information from a gene is used in the synthesis of a functional gene-product. These products are often proteins, but in non-protein coding, genes such as transfer RNA (+RNA), or small nuclear RNA (snRNA) genes produce a functional RNA.
It would account for such diverse symptoms and various disease associations to COVID-19.
The possibility of mast cells being employed in the service of gene expressive RNA functionality such as PLASMODIUM PATHWAY, as a replication genotype would increase the chances of the specificity of the harm plasmodia genus replication would do.
These could include the DNA association of the three genotypes (transposons & viruses) involved with the plasmodia genus involved in such disease as MALARIA. Other DNA associated genotypes of the plasmodium pathway CD44v, other than Malaria type infectious disease, are Sickle Cell Anemia (SCA), where the mRNA of the betaglobin protein is one of the subunits of hemoglobin, a protein necessary for oxygen-carrying function of red blood cells. Interestingly, SCA, which has a mutation in the amino acid sequence, leads to a clumping of deoxygenated hemoglobins, which changes the red blood cell shapes. This clumping, or aggregation of red blood cells was one of the symptoms associated with COVID-19. Therefore, it is suspect as to the cause of the aggregation of platelets. Consideration may also involve the Haldane Effect caused by release of erythrocytes, and which allows for 50% of the CO2 given off by the lungs.
Involvement includes, cerebral spinal fluid (CSF), which has an osteopontin-protein consistently elevated in patients with CNS, LCH.
Langerhans Cells Histiocyte (LCH), has in its employment peripheral monocytes which create active lesions of lesion V600E pathway. Acute-phase lTlH4 levels distinguish multi-system from single-system LCH via plasma peptidomics. Birbeck’s Granules are a significant connection to COVID-19 in their response to LCH, and may be the carrier of the antigen throughout the skin cells in the endothelial layer cells.
LCH is a proliferative disorder in which abnormal Langerhans Cells, or LC-types, intermingle with inflammatory cells. The appearance of LCH lesions are evident under a microscope and to which I believe are reactionary and produce inflammation as a response to the lesions which may occur on the IL-1 loop prolonged by BRAF-mutation. Other synonyms or IL-1 are, IL-18, cytokine IL1-F4, and Uniprot.-Q14116, structure-2VXT (with antibody).
This pathway CD44v which has the Langerin Cell involvement proliferating disease via peripheral monocytes should be further scrutinized as I believe the cures of multiple diseases are within its Chamber of Secrets. But, I will say that I see a connection between serum albumin, or lack thereof in certain cases, as well as fibrin (factor 1), Langerin lesions, and osmotic pressure.
I will furthermore say in my hypothesis of COVID-19, that it’s link to Langerin may be more significant than I first postulated. And whereby I would like to say:
The RNA replicates the DNA messaging of the “host cell” which has become the mast cell in connective tissues, as it tries to stop the antigen/eukaryote. Instead it’s a carrier of expressive genotype-behavior present on RNA and ribosomal carriers of traits, from antigen into plasma via dendrites, which also lead into capillaries of lungs. Osmotic pressure resulting from lipolysis (presence of oxLDL, and HILPDA in macrophage lipid droplets) may be causing dendritic force whereby capillaries are taking in unwanted lipid droplets, and therefore lesion formation as arteriosclerosis present.
Endothelial pathway using cerebral and stem cell (myeloid possibly) uptake and downward movements into branches of dendrite activity leading into capillaries. The incorrect signaling by basophils, corrupted cells, and leukotrienes into ignited white-blood cell behavior reactions to antigen’s presence in vivo, are being viewed as foreign particles in the plasma.
The fractures states of the quaternary structure is possibly due to a lesion on one of the folds, possibly loop 18, or loop 19 (IL-18, IL-19). Interleukin-18 is a member of the IL-1 family of cytokines.
Amino protein chains in plasma received corrupted files of protein combined with glycophospholipids. The coating of phospholipid onto the protein enzyme through TM, or as I refer to it, the Chamber of Secrets, went through hydrophilic rather than hydrophobic processes, or vice-verse depending on the structure that was required. What is required is also to break the adherence with polynomer receptors which will break the chain by bringing to state of homeostasis. Also, stopping covalent bonding mechanism. Two things are happening separately, and not as one and need to break the chain of covalent bonding, and one way to do this may be to introduce another catalyst to cause healthy bonding in Immunoglobulin, and separate issue is calm the reaction of foam cells during macrophage negative build-up.
The BCR is found only on the surface of B-cells and facilitates the activation of these cells and their subsequent differentiation, depending on which FcR it binds. The ability of antibody to bind to its corresponding FcR is further modeled by the structure of the glycans present at sites within its Fc region. THE ABILITY OF ANTIBODIES TO BIND TO FcR’s helps to direct the appropriate immune response for each different type of foreign object they encounter…
These (antibody factories) called Plasma cells, and also Memory B-cells, which will survive in the body and remember that same antigen or pathogen, or bacteria or chemicals, are important so that the B-cells can respond faster in the future if exposure to the COVID-19 happens again, and after the patient is well again. Phagocytosis acts in the same way with tissue cells.
Interaction of the B-cell with a T-Helper Cell is necessary to produce full activation of the B-cell and therefore, antibody generation continuity following antigen binding.
Antibody genes also reorganize in a process called, CLASS SWITCHING, that changes a different ISOTYPE of the antibody that retains the antigen-specific variable region. This allows a single antibody to be used by different types of Fc receptors, expressed on different parts of the IMMUNE SYSTEM.
A Paratope, also called an antigen-binding site, is a part of an antibody which recognizes and binds to an antigen. Good combined with bad. It is a small region of 5-10 amino acids, of the antibody’s Fc region; part of the fragment antigen-binding (Fab region), and contains parts of the antibody’s HEAVY and LIGHT CHAINS.
An epitope, which is also known as the antigenic determinant, is that part of the antigen to which antibodies bind. While the antigen evokes the antibody response in the host, the antibody does not bind to the entire protein, but only to that segment called the epitope.
Each of these antibodies bind to a specific epitope located on that protein. Binding between the antibody and the epitope occurs at the antigen binding site, which is called a paratope and is located at the tip of the variable region of the antibody.
Binding type proteins also play an important role in the natural immune response because they compete in their application to bind to proteins or ions that would have otherwise been benefitting to bacteria or replication of viruses.
It appears to me the focus should not be at the part of the antigen-epitope binding site, where the antibody has done its job in suppressing the antigen, but rather at the exposed areas not bound to any antibodies along the epitope binding site. However, there is also hope that if the binding site where the epitope has done its job and the antigen is bound to an antibody, that if the site is used as a way to destroy the antigen without destroying the antibody, then that also is an avenue to be taken and investigated to destroy the antigen!
Now I want to focus on COMPLEMENT PROTEINS WHICH ACT LIKE OPSONINS, such as C3b, C4b, and C1q, which are important Complement Molecules. These also serve as Opsonins. As a part of the alternative complement pathway, the spontaneous activation of a COMPLEMENT CASCADE converts C3 to C3b, which is a component that can serve as an Opsonin when bound to an antigen’s surface.
A Phenotype is defined as the physical and psychological characteristics of an organism from both genetics and environment, or a group of organisms having like-traits. Such an example would be a group of organisms which all are effected in the same ways via nature and how they were nurtured as well. These examples also include (but don’t have to), height, hair color, and shared commonality of levels of hormones, or blood cells. Also, common interaction of the genes of an organism. The reason animals, such as pigs, mice, or rats can be used for biological analysis is because many of the genes which are carried are similar to genes found in humans. Scientists would say this is due to the evolutionary process. I say it is because the same Creator created both. But the scientist community must observe both as only theory until proven fact. Though I could speak at more greater depth into this subject, for the sake of this paper, I will stay on topic.
So, earlier in the beginning page of this research and analysis of COVID-19, I alluded to the idea that the virus appeared to have genetic expression involved in its composition, as the virus appeared to have reactions in the body which are symptomatic to the cause of infectious mutations involving yeast infections or streptococcus varieties of bacteria.
Important to note is that Phenotype and genotype can share common ground but are still different. The Phenotype is the physical expression of those genotypes whereas, genotypes are genes of a particular DNA. I believe virus entry occurring in both, phenotype and genotype pathways, resulted in infecting normal functioning of cells in both the Adipose Tissues and Plasma cells throughout the body via glycerol macromolecules which are present in both tissue and blood. This would again account for the variations of symptoms associated with the COVID-19 due to the fact the Adipose and Blood Plasma glycerol macromolecules are present throughout every organ and cell region of the body and can combine to form complex multi-cellular organisms with specific bonds. I believe breaking apart these bonds will recombine the correct syncing and am doing research with respect to Catalase.
The chemical reaction of the surface reactors to the bacteria (via transmission in vitro through Phenotypes and/or Genotypes) in the phagocyte normally do a binding activation that leads to the dissemination of the bacteria by the phagocyte COMPRISED OF OXIDANTS AND NITRIC OXIDE (also known as phagocytosis). But in the case of the afore-to-mentioned situation occurring where the phagocyte, becomes a host to the protein-antigen-pathogen enzyme, and allows it play the role of opsonin and thereby deceive the process of phagocytosis, it is apparent that the binding activation for oxidants and NO has been canceled. Which again, leads to free-radicals being expressed. Nitric Oxide is also required for maintaining of healthy cell barriers which do not permit the re-entry of virus back in vitro once the virus has been successfully driven out of the body. So, making sure NO is re-established after stabilization of the body is of paramount importance.
More about the effects Nitric Oxide (NO) has on the body is very important to outline regarding pathogenic and chronic disease but not for this papers research emphasis. But for this research I have found through research findings that NITRIC OXIDE (NO) HAS POSITIVE EFFECTS IN VITRO AS THE BODY IS USUALLY LACKING IN HAVING ENOUGH NITRIC OXIDE, WHICH IS BENEFICIAL IN THE BINDING WITH FREE-RADICALS WHICH PROTECT AGAINST GOOD CELL DEATH.
NITRIC ACID (NO), ATTACH TO FREE-RADICALS THEREFORE INDISPOSING THEM FROM THEIR ATTEMPTS TO KILL GOOD CELLS.
However NO is usually taken by supplements unless doctor prescribed. And its efficacy is still being discussed but be warned that people with cirrhosis, and in conjunction with liver scarring, low blood pressure, or diabetes should consult their physician first as NO may interfere with medicines they’re on. Also, people with the rare, genetic condition called, Guanidinoacetate methyltransferase deficiency MUST NOT take NO. This is where a person lacks an enzyme that converts arginine into creatine, which is a waste product.
As I look over my research paper and notes, I am beginning to see some alignments whereby I’m noting more connections being made. I will try to summarize these thoughts as best as I can.
With regard to genetic expression and the coding of cellular signaling pathways which can be disrupted when correct signaling is inhibited or altered, I find myself being lured by the mention in my notes of p70S6K. Another name for this is Ribosomal Protein S6 Kinase beta-1, or S6K1, all of which denote synonyms for a downstream protein/enzyme which is activated to IL-3. Its target is the S6 ribosomal protein. The S6 ribosomal protein, also referred to as r-protein or rProtein, is any of the proteins which work in conjunction with rRNA, make up what’s called the ribosomal subunits involved in the cellular process of TRANSLATION.
Studies involving E. Coli with respect to their adherence to ribosomes of DNA have been able to isolate ALL THE RIBOSOMAL PROTEINS and most of their specific antibodies which have been produced in reaction to their presence. In other words, natural ribosomal products produced by a variety of organisms such as prokaryotes, eukaryotes, and archaea, are characterized by a wide range of biological functions. However, if genome sequencing is what is being dealt with here, then the chemical structures found in the ribosomal products are more definable from the genome data than are the natural products, which is to say they should be able to be identified with rapidity. If this has not been able to be a quick identifier of the DNA structure of the pathogen/virus, then it is a safe bet, in theory, that it is a natural variety of organism, as discussed.
Complementary-Determining-Regions (CDR’s) have been isolated for determining of the proteins to the correlating ribosome. Therefore my research finds that with respect to the invader having personality associated markers (gene expressions) with what appears may be two interacting virus antigens, I have found that it correlates in many respects with the symptoms of both. And evidence supports the fact that when two bacterial allergens are transported onto peptide chains, they are more indestructible and variety driven than otherwise would be. With that in mind, one of my more recent theories involves the interruption of the correct TRANSLATION OF MACROMOLECULES IN THE BBB (Blood Brain Barrier) due to mixing of these transport peptide chains carrying gene expressive traits, via nRNA, or other.
*** The BBB is the intersection of ENDOTHELIAL CELLS with extracellular fluids of the central nervous system (CNS) with respect to where the neurons reside and the fact the BBB is formed by the endothelial cells of the capillary wall (astrocyte end-feet ensheathing the capillary), and pericytes which are embedded in the capillary basement membrane, are all involved in the systematic passage of some molecules (macromolecules) via PASSIVE DIFFUSION, AND TRANSPORT. If the macromolecules such as Birbecks Granules were to adapt similar transmitted genotype behaviors to the other peptide enzyme then the possibility is that one of the protein enzymes may be connected to a disease and therefore if there is a solution to one, it may correct the other. This could also be affiliated with certain disease doors via v600E disease pathway.
One such example, may be cancerous cells in the breast that suddenly spread into the brain causing lesions when it was initially thought to be COVID-19, AND PAST BREAST CANCER RELATED ACTIVITY HAD BEEN IN REMISSION FOR YEARS. Therefore, I suggest that if these are correlated via Langerhans Cells that possibly the lesions are resulting from this translation of macromolecules at the BBB and mixing of transport chains which opened the door from previously retentive breast cancer.
I therefore propose the antigen mutates by activating the genotype expressive cell which is most vulnerable in the weakened immunity of an individual. So, if a person for example, has diabetes, it mutates to that expression in vivo. The chain of virulent activity may be stopped by certain successful treatments penetrating to what specific disease has been brought on by COVID-19.
With this in mind, and regarding the former remission of breast cancer, I found a treatment that has been used in certain cancers that link to gateway V600 pathway, as a targeted therapy.
It’s called, Vemurafenib (Zelboraf ®) and it is targeted cancer therapy treatment which uses the V600 gateway. I theorize that if either are treated effectively, the COVID-19, or the disease itself, then it will break the chain of virulent activity that has escalated to the point of adopting a specific disease.
IN THE END, PEOPLE WITH CERTAIN DISEASES MAY FIND CURES FOR THEIR DISEASE IF COVID-19 HAS BEEN BONDED TO THE LANGERHANS CELLS, AND CORRECT THERAPEUTIC DRUGS TARGET THAT SPECIFIC DISEASE OR KNOWN PATHWAY, SUCH AS CD44V, OR V600E, ETC.
When IgE is active, the antibody triggers allergic reactions which are called hypersensitive reaction. Important to note is how IgE antibodies reside in the LUNGS, SKIN, AND MUCOUS MEMBRANES. These are specific sites to which COVID-19 has expressed signs of invasion by producing inflammatory reactions. As the “allergen” response is triggered by the E. Coli , or other Streptoccoci bacterial infection for example, it incites the inflammatory responses associated with T-cell activation and B Cell receptor activations via IL-6, and secretion of type 1 cytokines, and IL-12, among others.
These activations caused by various molecular stimuli via OXIDIZED MACROPHAGE PERFORMANCE, are present in the Endothelial lining and present oxidized-LDL, oxidized-cytokines, pathogen associated macromolecules, and advanced glycosylation end products (AGE).
The various negative performing molecular stimuli which are produced via macrophage inflammatory reactions which include the release of apoB-containing-Lipoproteins, which are artery clogging induced inflammatory responses which cut off air passageways. This is another symptom involving COVID-19’s virulent activity.
Now that I am making my final summation regarding my theories regarding (COVID-19) pathogens entrance, travels and symptoms, throughout the body, I MAKE A FINAL REALIZATION WITH RESPECT TO THE INITIAL BINDING SITES AND SYMPTOMS ASSOCIATED WITH THOSE SITES OF ACTIVITY AND A BIG FIND REGARDING WHAT I BELIEVE TO BE GROUND ZERO, and how I initially found this.
Initially patients began to report symptoms in lungs, skin, and mucous membrane regions. I decided early on that the mode seemed to be the ADIPOSE TISSUES, which is still a correct analysis based upon the evidence presented. However, as I looked at the overthrowing of the Immunological antibodies and their inability to properly function I began to look more closely at the Isotype IgE with respect to the antibodies normal residing in the lungs, skin, and mucous membranes specifically. When allergens are triggered with respect to these areas, the allergen binds to specific immune cells called, basophils and mast cells.
I focused on histamine and in round-about ways found Histiocytosis. I looked this up and found Langerhans cell histiocytosis (LCH), which is a rare disorder in which the body makes too many dendritic cells. Dendritic cells are a form of histiocyte, or white blood cell. THESE CELLS PLAY IMPORTANT ROLES IN THE BODY’S IMMUNE SYSTEM. THEY CAN BE FOUND IN THE SKIN, LUNGS, STOMACH, BONE, EYES, AND INTESTINES. This fits in conjunction with COVID-19’s symptom areas.
THOUGH I DO NOT BELIEVE EVERYONE THAT CONTRACTED COVID-19 HAS THIS RARE DISORDER, WHAT I DO BELIEVE IS THE FUNCTION OF THIS PARTICULAR ANTIBODY SITE HAS BEEN COMPROMISED IN REGARD TO THE PRODUCTION OF IMMUNE RESPONSE AND COVID-19’s PATHOGENIC TAKEOVER.
The pathway that Langerhans cells travel is like a template leading the scientist to be able to know where the pathogen has traveled, but are not related to the actual disease but rather its replicating pathway with respect to a mutual protein affiliation.
Langerhans cells (which derive from the primitive erythromyeloid progenitors that arise in the yolk sac outside the embryo in the first trimester of pregnancy) and under normal circumstances persist throughout life, and are replenished by normal means as needed.
Obviously, this is just a template I am referring to by noting the full understanding of what Langerhans cells do, but the part about pregnancy is not regarded in this case, but only the proliferation of regenerative cell structures. For example, if the skin becomes severely inflamed, possibly due to infection, blood monocytes are recruited to the affected region and differentiate into replacement Langerhans cells.
The migration of the protein itself, known as Langerin, is a protein found in Langerhans cells (LC) and dendritic cells. LC contain organelles called, Birbeck granules, which are present in all layers of the epidermis and are most prominent in the stratum spinosum. They also occur in papillary dermis, with particular aggregation around blood vessels, as well as in the mucosa of the mouth, foreskin (male), and vaginal epithelium (female). They are also found in other tissues such as the lymph nodes.
I found with respect to the template of the langerin protein and the antigen pathway; the CD4 T lymphocytes and macrophage need to be studied, as well as C-type lectin receptors (CLR’s), and CD4 and chemokine co-receptors (CCR5 and CXCR4), which is the classical pathway used by HIV-1 to enter CD4 T lymphocytes, and macrophages, and may be in this instance as well.
These CLR’s are used to distinguish dendrite cell subsets in mucosal tissues.
I could go on about my finding involving carbohydrates and their affiliations with regard to glycosidic bonds (glucose) which determine polysaccharide structures and their proliferation throughout the bodies systems involving COVID-19 and its path via fibronectin features, or the connection I see to Heparin Proteoglycan, (with regard to quaternary structures of crystal-like features), but I believe I have found COVID19’s GROUND ZERO to cut it off at the head, and I leave it up to anyone reading this that may be a scientist or doctor to decide if what I think may be true, or not.
I will continue to give analysis and my opinions regarding further theories and research finds if I am asked but I felt the information I have now will do much good. If I have made any errors I apologize. I only just learned all this about biological terminology and such in the last 10 and a half weeks since I first felt called to do it.
I took one class of AP-Biology in high school and have not invested time to update my information about cellular biology until now. I had received an award from a doctor upon graduation as well as the highest recommendations and letter from my professor stating his desire that I become a biologist, but I declined in order to do my fine art. But, when God equips, we can do anything through Christ, whom gives us strength, and the mind of Christ.
I wanted to fulfill this calling in order to provide alternative responses for cures via therapeutics and not have to depend on vaccines. However, I have no problem with vaccines provided they are proven to be safe and had tests to prove its human safety check-points. I just am pro-options.
My hope is also that pharmaceutical companies will open branch divisions dedicated to therapeutic drug options and organics, which I believe is the wave of the future. I found a company recently trying to do just that.
Thank you to all whom used my information and hopefully, I meant well. I don’t want one more person to die, I want people to live.
I pray the good Lord grant us all answers through science, and discovery because He is science.
Job 38 & 39 NIV.
JoAnn Peralta-Fine Artist