Are you as tired of warnings turning out to be predictions as I am? The concept of a warning being ostensibly about something that “might” happen, usually means there is a chance it “won’t” happen, particularly if necessary actions to avoid it take place. But what happens if there are “no” actions one can ostensibly take to ensure the warning doesn’t come to pass? Will it come to pass anyway? Not necessarily. Just look at the long list of climate change warnings since the 70’s that have yet to come to pass, and many of them were slated to have occurred long before now. But when you read statements by people such as Bill Gates, WEF speakers, One Health proponents, etc, all saying variations of “the coming decade of pandemics“, and then hear people such as Gates in early 2022 discussing the possibility of hemorrhagic fever being one of those pandemics, you pay attention and log such statements at the back of mind. Why? Because you may have to pull them out of memory and reference them again. A good way to do this is to “save to pdf” articles where these statements are coming from.
It appears that Gates’ prediction of a coming hemorrhagic fever pandemic caused various research labs that he funds (directly or indirectly), to hop-to, and dig up “the next big thing”, then crow about it when they found it.
EDIT June 28, 2024
It appears Gates isn’t letting any grass grow under his feet! He’s determined to push his agenda forward as quickly as possible! Check out this article on his mosquito experiment supposedly reducing disease-carrying threats such as Dengue fever. In part two of the above article, clickable at the end of it, we discover:
“For their complex sci-fi process, they used African green monkey kidney cells along with mouse monoclonal anti-alphavirus antibodies. The DENV-2 genomic fragment was then inserted into a plasmid and transformed by Escherichia coli.
This GMO mosquito is also funded by DARPA’s Safe Genes Program. And in case you missed my two-part on Substack, they used Plasmid and vats of E.coli to scale up their COVID-19 jibjab and although Pfizer knew there was contamination, they injected humans anyway.”
““I have always said that this is going to make the problem way worse and they’re finding Wolbachia genes in people with cancer. It synergizes other infections too and parasites, so it helps the other bad parasites and any tick-borne infections.”
“In his book, Finnegan writes: “It does not appear that the Wolbachia are as harmless and non-transmissible as they thought, because there is some evidence that Wolbachia antigens are being found in people with cancer, and the bacteria has also been given antigens from the herpes-simplex virus which would certainly help it acquire human pathogenicity.”
He also sent me a study on the detection of Wolbachia genes in a patient with non-Hodgkin’s lymphoma.
Also consider that that after the mosquito initiative began, dengue cases have risen sharply rather than fallen. “
These notes are important as you read the rest of this article.
end edit
Let’s go back to 2015, to a research paper published January 1st in the journal: American Society for Microbiology. The article in question was received by the journal, September 17, 2014, accepted on October 23, 2014 and officially published October 29, 2014 for the January 1st 89th issue of this journal. There are a few quotes here, and I will reference them where appropriate here as we move along.
“Simian hemorrhagic fever virus (SHFV) causes a severe and almost uniformly fatal viral hemorrhagic fever in Asian macaques but is thought to be nonpathogenic for humans. “
Simian hemorrhagic fever virus (SHFV) causes highly lethal disease in Asian macaques resembling human illness caused by Ebola or Lassa virus. However, little is known about SHFV’s ecology and molecular biology and the mechanism by which it causes disease.”
Asian macaques are a breed of monkey. Skip ahead to September 28, 2022. We have a strangely-worded observation and we run across two contradictory statements:
“We find that CD163 acts as an intracellular receptor for simian hemorrhagic fever virus (SHFV; a simian arterivirus), a rare mode of virus entry that is shared with other hemorrhagic fever-causing viruses (e.g., Ebola and Lassa viruses). Further, SHFV enters and replicates in human monocytes, indicating full functionality of all of the human cellular proteins required for viral replication. Thus, simian arteriviruses in nature may not require major adaptations to the human host.”
(2022), Click that link, go to the Conflict of Interest paragraph, and then read anything further related to the above link with a good dose of salt!
Hold on a moment. . . “may not require major adaptations to the human host”??? Why would such a virus “require adaptation”? There is actually a fair bit of information out there regarding CD163 and it’s role in the human body. In 2014, we supposedly didn’t know about the mechanism Simian Hemorrhagic Fever Virus used, but not only do we supposedly just discover it here in 2022, we actually knew about this back in 2019, particularly if we bother to connect the dots that Warren et al., threw out for us in the exact same paper claiming human immunonaivity against such threats. By the time we are done today, those dots very well may have you clopping your head or banging it on a desk (just not your keyboard, ok?) due to the apparent lack of professional ability to do this themselves.
The biggest dot here, is the mention of Ebola virus, which some research papers simultaneously refer to as Ebola virus disease. From where I sit, the differences are in the progression of the body’s response to the threat, not a change in the threat itself, so the term differences are misleading. Somehow, it made sense to the paper authors to refer to it this way. Unrelated to the paper I will quote fairly extensively from, my Liberian cousin-in-law was on the front lines of the Ebola outbreak that swept through Liberia awhile back. I lost a 2nd cousin to that outbreak as every day, my cousin-in-law was on the front lines in med tents working to save lives. It was noted back then, that Ebola was a common threat in various regions across Africa, but that the Liberian outbreak was the worst anyone had ever seen it. At the time, I was quite suspicious about how severe this particular outbreak was, and equally suspicious at how several medical personnel arrived back in the US and Canada, with the World Health Organization trying to whip the world into a panic over a potential global pandemic that didn’t materialize. This suspicion was due to the WHO efforts to create global panic a few previous times already in that decade! It seemed as if they were determined for some reason, to get a global health emergency going and it kept fizzling. The Ebola outbreak in Liberia seemed poised to give WHO what they wanted, but the disease did not take off in western nations as expected. It stayed localized to Liberia and surrounding nations.
In February 2019, the CDC published an article about the Ebola virus that give us huge clues to it’s behaviour and successful treatment. For those who have followed me since late 2020, you’ll know that in early 2021, my daughter and I released a PDF of foods that have medicinal properties similar to HCQ and Ivermectin, the two drugs used most effectively against both Malaria and Ebola in the countries of Uganda and India. This pdf was created due to government idiotic behaviour around these two drugs in the treatment of COVID-19. Keep in mind, these are anti-parasitic medications.
Back to the February 2019 article now. The CDC noted that elevated levels of cytokines are associated with the Ebola virus. But they mentioned that cytokine storms were associated with those who died from the virus. In addition:
“This type of hyperinflammatory state is reminiscent of 2 rheumatologic disorders known as macrophage activation syndrome and hemophagocytic lymphohistiocytosis, which are characterized by macrophage and T-cell activation….that directed anti-inflammatory therapies could be beneficial in the treatment of EVD. . . The similarities between EVD and HLH have not gone unnoticed by other clinicians; a group in the Netherlands has published an opinion piece suggesting a connection between the 2 diseases”
Remember that EVD is Ebola virus disease. HLH is an easier-to-remember term than hemophagocytic lymphohistiocytosis and another term is going to crop up shortly: MAS, or macrophage activation syndrome.
So the dots so far:
- Simian hemorrhagic fever uses the same CD163 receptor to enter cells as Ebola.
- Ebola shows the same kind of immunological behaviour as MAS and HLH, that are considered to be two rheumatoid diseases, in other words, behaviour that tends to show up in rheumatoid arthritis.
Now:
“HLH can occur as a primary genetic disorder or a secondary consequence of another medical condition, including infection (9). Secondary, virus-associated HLH is most commonly reported after Epstein-Barr virus (EBV) infection, and even though EBV infection is exceedingly common (seroprevalence in adults 80%–90%) (10), development of EBV-associated HLH is still a rare event, estimated at 0.4 cases/1 million population (9). Other hemorrhagic fever viruses, such as Crimean-Congo hemorrhagic fever virus (11) and dengue virus (12), have also been reported to trigger HLH.”
Hold on a moment. . . Epstein-Barr??? Isn’t that seeing a recurrence in those who got the COVID shot??? Incidentally, I did not know Epstein-Barr was as prevalent as this 2019 article claims.
The researchers for this article then began delving into a few other markers present in ebola that are also markers for HLH and MAS. Due to our focus here on food as medicine, these findings are of note. First, they mention that high levels of triglycerides and low levels of fibrinogen are often seen in both HLH and MAS, but not previously noted for ebola. When the researchers dug into the data, they found high levels of triglycerides in severely ill patients with ebola, and extremely high levels in fatal cases. Fasting levels could not be determined, but high and extremely high levels did correlate with severe and fatal disease.
“The elevated triglycerides seen in severe and fatal cases of EVD would be consistent with this finding, considering these same patients have marked increases in proinflammatory cytokines. Therefore, the finding of elevated triglycerides probably represents a response to rather than an initiator of pathology.”
Another statement in this CDC article shows just how nasty our mainstream medical systems got when they went after Dr. Charles Hoff here in BC Canada over the past couple years, as he used the D-dimer test on his post-vaxx patients:
“Two other laboratory findings often reported in HLH and MAS are elevated transaminases and D-dimers (Table) (13). Aspartate aminotransferase and D-dimers are elevated in patients with EVD, and elevated levels of these analytes are associated with fatal outcome”
You can’t claim a test is useless when you use it yourself! This type of test was successfully used in observing fatal Ebola cases! Hmmm!
However, we’re not done with the connections between HLH, MAS and Ebola! According to this CDC article, all three are inflammatory syndromes characterized by fever, cytokine storms, liver dysfunction and by extension, drastically reduced ability for the blood to clot.
Exceptionally high levels of iron were found in patients with ebola virus, a predictor of HLH as it turns out. To the notes above regarding CD163,
“CD163 expression was reported on hemophagocytic macrophages in the skin of patients with HLH, and high serum levels have been noted in patients with HLH and MAS. sCD163 has also been associated with disease severity in hemorrhagic fever with renal syndrome (which occurs after hantavirus infection) and dengue hemorrhagic fever “
“Elevated levels of macrophage activation marker sCD163 were seen in all patients with EVD, and this marker was associated with both disease severity and fatal outcome. Elevated levels of sCD163 in disease pathogenesis have also been reported for dengue virus and hantavirus infections (14,35), and sCD163 was an independent predictor of all-cause mortality in HIV-infected patients (42).”
A predictor of all-cause mortality in HIV-infected patients now. . . Hmmm. . .
Hemophagocytic simply refers to macrophages (white blood cells) that break down spent blood cells. As we will see in further quotes here, CD163 mentioned by itself, refers to the receptor that is attached to the macrophage, while sCD163 is the soluble receptor that has been discharged, cut off, or “cleaved” as some researchers put it, and is floating free in the blood serum. High levels of sCD163 is often considered a marker for various hematological, or blood-borne diseases. Notice the other hemorrhagic fever references in the above quotes? We can learn from these references.
Further to the CD163 discussion, we come back to the liver:
“that we found elevated levels of sCD163 and abundant CD163-positive macrophages in the liver surrounding areas with extensive viral antigen is not surprising. Liver macrophages include mostly Kupffer cells, which are usual constituents of the liver, but during inflammation, monocytes are recruited from the periphery that can differentiate into macrophages in this tissue (45). Kupffer cells express various markers and are thought to have various functions. CD163 is classically considered a reparative marker of an M2 type of macrophage, but this marker is not definitive because inflammatory macrophages can also express CD163”
White blood cells come in various forms, with M2 being one of them. Kupffer cells are the liver’s primary method of doing it’s job in the body.
Iron storage proteins are referred to in this CDC article as: ferriton. Refer to the article link to follow footnoted numbers.
“In healthy persons, the ferritin level is 10–250 ng/mL and used clinically as a marker of iron storage (26). Ferritin is also known as an acute-phase reactant that is elevated nonspecifically in the context of inflammation. In HLH and MAS, ferritin levels can be markedly high. Hyperferritinemia was observed in patients with EVD, where ferritin levels were as high as 1 × 105 ng/mL, which is 3 logs of magnitude over the upper limit of normal. In HLH and MAS, the source of ferritin causing the extremely high blood levels is thought to be the activated macrophage population (38,39). In EVD, the liver could also be the source of the ferritin, as has been noted in animal models”
Seeing as the discussion around inflammatory blood-borne diseases keeps bringing up CD163 and macrophages, and the fact that this receptor is exclusive to both monocytes and macrophages, let’s spend some time learning a bit more about this receptor, particularly because the predicted coming pandemic uses this receptor to jump to humans. We’ll go through another round of various quotes from various papers. Stick with me, because we’ll be returning to some of these papers in their suggestions around treatment and management of the diseases discussed, and CD163’s role in those.
Back in 1999, the following quote appeared in the journal, Pathobiology:
“CD163 is a recently identified member of the scavenger receptor cysteine-rich superfamily expressed on peripheral blood monocytes and most tissue macrophages.”
More specifically, CD163 belongs to the Scavenger receptor cysteine-rich (SRCR) class B family of membrane proteins.
In Antioxid Redox Signal. 2013 Jun 10
We read that CD163 indirectly contributes to the body’s anti-inflammatory response. Researchers divide up areas of proteins and molecules into domains and regions.
“the calcium-binding SRCR domain 3 of CD163 has been shown to be essential for the binding of Hb-Hp(hemoglobin/haptoglobin) to CD163”
Pay special attention to this next set of quotes, note locations of the body in particular:
“Human CD163 expression is restricted to the monocytic–macrophage linage with high expression in, for example, red pulp macrophages, bone marrow macrophages, liver macrophages (Kupffer cells), lung macrophages, and in macrophages of several other tissues“
What areas of the body have been under particular attack over the last three years?
In this next paragraph, note what “downregulates” or lowers, CD163 expression. Where have you heard THIS before?
“The most potent stimulators of CD163 expression known are glucocorticoid, interleukin (IL)-6, IL-10, and heme/Hb, whereas IL-4, lipopolysaccharide (LPS), TNF-α and interferon γ, CXC-chemokine ligand 4 (CXCL4), and granulocyte–macrophage colony-stimulating factor downregulate CD163 expression”
“CD163-expressing macrophages have been detected in sites of inflammation, such as chronically inflamed arthritis joints (8, 33), atherosclerotic plaques (96), and the vicinity of tumor cells (tumor-associated macrophages)”
We’re going to get into a bit of a science lesson now. Anywhere you see Hb, it means: hemoglobin, the protein found in red blood cells that carries iron and oxygen in the blood. Athero- means artery or arterial. Lesions are tiny tears that bleed. Haptoglobin is a protein produced by the liver that binds with hemoglobin. This protein is present in the bloodstream serum, binding to and removing free hemoglobin from the bloodstream, reducing inflammation and oxidative stress. Read more about haptoglobin here: Hemolysis is the breakdown of red blood cells.
“When activated, macrophages release reactive oxygen intermediates and nitric oxide extracellularly and can cause extracellular killing of parasites and microorganisms. Macrophages secrete a number of cytokines involved in inflammation and the immune response
Macrophages express monocyte-associated cell surface antigens CD11b, CD14, CD64, CD68 and CD163 and are CD45 and HLA-DR-positive and their granules contain acid hydrolases and lysozyme.”
SN Wickramasinghe, … WN Erber, in Blood and Bone Marrow Pathology (Second Edition), 2011
The Antioxid article we’ve been quoting above about CD163 goes on to say:
“CD163-expressing macrophages have been detected in sites of inflammation, such as chronically inflamed arthritis joints (8, 33), atherosclerotic plaques (96), and the vicinity of tumor cells (tumor-associated macrophages)
Studies of atherosclerosis (arterial inflammation involving lesions in arterial walls) (16) and Hb (49) suggest that CD163 and Hb from local microbleedings (plaque hemorrhage) have an atheroprotective role via the metabolism of Hb leading to polarization of macrophages. These studies have led to a definition of a new class of CD163-positive atheroprotective and anti-inflammatory macrophages in atherosclerotic lesions”
“CD163 is highly expressed on phagocytic macrophages. Upon hemolysis, released hemoglobin (Hb) is rapidly bound by the acute-phase protein Hp forming the haptoglobin–hemoglobin (Hp-Hb) complex. The complex is subsequently bound and removed from the circulation by CD163-positive macrophages in the liver, spleen,and bone marrow. The uptake of Hb by macrophages contributes to the recycling of iron and also to the inflammatory response. The uptake of Hb in macrophages and subsequent degradation of heme by heme oxygenase-1 (HO-1), produce the anti-inflammatory metabolites, Fe2+, CO, and biliverdin. Biliverdin reductase converts biliverdin to bilirubin, which is secreted to the cell exterior. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars.”
Remember what was said earlier in Ebola, HLH and MAS patients about high levels of iron? Remember what was said about these three diseases and liver dysfunction? Now for a carbon monoxide surprise, written in the language of chemistry simply as CO.
“Among the many effects of CO, where some overlap those of NO, this well-known, but potentially very toxic CO gas, is a potent inhibitor of proinflammatory cytokines, such as IL1 and TNF-α and a stimulator of IL-10 (61). In malaria, where the plasmodium parasites may cause severe hemolysis and heme intoxication, CO is reported to have a specific cytoprotective role because it binds to free Hb and thereby prevents heme release from Hb (32).”
There’s that connection between parasites and severely high levels of destruction of blood cells and iron intoxication (heme). This is a clear case of a little Carbon Monoxide is useful, but that amount is very small with what we know of CO poisoning, which can occur when wearing a mask for hours on end!
“Elegant studies of cells transfected with catalytic inactive HO-1 have shown that HO-1 itself is involved in cell signaling and different changes in phenotype, including an upregulated expression of catalase, glutathione peroxidase,”
Now that’s a mouthful! Iron oxygenase, HO-1 is apparently involved in cell signalling, the method by which cells in the body talk to each other to say what they need. But look at what it gets involved with: among other things, glutathione peroxidase! Now where have you been hearing about the necessity of glutathione?!
“African swine fever virus (ASFV) and the porcine reproductive and respiratory syndrome virus (PRRSV) are the two virus reported to bind CD163 (21, 101, 113). The binding of virus to CD163 seems important for the virus infection, but in different ways. ASFV is proposed to exploit CD163 for attachment and internalization (101), whereas PRRSV data suggest a role for CD163 during virus uncoating (113). Minor envelope glycoproteins GP2a and GP4 of PRRSV are reported to interact with CD163 (24).”
Remember, visit the article link I’m quoting from, to visit their footnote numbers for your own research. PRRSV is an arterivirus in the same family as simian hemorrhagic fever virus. The mention here is to show how this family of viruses seems to be attaching to CD163.
“Several other diseases, where inflammation is an important component of the pathogenesis have increased levels of soluble CD163. This includes acute diseases, such as bacterial sepsis/infection (54, 76, 79), hepatitis (44), and malaria (58) as well chronic inflammation, such as rheumatoid arthritis (39, 66), Crohn’s disease (76), scleroderma (82), coeliac disease (23), and atherosclerosis (4, 73) (Table 3). Generally, the increase in the CD163 level is much more pronounced in acute inflammations, such as bacteremia/sepsis, where the CD163 level also has negative correlation to survival (79).”
My, what a common list we have there! Question as you continue reading . . . How are many of those diseases currently treated?
CD163 has been found elsewhere too:
“… it is known that in MS brain tissue CD163+ perivascular macrophages express molecules for antigen recognition and presentation, and a strong accumulation of CD163+ macrophages/microglia has been observed in acute active lesions and at the rim of chronic active lesions of MS, altogether suggesting that CD163 might contribute to the resolution of inflammation in MS.
Clara Matute-Blanch, … Manuel Comabella, in Handbook of Clinical Neurology, 2018
Notice the role of iron in the following two quotes from the next paper, and notice the dates of these papers too:
“Besides the prevention of oxidative stress caused by heme (damage to the kidney proximal tubules) and downstream metabolic pathway of Hb [28, 36], the removal of Hb by Hp binding establishes an iron-poor environment [37] and as a result heme iron is unavailable for bacterial growth [38]. Iron is an essential element for nearly all living organisms [39] and the induction of a host acute-phase response limits the amount of circulating iron, primarily accomplished through a reduction in dietary iron absorption and by iron sequestration [40, 41]. Moreover, iron plays multiple roles in viral infections [42] and elevated ferritin concentrations are strongly associated with an earlier mortality in HIV [43].
Elevated sCD163 concentrations are found in pneumonia/sepsis in hematological patients, mononucleosis, leishmaniasis, myelomonocytic leukemia, reactive hemophagocytic syndrome, and fulminant hepatitis”
Ishmael Kasvosve, … Joris R. Delanghe, in Advances in Clinical Chemistry, 2010
Elevated ferritin is strongly associated with what??? Remember, Ferritin is iron storage, so that iron is not available for use by the body.
Now for another acronym that you are encouraged to click the link to learn more about:
” CD163 has been recognised as an atherosclerotic plaque modulator due to its anti-inflammatory and anti-atherogenic abilities [89, 90].
Gutierrez-Muñoz et al. also state that CD163 expressing macrophages exert a protective role by blocking TWEAK’s effect on atherosclerosis development and progression (Fig. 3) [94].
Similar to other inflammatory pathologies, in atherosclerosis, there is increased infiltration by TWEAK expressing macrophages, increased CD163 expressing monocytes and increased Fn14 receptor expression. The concentration of sTWEAK is also reduced. It is proposed that CD163 binds to TWEAK, which stops macrophage migration and further infiltration.”
Published: 20 September 2021
The TWEAK/Fn14/CD163 axis—implications for metabolic disease
Further to the role that CD163 has on the travel and management of not only inflammation, but blood cells:
“The increase in intracellular hemoglobin concentration is a result of a combination of enhanced protein expression and uptake from the extracellular space via a CD163-dependent mechanism. Intracellular hemoglobin preferentially localizes to the mitochondria, where it interacts with complex I and, on the one hand, increases mitochondrial respiratory rate and mitochondrial membrane potential, and on the other hand, protects from H2O2-induced cytotoxicity and mitochondrial DNA damage.
Cellular hemoglobin uptake is mediated by CD163 (scavenger receptor cysteinerich type 1 protein M130), a membrane transporter protein (17).
… uptake of hemoglobin into mononuclear cells from the circulation via CD163 is viewed as a protective pathway that serves to reduce circulating free hemoglobin levels (17).”
https://molmed.biomedcentral.com/counter/pdf/10.2119/molmed.2015.00187.pdf
I’m going to share a couple paragraphs from yet another paper here, then reword it for you to ensure you get a solid idea of just how important the CD163 receptor is to proper functioning of your body.
“The haptoglobin- (Hp-) CD163-heme oxygenase-1 (HO-1) pathway is an efficient captor-receptor-enzyme system to circumvent the hemoglobin (Hb)/heme-induced toxicity during physiological and pathological hemolyses. In this pathway, Hb tightly binds to Hp leading to CD163-mediated uptake of the complex in macrophages followed by lysosomal Hp-Hb breakdown and HO-1-catalyzed conversion of heme into the metabolites carbon monoxide (CO), biliverdin, and iron. The plasma concentration of Hp is a limiting factor as evident during accelerated hemolysis, where the Hp depletion may cause serious Hb-induced toxicity and put pressure on backup protecting systems such as the hemopexin-CD91-HO pathway. The Hp-CD163-HO-1 pathway proteins are regulated by the acute phase mediator interleukin-6 (IL-6), but other regulatory factors indicate that this upregulation is a counteracting anti-inflammatory response during inflammation. The heme metabolites including bilirubin converted from biliverdin have overall an anti-inflammatory effect and thus reinforce the anti-inflammatory efficacy of the Hp-CD163-HO-1 pathway.
The CO cleaved from hydroxyheme is primarily removed from the body via respiration. CO diffuses readily cross-cell membranes and binds Hb with approximately 200-fold higher affinity than O2. Provided adequate circulation and respiration, it is then transported to the alveoli and diffuses to the alveolar gas.”
Published online 2013 May 27
A triad made up of haptogloin, CD163 and heme oxygenase-1 is an effective system to get around the hemoglobin/heme-induced toxicity during physiological or disease-caused breakdown of the blood. Hemoglobin binds tightly to haptoglobin, leading to mediation by CD163 in the Hb/Hp complex in white blood cells followed by breakdown and conversion of heme into the metabolites: carbon monoxide, biliverdin, and iron. The concentration of haptoglobin in blood plasma may cause serious hemoglobin-induced toxicity and put pressure on backup protective systems. Our triad proteins are regulated by interleukin-6, but other factors show this increased regulation is counteracting anti-inflammatory responses during inflammation. Heme metabolites including bilirubin (from biliverdin) have an overall anti-inflammatory effect, reinforcing the anti-inflammatory efficiency of our triad even though interleukin-6 is otherwise working against the triad.
So let’s try to summarize here, as we prepare to look into what we can do to stay healthy in the face of the “new” potential threat:
- Simian hemorrhagic fever virus apparently comes from monkeys. Ostensibly the same vector as HIV, and in many ways behaving much like HIV does.
- This potentially new zoonotic threat to humanity uses the CD163 macrophage receptor to gain access to the body’s cells, just as it has now been discovered that other blood-borne diseases do.
- Simian hemorrhagic fever has a lot in common with Ebola, which shares three primary disease activities with HLH and macrophage activation syndrome. Those three are: cytokine storms, liver disfunction and by extension, drastically reduced ability for the blood to clot.
- CD163 and sCD163 are used as markers for various diseases.
- CD163 belongs to a calcium-binding group of proteins, and is cysteine-rich.
- Glucocorticoids and Interleukin-6 stimulate CD163
- Interferon Y (gamma) is among components that calm down CD163
- Liver and kidney damage caused by various diseases, can lead to HLH and MAS secondary diseases. One of the precursors is Eptstein-Barr.
- Parasites that cause Malaria can severely induce the breakdown of blood cells and contribute to heme toxicity due to kidney disfunction.
- Many of the common ailments associated with high CD163 presence, are classified in one way or another, as inflammatory diseases such as rheumatoid arthritis, Cron’s disease, Multiple Sclerosis, scleroderma, atherosclerosis, etc.
- CD163 assists with intracellular uptake of hemoglobin where the hemoglobin localizes to the mitochondria, enabling improved mitochondrial respiration and membrane potential.
Now we are going to revisit some of the previously-shared papers, and go over some of their thoughts on various treatments. Keep in mind that this section very much comes from mainstream medical sciences, and at one or two points at least, probably heavily influenced by string pullers as well. But these quotes give us an idea of what has been or is being considered in the above discussions.
“Treatment of target cells with proteases (proteinase K, papain, α-chymotrypsin, and trypsin) abrogated entry, indicating that the SHFV cell surface receptor is a protein.
… treatment of cells with antibodies targeting CD163, a cell surface molecule identified as an entry factor for the SHFV-related porcine reproductive and respiratory syndrome virus, diminished SHFV replication, identifying CD163 as an important SHFV entry component.”
Simian hemorrhagic fever virus cell entry is dependent on CD163 and uses a clathrin-mediated endocytosis-like pathway
Proteases, also known as proteolytics, are found in such foods as:
- Pineapple,
- Papaya,
- wheat bran,
- rye, and
- kiwi.
Trypsin is created in your pancreas as a direct result of eating protein.
EDIT April 15, 2023
Mercola recently shared an article on three enzyme supplements that aid in fibrinogen break-down/management, so that your arteries don’t clog with blood clots. He too mentions proteolytic enzymes. He writes:
“Fibrinolytic enzymes are antihypertensive, anti-atherosclerotic, lipid-lowering and antiplatelet agents, which also have neuroprotective effects”
He quotes one researcher as saying:
““There is evidence in both animals and humans that fibrinolytic therapy in acute lung injury and acute respiratory distress syndrome (ARDS) improves survival, which also points to fibrin deposition in the pulmonary microvasculature as a contributory cause of ARDS.”
Study co-author Mauro Giacca, a professor at King’s College London, is quoted:
“Dissolving scar tissue is another area in which enzymes, particularly proteolytic enzymes, may be useful.”
End edit
“…substantial immunoreactivity of host tissues to a CD163-specific antibody, predominantly in areas of extensive immunostaining for Ebola virus antigens, was observed in fatal cases. These data suggest that host macrophage activation contributes to EVD pathogenesis and that directed antiinflammatory therapies could be beneficial in the treatment of EVD.
…as the marker sCD163 indicates, inflammation can persist, even after viral load control, so improving patient outcomes will probably require both directed antiviral therapies early in the disease course and carefully timed host-directed antiinflammatory therapies.”
Volume 25, Number 2—February 2019
Many, many foods are anti-inflammatories! Both Pineapple and Papaya mentioned above, are also listed as being anti-inflammatory.
“glucocorticoids promote the resolution of inflammation by skewing macrophage polarization towards an M2-like (termed M2c) highly phagocytic phenotype, promoting the clearance of microorganisms, apoptotic cells and debris. M2c macrophages show high expression of the hemoglobin scavenger receptor, CD163 as well as the protein S/Mer tyrosine kinase pathway, important for the engulfment and clearance of apoptotic cells (Martinez et al., 2008). They secrete the antiinflammatory cytokines, IL-10 and transforming growth factor (TGF)-β, important in terminating an inflammatory response as well as inducing tolerance via the adaptive immune system
Glucocorticoids also reduce pro-inflammatory cytokine levels via induction of tristetraprolin, which targets their mRNAs for degradation.
Nitric oxide is an important intra- and intercellular signaling molecule in shaping the innate and adaptive immune response, with potential for both detrimental and protective effects. Glucocorticoids suppress the cytokine induction of inducible nitric oxide synthase (iNOS/NOS2) expression, decreasing nitric oxide release by endothelial cells. This inhibition, mediated by the glucocorticoid second-messenger annexin A1, may prevent overshoot of an early endothelial cell-mediated inflammatory reaction ”
Karen E. Chapman, in Encyclopedia of Endocrine Diseases (Second Edition), 2018
Karen’s suggestion to use glucocorticoids is a multi-edged sword and as such, I cannot echo her recommendation. While cortisol does tamp down stress-induced inflammatory behaviours around the body, regardless of what caused that stress be it internal disease or external exacerbation causing asthmatic inflammation, medical experiences taking cortisol in various forms by various family members has not ended well in the long run. Perhaps short-term, emergency-only, immediate use cases could use the injection whether by puffer, syringe, or other dispensing methods as an emergency method for quickly bringing down runaway inflammation. But outside of a flat-out life or death emergency, I am unable to recommend this option.
The note above about Nitric Oxide is important as it also regulates elasticity of your blood vessels such as veins and arteries so that they can dilate and shrink as needed, allowing blood to flow through them unhindered. Care should be taken in restricting this component of bodily function.
“The use of resveratrol decreases CD163 expression which has been shown to increase levels of sTWEAK in people with T2D [85]. Resveratrol also increases expression of SIRT1 and 5′ AMP‐activated protein kinase (AMPK), which together inhibit NF‐κB and therefore, further increase sTWEAK concentration [46, 85]. The increase in sTWEAK was connected to increased expression of p53 and p21 genes required for inhibition of apoptosis, cell cycle regulation and tumour suppression [46, 85]. ”
Published: 20 September 2021
The TWEAK/Fn14/CD163 axis—implications for metabolic disease
Resveratrol is found in:
- the skin of red grapes,
- cocoa and
- blueberries.
Incidentally, anthocyanins, present in all fruits that have a darker red-to-purple skin colouration, have also been known to bring down inflammation.
WARNING!
“The nonshed membrane form of CD163 in macrophages constitutes a target for drugs to be directed to macrophages in inflammation. This approach has been used in an animal inflammation model to highly increase the apparent therapeutic index of anti-inflammatory glucocorticoid drug that was coupled to an anti-CD163 antibody.
The specific expression of CD163 in monocytes/macrophages makes the receptor an interesting gate for drug delivery. This may apply to different kinds of disease, including inflammatory disorders, certain cancers of myeolo-monocytic origin, infections, where the macrophages harbor the pathogen (e.g., mycobacterium, HIV, or leishmania parasites), and rare genetic disorders (e.g., Gaucher’s disease affecting macrophages).
The CD163-expressing macrophage is an interesting therapeutic target because CD163 macrophages are present at the site of inflammation where they, despite an overall anti-inflammatory function, also produce inflammatory cytokines, such as TNF-α. This cytokine is largely produced by macrophages and the efficacy of anti-TNF-α biological drugs (35) suggests that the macrophage is an obvious target for anti-inflammatory therapy. “
WARNING #2
“An alternative type of conjugate vehicles targeting CD163 has recently been constructed and analyzed in vivo and in vitro (27). This type of conjugate vehicle is a pegylated liposome (stealth liposome) protected with polyethylene glycol that prevents nonspecific targeting and intravascular rupture. Anti-mouse CD163 is linked to the phospholipid layer by a hydrophobic linker. Loading the liposomes with the cytotoxic agent doxorubicin revealed strong CD163-dependent cytotoxic effects in cultured CD163-expressing cells. In vivo analysis of calcein-loaded anti-CD163 stealth liposomes showed accumulation in mainly the liver that contains the majority of the body macrophages. A much lower uptake was seen with nontargeting liposomes (27).
The latest novel connection between CD163 and inflammation concerns the use of CD163 and a target for drug delivery to macrophages. By the use of targeting antibodies or ligands directly coupled to drugs or to liposomes encapsulating drugs, it is now possible to direct in principle any kind of drug, such as cystostatic and anti-inflammatory compounds, directly to macrophages in the inflammatory process. The first reports (26,37) using this technology seem rather promising for the development of conjugate glucocorticiods with far lower side effects and higher potency than the nonconjugated glucocorticoid used in therapy today.
Polyethylene Glycol was used in industrial applications as a cleanser for refrigeration systems where my brother worked for awhile, and often shows up in various packaged foods such as artificial extracts, pre-packaged bakery mixes, in their ingredient lists, often near the top of the list. PEG-ylated anything, if I happen to catch the ingredient list, is always tossed. This lady gives a reasonable breakdown as to why. The idea of putting petroleum-based products on or in our bodies has been getting negative feedback for awhile now, with the most common one being Vaseline. You can now make similar products using coconut oil, however, I doubt coconut oil would work in the above application very well. The idea that peg-ylated anything would congregate in the liver, is also troubling.
The two paragraphs on this above from the Antioxid article contradict each other in that one paragraph claims these liposomes congregate in one area more than others, while the other paragraph claims this medicine delivery vector could target anywhere inflammation occurs in the body. These kinds of contradictions need to be observed and noted. Liposomal therapy is apparently the new rage in nutrition and medicine delivery with one doctor I sat under recently in a seminar, sharing briefly how you can make your own liposomal nutritional supplements. I am not sure yet what I think of this delivery method, other than to say, stay away from PEG-related versions!
Recapping the food as medicine discussion, including what my household learned regarding alternatives to HCQ and Ivermectin:
From studies my daughter and I did on ebola and malaria in late 2020/early 2021, quercetin and quinone foods were high on the list, placing foods found in the citrus, lamiceae, and fabiceae groups front and center. Spring of 2021, word sprang out regarding Shikimate found in pine needles, which would also be found in dandelion, cucumber, gingko biloba, licorice root, star anise, and wheatgrass. A much larger list of foods, herbs and spices related to that discussion is available here.- Dandelion, licorice root, oranges, and mint, are among others on that list that are anti-inflammatory.
- Proteases, also known as proteolytics, are found in such foods as: Pineapple, Papaya, wheat bran, rye, and kiwi. Trypsin is created in your pancreas as a direct result of eating protein.
- Both Pineapple and Papaya mentioned above, are also listed as being anti-inflammatory.
- Resveratrol is found in the skin of red grapes, cocoa and blueberries.
- Incidentally, anthocyanins, present in all fruits that have a darker red-to-purple skin colouration, almonds, and artichokes, have also been known to bring down inflammation.
While quoted articles did not list treatments to maintain a healthy mitochondria, this was due to discussions being about providing the mitochondria with it’s necessary hemoglobin, and aiding it in its respiratory functions within the cell.
- Foods containing a range of B vitamins, most notably Vit B1 (Thiamine) are helpful for the mitochondria.
- CoQ10, available in red meat alongside zinc, also benefit the mitochondria.
- Foods containing selenium and Vitamin C should be on the list as well. Brewer’s Yeast for example, contains both selenium and B vitamins.
In a recent seminar I sat in this month (October 2022), Licorice root was noted as a useful treatment for Epstein-Barr virus. This virus has a decent write-up here. It appears that COVID-19 shots are reactivating this virus, as it is being reported as an adverse event after various people have received one or more jabs.
Considering that HLH and MAS can occur following a bout of the Epstein-Barr virus, and considering how similar these two are in behaviour to Ebola, and that the “new” monkey virus behaves similar to Ebola. . . the dots suggest the “new” virus could be a cover for the HLH/MAS fallout following resurgence of Epstein-Barr due to the “vaxx”.
The minerals you want to focus on for healthy mitochondrial behaviour, are:
- Magnesium,
- manganese,
- zinc, and
- Phospherus.
Remember that CD163 binds calcium, while Epstein-Barr increases calcium uptake by the mitochondria. (read more about this here ) Magnesium helps to balance out the calcium. Zinc helps both minerals come and go from the cell as needed. Vitamin C is necessary to release zinc from your protein sources.
If you have gotten your Hepatitus B vaccine in the past, or you have an old-style filling in your mouth, you want to be detoxing mercury using:
- coriander,
- curcumin,
- pre and probiotics,
- fennel, etc.
Detox from aluminum with coriander, horsetail.
Glyphosate also negatively impacts your mitochondria, and studies have noted that countries where Glyphosate had higher usage, cases of COVID-19 were also higher. So if you live in an area where RoundUp is in heavy use, you will want to mitigate this as well. Such mitigation can be done with:
- dandelion root,
- ginseng,
- Mushrooms and
- milk thistle.
These help protect the liver and endocrine system from the damage glyphosate can cause. Citrus fruits and kelp are also of benefit,
- citrus for their anti-oxidant behaviour and
- kelp for it’s toxin absorption behaviour, as well as iodine to protect the thyroid.
- Ginko Biloba is another protectant from glyphosate toxicity.
- Foods high in sulfur such as your cruciferous vegetables are great for detoxing glyphosate.
There are many great sources online to help you formulate the detox regimen that works best for you.
Vitamin C and Zinc are your primary food nutrients to load up on for all respiratory illnesses, in addition to stomach and intestinal bugs. The fact that these blood-borne diseases also attack bone marrow, spleen, and liver, mean that Vitamin C is a huge boon for your body there as well, because Vitamin C aids in strong bone creation, thereby aiding in the creation of healthy blood cells. The lists are long for liver tonics, kidney tonics, blood supports, etc. If you would appreciate customized grocery lists for yourself and your household, fill out the free session request form, and after completing your intake form, we’ll go over how best to begin your nutritional/medicinal health journey to fortify your body in the “new” viral landscape.
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