MTHFR Support & Nutrigenomics Wellness
COVID-19 Genes and SNPs
What follows is a collection of genes and SNPs that we have found to be relevant to the current Coronavirus epidemic, COVID-19 (aka SARS-CoV-2), and their implications. This app was created by Sterling Hill of MTHFR Support in conjunction with Cynthia Smith of Nutrigenomics Wellness.
In addition to primary SNPs we have also included some secondary gene SNPs that are related to a downstream cytokine storm that may occur in some folks. The secondary genes may give further insight into individual impairment based on your individual biochemistry to sense COVID-19 virus in your body and address your individualized response to COVID-19. We have also selected relevant genes that are associated with protection of cell wall permeability and may assist with modulation of your immune system.
All of the SNPs mentioned here can be found on our new COVID-19 report available on Sterling’s App.
It is important to note that neither this information nor the COVID-19 report constitutes a medical diagnosis or advice and does not replace medical advice from your Physician. Rather, our goal is to share info that may be relevant to your personal health.
This information should not be used without the advice of a medical doctor and does not replace medical advice from your physician. We understand that many are concerned about COVID-19 and are working hard to help provide you with information regarding your genetics.
Any information provided herein regarding nutraceuticals should not take the place of medical advice from your Physician. The CDC and Physicians have advised the public to support their immune system via hand washing, etc., and both macro and micronutrients during this COVID-19 outbreak.
Like many things regarding health, genetic knowledge is one data set, that in conjunctions with other data sets and lifestyle information, that can be utilized to optimize your overall health. Genetics can enable you to identify individualize “weak links” in your health “chain”, and then address them.
When using genetic results as a data set, to optimize your health please consult an experienced Practitioner. You may find one near you on our Find a Practitioner map.
Here at MTHFR Support we are doing our best to provide you with the most up to date information as you have requested.
NOTE: COVID-19 and SARS-CoV-2 terms are interchangeable.
Some of the research I have cited pertains to original SAR outbreak in 2002-2003 (called SARS-CoV), but some of the same principles apply to the immune system domino effect upon SARS-CoV-2 first docking with ACE2 receptors.
COVID-19/SARS-CoV-2 in 2020 is more easily transmitted than SARS-CoV from 2002-2003, but SARS-like impacts with SARS-CoV-2 are lesser.
Having said that however, a new FURIN cleavage system in SARS-CoV-2 has made this strain more transmittable. The FURIN cleavage system was not present in coronavirus in original SARS-CoV 2002-2003 version.
I have attempted to list the enzymes/receptor proteins below in the sequential order in which they are impacted, subsequent to the docking of the COVID-19 virus onto ACE2 receptors. In some cases however, the enzymes/receptor proteins are working in parallel with the immune system.
Here is a simplified summary of the sequence of events:
Following docking of SARS-CoV-2 onto ACE2 receptors (mostly in lungs and GI), and virus-cell membrane fusion via TMPRSS2 and FURIN, a cascade of enzymatic steps and subsequent immune system mobilization occurs. Once infected, GI/lung cells are hijacked into making more viruses. The immune system reacts by stepping up its response. This response includes a robust elevation of a pro-inflammatory cytokines including IL-1b, early in the infection process. As described below, NLRP3 inflammasomes, CASP1, PYCARD, and HMGB1, play prominent roles in this process.
SARS-CoV-2 infects alveolar endothelial cells (see, ACE2 below) and/or macrophages. Subsequently, the immune system mobilizes a response including generation of various pro-inflammatory cytokines (e.g., IL-1, IL-6, TNF, and IFN-γ).
In some, this immune system mobilization is “overexpressed”, and can result in a severe and highly lethal respiratory disease. This severe respiratory disease is characterized by a prominent pro-inflammatory response (cytokine storm), and is referred to a bilateral pneumonia.
It should be noted that pro-inflammatory cytokines are double-edged swords that not only mobilize human immune system defense but can also drive pathologic inflammation, and therefor can play both anti-viral and pro-viral roles during a SARS-CoV-2 infection.
Postmortem data from fatal cases of the 2002-2003 SARS-CoV outbreak showed diffuse alveolar damage including collapse and fibrous tissue in alveolar spaces, significant monocyte–macrophage infiltration, and elevated serum cytokines. https://ajp.amjpathol.org/article/S0002-9440(10)61329-6/fulltext
It was interesting to note that during the 2002-2003 SARS-CoV, AIDS patients with deficient immune system were somewhat resistant to SARS infection, raising a possibility that an excessive immune response is attributable to the lethality of patients who die of SARS. Because death due to SARS may be the result of an overactive immune system response, scientists speculate that HIV patients’ weakened immune systems may put them at a lower risk of developing the disease.
Angiotensin-converting enzyme 2 (ACE2)
- ACE2 gene encodes the angiotensin-converting enzyme-2
- ACE2 acts as a cell surface receptor for Human coronavirus. Normally, the ACE2 receptor plays an important role in regulating the body’s blood pressure and fluid balance.
- The surface expression of the ACE2 protein occurs on lung alveolar epithelial cells and enterocytes of the small intestine. As such, ACE2 is abundantly present in humans in the epithelia of the lung and small intestine.
- The coronavirus gains entry into a cell via exploiting ACE2 and type II transmembrane serine proteases (TMPRSS2) see below.
- Basically, the coronavirus S (spike) protein of COVID-19 binds to ACE2 with high affinity.
- Binding of the coronavirus S protein to ACE2 triggers a conformational change in the S protein of the coronavirus, allowing for proteolytic digestion by host cell proteases (TMPRSS2), thereby facilitating COVID-19 virus to human cell membrane fusions, and subsequent inflammatory immune system response (IL-6, and IL1B) see below.
- NOTE: Although ACE inhibitors and ARBs are useful drugs in the treatment of high blood pressure, CAD and diabetes, (used to reduce blood pressure, decrease risk of progressive kidney disease, and decrease risk of dying if one is at high cardiovascular risk), there are ongoing questions as to whether taking ACE inhibitors or ARBs increase or decrease ones susceptibility to the more severe symptoms of COVID-19.
- A March 2020 article in the Lancet, entitled, Are patients with hypertension and diabetes mellitus at increased risk for COVID-19 infection?, suggested that because the expression of ACE2 is substantially increased in patients with diabetes, heart disease, etc., who are treated with ACE inhibitors and angiotensin II type-I receptor blockers (ARBs), “…they are at higher risk for severe COVID-19 infection and, therefore, should be monitored for ACE2-modulating medications, such as ACE inhibitors or ARBs”
- ACE2 has binding sites for Zinc and Chloride
Transmembrane protease serine 2 (TMPRSS2)
- TMPRSS2 is a Serine protease that proteolytically cleaves and activates the viral spike glycoproteins which then facilitates virus-cell membrane fusions; spike proteins are synthesized and maintained in precursor intermediate folding states and proteolysis permits the refolding and energy release required to create stable virus-cell linkages and membrane coalescence. This Serine protease facilitates human COVID-19 infection via two independent mechanisms, (1) proteolytic cleavage of ACE2, which might promote viral uptake, and (2) cleavage of coronavirus spike glycoprotein which activates the glycoprotein for cathepsin L-independent host cell entry. Essential for spread and pathogenesis of COVID-19.
- This Serine protease is expressed in type II pneumocytes in the lung (at protein level). Expressed strongly in small intestine.
- It is involved in the activation of viral glycoproteins/viral entry across a range of viruses, including SARS-CoV-2.
- NOTE: Recommended by Chinese and South Korean health authorities for the treatment of COVID-19 hydroxychloroquine and its related drug chloroquine. Hydroxychloroquine is a decades-old and inexpensive anti-malaria drug to treat coronavirus, and MAY enable faster healing times and shorter hospital stays in those who contract the infection.
- Brand names of Hydroxychloroquine include Plaquenil, Hydroquin, Axemal (in India), Dolquine, Quensyl, Quinoric
- SARS-CoV-2 entry into cells is partially blocked in vitro by the protease inhibitor via serine protease inhibitor camostat mesylate.
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4774534/, ”…Serine protease inhibitors blocked coronavirus entry into caco-2 cells, and Camostat protected 6 of 10 mice from lethal infection with SARS-CoV-2.” https://en.wikipedia.org/wiki/Camostat
- Furin is an enzyme encoded by the FURIN gene. Furin is a proprotein convertase and acts to cleave sections of inactive proteins, in order to activate them. The Furin enzyme is highly expressed in lungs.
- NOTE: Proprotein convertases are a family of nine serine secretory proteases proteins that activate other proteins. Many proteins are inactive when they are first synthesized, because they contain chains of amino acids that block their activity. Proprotein convertases remove those chains and activate the protein.
- The proprotein convertase family is responsible for the activation of a wide variety of precursor proteins, such as growth factors, hormones, receptors and adhesion molecules, as well as cell surface glycoproteins of infectious viruses
- In addition to processing cellular precursor proteins, Furin is also utilized by a number of pathogens. For example, the envelope proteins of viruses influenza, HIV, SARS-CoV-2 and several filoviruses including Ebola Marburg virus must be cleaved by furin or furin-like proteases to become fully functional and active.
- As previously discussed, the spikes “crowning” the SARS-CoV-2 must attach (AGT2), fuse (TMPRSS2) and gain entry to cells.
- David Veesler, senior author of the report referenced below and assistant professor of biochemistry at the UW School of Medicine, said that “The spike is the business part as far as viral entry. It is in charge not only of attachment at the host cell surface, but also of fusing the viral and host cell membranes to allow the infection to start.”
- He goes on to say that, “…unlike SARS-CoV, SARS-CoV-2 includes a furin cleavage site at a boundary between two subunits of the spike protein. It is not yet known if this difference is expanding the kinds of cells the SARS-CoV-2 could infect or enhancing its transmissibility, in a way that might be similar to that of highly pathogenic avian flu viruses.”
- Thus, when SARS-CoV-2 attaches to ACE2 cell surface receptors in the respiratory tract, it may then successfully exploit this Furin enzyme to activate its own surface glycoprotein to gain entry to respiratory tract cells. This makes SARS-CoV-2 a very easily transmittable virus. This was not the case with 2002-2003 SARS-CoV.
- Binds 3 calcium ions per subunit
- Optimum pH is 6.0
NACHT, LRR and PYD domains-containing protein 3 (NLRP3 aka CIAS1, Cryopyrin, NALP3, and Pypaf1)
- NLRP3 is a protein encoded by the NLRP3 gene.
- As the sensor component of the NLRP3 inflammasome, NLRP3 plays a crucial role in innate immunity (first line of immune defense against non-self pathogen such as SARS-CoV-2), and inflammation.
- NLRP3 regulates the secretion of pro-inflammatory cytokines interleukin 1 beta (IL-1β) and IL-18.
- In response to pathogens and other damage-associated signals, NLRP3 initiates the formation of the inflammasome polymeric complex, made of NLRP3, PYCARD see, below and CASP1, see below.
- Recruitment of proCASP1 to the inflammasome promotes its activation, and CASP1-catalyzed IL1B and IL18 maturation and secretion in the extracellular milieu.
- NLRP3 activation stimuli include extracellular ATP, reactive oxygen species, K+ efflux, etc., crystals of monosodium urate or cholesterol, amyloid-beta fibers, cytosolic dsRNA, etc.
- NOTE: Coronaviruses are positive-sense RNA viruses that generate double-stranded RNA (dsRNA) intermediates during replication, yet evade detection by host innate immune sensors. https://www.pnas.org/content/pnas/early/2017/05/02/1618310114.full.pdf
- NLRP3 activation further occurs in the presence of cytosolic dsRNA and is mediated by ATP-dependent RNA helicase (aka DHX33)
- DHX33 Independently of inflammasome activation, regulates the differentiation of T helper 2 (Th2) cells.
- “…melatonin has been evidenced to significantly inhibit airway inflammation, and suppress TLR3/4-mediated inflammation in liver injury. Most notably, NLRP3 is a novel molecular target for melatonin in murine model of septic response, liver injury and acute lung injury…”
- Melatonin exhibits immunomodulatory properties.
- There is evidence that melatonin levels are disrupted (decreased) by electromagnetic fields such as those associated with high frequency electromagnetic fields (EMFs), particularly those associated with 4G and 5G technology.
- Melatonin is a natural hormone produced by pineal gland activity in the brain that regulates the body’s sleep-wake cycle.
- The pineal gland is likely to sense EMFs as light but, as a consequence, may decrease the melatonin production.
- High melatonin folks include children and women in 3rd trimester of pregnancy. Elders have lower melatonin levels.
- Melatonin peaks in early childhood (130 pg/ml)
- Melatonin begins slow decline at puberty
- 20 yrs old — 80 pg/ml
- 40 yrs old — 35 pg/ml
- 50 yrs old — 20 pg/ml
- 60 yrs old — 5 pg/ml
- 70 yrs old – negligible
Apoptosis-associated speck-like protein containing a CARD (PYCARD aka ASC)
- PYCARD is a protein that functions as key mediator in apoptosis (programmed cell death) and inflammation.
- The PYCARD protein is involved in macrophage pyroptosis, (a caspase-1-dependent inflammatory form of cell death) and is the major constituent of the ASC pyroptosome which forms upon potassium depletion and rapidly recruits and activates caspase-1.
- NOTE: ASC can be either apoptosis-associated speck protein containing a CAR, or Caspase activation and recruitment domain).
- NOTE: Pyroptosis is highly inflammatory form of programmed cell death that occurs most frequently upon infection with intracellular pathogens.
- NOTE: Pyroptosis pyroptosis requires the function of the enzyme Caspase-1
- In innate immune response (first line of immuhne defense against non-self pathogen such as SARS-CoV-2), the PYCARD protein is believed to act as an integral adapter in the assembly of inflammasome which activates caspase-1, thereby leading to processing and secretion of pro-inflammatory cytokines.
- CASP1 gene encodes the protease (enzyme) caspase-1
- CASP1 is an organosulfur-based protease that cleaves Interleukin-1 beta, thereby releasing the mature cytokines which are involved in a variety of inflammatory processes. Important for defense against pathogens.
- Upon inflammasome activation, during DNA virus infection but not RNA virus challenge, CASP1 controls antiviral immunity through the cleavage of Cyclic GMP-AMP synthase, rendering it inactive.
- NOTE: Cyclic GMP-AMP synthase is a component of the innate immune system which detects the presence of cystolic DNA and, in response, trigger expression of inflammatory genes that can lead to cell death or to the activation of defense mechanisms.
- DNA is normally only found in the nucleus of the cell.
- Localization of DNA to the cytosol is associated with tumorigenesis, a viral infection or an invasion by some intracellular bacteria. The cGAS – STING pathway, including Cyclic GMP-AMP synthase, acts to detect cytosolic DNA and induce an immune response.
Interleukin-1 beta (IL1B aka IL-1β)
- Interleukin-1 beta is a cytokine protein that is encoded by the IL1B gene
- As a caspase activation-dependent cytokine, regulated by the release of inflammasomes (NLRP3, see above)
- IL1B is Potent proinflammatory cytokine, and induces prostaglandin synthesis, neutrophil influx and activation, T-cell activation and cytokine production, B-cell activation and antibody production, and fibroblast proliferation and collagen production.
- The IL1B production occurs in 2 steps, each being controlled by different stimuli.
- First, inflammatory signals, such as LPS, stimulate the synthesis and promote the accumulation of cytosolic stores of pro-IL1B (priming).
- Second, additional signals are required for inflammasome assembly, leading to CASP1 activation, pro-IL1B processing and eventually secretion of the active cytokine. IL1B processing and secretion are temporarily associated.
- NOTE: Blocking the activity of IL-1 beta has entered the clinical arena of treating autoimmune diseases
High mobility group protein B1 (HMGB1)
- HMGB1 is a multifunctional redox sensitive protein with various roles in different cellular compartments.
- HMGB1 is also released passively by necrotic cells, and actively by macrophages/monocytes in response to exogenous and endogenous inflammatory stimuli.
- It activates macrophages/monocytes to express proinflammatory cytokines, chemokines, and adhesion molecules.
- A caspase activation-dependent cytokines, regulated by the release of inflammasomes (NLRP3, see above)
- Activation of the NLRP3 inflammasome is required for HMGB1 secretion.
- The active cytokines and HMGB1 stimulate inflammatory responses. Inflammasomes can also induce pyroptosis, an inflammatory form of programmed cell death.
Interleukin-6 receptor subunit alpha (IL-6)
- Interleukin 6 is encoded by the IL6 gene
- IL6 is a pleotropic cytokine produced in response to tissue damage and/or infections.
- IL6 IL-6 stimulates the inflammatory and auto-immune processes in many diseases
- IL-6 is a cytokine with a wide variety of biological functions. It is a potent inducer of the acute phase response. It plays an essential role in the final differentiation of B-cells into Ig-secreting cells Involved in lymphocyte and monocyte differentiation. It acts on B-cells, T-cells, hepatocytes, hematopoietic progenitor cells and cells of the CNS. It is required for the generation of T(H)17 cells. In some cases, it also acts as an anti-inflammatory myokine. It is discharged into the bloodstream after muscle contraction and acts to increase the breakdown of fats and to improve insulin resistance. It induces myeloma and plasmacytoma growth and induces nerve cells differentiation.
- It is worth noting that, “While several studies show the essential role of IL-6 to mount a proper immune response during some viral infections, others link this cytokine with exacerbation of viral disease. These latter findings lend support to the hypothesis that up-regulation of IL-6 during certain viral infections may promote virus survival and/or exacerbation of clinical disease.”
- “The clinical picture of severe acute respiratory syndrome (SARS) is characterized by an over-exuberant immune response with lung lymphomononuclear cell infiltration and proliferation that may account for tissue damage more than the direct effect of viral replication.”
Nitric oxide synthase 3 [endothelial] (NOS3 aka eNOS, Constitutive NOS)
- There are three types of NOS; NOS1 (Nitric oxide synthase 1, neuronal), NOS2 (Nitric oxide synthase, inducible; aka iNOS), NOS3 (Nitric oxide synthase, endothelial; aka eNOS)
- NOS2 enhances the synthesis of pro-inflammatory mediators such as IL6 and IL8
- NOS3 produces nitric oxide (NO) that is implicated in vascular smooth muscle relaxation through a cGMP-mediated signal transduction pathway. NO mediates vascular endothelial growth factor (VEGF)-induced angiogenesis in coronary vessels and promotes blood clotting through the activation of platelets.
- eNOS is primarily responsible for the generation of NO in the vascular endothelium, a monolayer of flat cells lining the interior surface of blood vessels, at the interface between circulating blood in the lumen and the remainder of the vessel wall. NO produced by eNOS in the vascular endothelium plays crucial roles in regulating vascular tone, cellular proliferation, leukocyte adhesion, and platelet aggregation. Therefore, a functional eNOS is essential for a healthy cardiovascular system.
- Catalytic activity:
- 2 L-arginine + 3 NADPH + 4 O2 = 2 L-citrulline + 2 nitric oxide + 3 NADP+ + 4 H2O
- Cofactors: Heme, FAD, FMN, 5,6,7,8-tetrahydrobiopterin
Encouraging Nitric Oxide production inhibits the replication cycle of Severe Acute Respiratory symptoms of SARS-CoV-2
“Our results demonstrated that NO specifically inhibits the replication cycle of SARS CoV, most probably during the early steps of infection.”
- innate immune receptor which acts as a cytoplasmic sensor of viral nucleic acids and plays a major role in sensing viral infection and in the activation of a cascade of antiviral responses including the induction of type I interferons and proinflammatory cytokines.
- The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of proinflammatory cytokines, contributes to the severe forms of the disease
- Further Resources
- Analyses suggest that African-Americans and Chinese with low Tmaf of rs1990760 are more vulnerable to SARS-COV2 infection, apart from other genetic factors or socioeconomic conditions in these population. Taken together, an IFN-beta supplement might aid in preventing COVID-19 infection and help in development of herd immunity – PubMed
Interferon-alpha/beta receptor 1 (IFNAR1)
- Interferon-alpha/beta receptor 1 alpha chain is a protein that in humans is encoded by the IFNAR1 gene.
- IFNAR1 is a type of interferon that helps regulate the immune system.
- All type 1 interferons bind to IFN-α receptors that consist of IFNAR1 and IFNAR2 chains.
- IFNAR1 is a component of the receptor for type I interferons.
- Genetic transfer of a functional human interferon alpha receptor into mouse cells: cloning and expression of its cDNA
- Formation of a uniquely stable type I interferon receptor complex by interferon beta is dependent upon particular interactions between interferon beta and its receptor and independent of tyrosine phosphorylation
- Formation of a uniquely stable type I interferon receptor complex by interferon beta is dependent upon particular interactions between interferon beta and its receptor and independent of tyrosine phosphorylation
- Structural linkage between ligand discrimination and receptor activation by type I interferons
- A B cell auto-immune phenocopy of inborn errors of type I IFN immunity underlies life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men.
People who are G6PD deficient can end up with iron overload and a cytokine storm especially when given ascorbic acid. Many practitioners have discovered throughout the years it is best for G6PD deficient individuals to have food based C which is ascorbate form. As we know with an elevation of serum ferritn that those individuals are in a cytokine flare. So it is best to speak with a medical professional if you are G6PD deficient before taking any ascorbic acid supplements.
C rich foods are always safer for G6PD deficient people than ascorbic acid. Please speak with your doctor who can advise you on what C rich foods to consume during the COVID-19 outbreak. Remember that just because you have a mutation does not mean that it is always problematic.
The World Health Organization (WHO) breaks G6PD into these classifications:
- Class I: Severe deficiency (<10% activity) with chronic (nonspherocytic) hemolytic anemia
- Class II: Severe deficiency (<10% activity), with intermittent hemolysis
- Class III: Mild deficiency (10-60% activity), hemolysis with stressors only
Acute respiratory distress syndrome (ARDS) caused by SARS-CoV-2 is largely the result of a dysregulated host response, followed by damage to alveolar cells and lung fibrosis. Exacerbated proinflammatory cytokines release (cytokine storm) and loss of T lymphocytes (leukopenia) characterize the most aggressive presentation. We propose that a multifaceted anti-inflammatory strategy based on pharmacological activation of nuclear factor erythroid 2 p45-related factor 2 (NRF2) can be deployed against the virus. The strategy provides robust cytoprotection by restoring redox and protein homeostasis, promoting resolution of inflammation, and facilitating repair. NRF2 activators such as sulforaphane and bardoxolone methyl are already in clinical trials. The safety and efficacy information of these modulators in humans, together with their well-documented cytoprotective and anti-inflammatory effects in preclinical models, highlight the potential of this armamentarium for deployment to the battlefield against COVID-19.
What Is NRF2 And Why Is It Important?
NRF2 is a nuclear transcription factor that binds to antioxidant response. It is also called erythroid-related factor 2. It is a powerful protein that is latent in each cell in our bodies.
NRF2 migrates into the cell nucleus and bonds with our DNA. It does this at our antioxidant response element which is the regulator of our antioxidant response system. As we age this system starts to decline.
Among patients with immune-mediated inflammatory diseases (IMIDs) who get COVID-19, the risk for hospitalization and death is lower if they are receiving tumor necrosis factor (TNF) inhibitor monotherapy, compared with receiving most other common drugs for these conditions, with or without TNF inhibitors, according to a study published October 18 in JAMA Network Open. The only combination not associated with an increased risk for hospitalization or death was TNF inhibitor therapy with methotrexate
What Is TNF?
Tumor necrosis factor is produced by cells in your immune system that promote inflammatory responses. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen-causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, under certain conditions it can stimulate cell proliferation and induce cell differentiation. Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Upregulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key ‘Ser-418’ residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective.
Patients hospitalized with severe COVID-19 infections who have high levels of the blood clotting protein factor V are at elevated risk for serious injury from blood clots such as deep vein thrombosis or pulmonary embolism, investigators at Massachusetts General Hospital (MGH) have found.
What Is FVL/ Factor V Leiden?
FVL is one mutation of a clotting factor in the blood. Protein C, an anticoagulant protein that normally inhibits the pro-clotting activity of factor V, is not able to bind normally to factor V, leading to a hypercoagulable state. People with epigenetic expression of FVL usually end up with DVT (deep vein thrombosis) or pulmonary embolism.
Higher levels of D-dimer, thrombocytopenia and prolonged prothrombin time in COVID-19 patients suggest the occurrence of DIC, yet in DIC the levels of D-dimer is higher than that of COVID-19 and thrombocytopenia is more predominant.
What Is Factor II Prothrombin G20210A?
It is a genetic condition that raises your chances of forming a blood clot and is almost always in 3% of caucasions. People with epigenetic expression of F2 Prothrombin G20210A usually end up with DVT (deep vein thrombosis) or pulmonary embolism.
Chloroquine has infrequently been reported to cause hemolysis in G6PD-deficient patients and caution is advised for its use.11 Hydroxychloroquine, its molecular variant, is generally considered safe. Both antimalarial drugs are being trialed as possible treatments for COVID-19. However, a recent report described an acute hemolytic episode occurring in a COVID-19 patient with G6PD deficiency who was treated with hydroxychloroquine.12 Hydroxychloroquine may increase the oxidative stress in COVID-19 patients with G6PD deficiency, thereby serving as a trigger for hemolytic anemia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7275177/
Back in January of 2020 when I built the COVID-19 report , I had G6PD down as a suspect and contacting scientists and doctors warning them of giving these patients HCQ. I received tons of backlash for this but here it is. Here is an interview I did with My Black Health. https://www.youtube.com/watch?v=Wn5ovUjxVbE
This gene gives us the ability to produce an enzyme called α1,2-fucosyltransferase. When you are homozygous for any of these FUT2 SNPs on this report you only have the ability to produce 4% to 6% of this enzyme on our own. α1,2-fucosyltransferase is used to produce glycans and having trouble producing this can lead to some health issues. This enzyme is needed to help the body’s natural defense system. FUT2 non secretors can have immune system impairment from diarrhea, poor beneficial gut bacteria to throat infections, ear infections and even how you respond to viruses.
Having a diet rich in oligosaccharides and polysaccharides can help vastly improve your ability to hold onto beneficial bacteria in the body. So what are some beneficial oligosaccharides and polysaccharides that and FUT2 can put in their diet to help regulate their immune system?
- Dandelion Root
- Burdock Root
- Jerusalem Artichoke
- Supplements containing oligosaccharides and polysaccharides
Of course when wanting to get some of these in your diet, work with your doctor to see which ones would be healthiest for you and it is always wise to eat organic and not to microwave your food.
Now does being a FUT2 non secretor help you?
Well we now know that FUT2 non secretors have more issues with bacteria and less issues with certain viruses.
So here is a little something about FUT2 showing that non secretors may have some protection against certain viruses. A few of my FB followers shared this information with me. I would encourage anyone who would like to know more about FUT2 to follow the FUT2 non secretor group on FB
Being a non-secretor seems to offer some protection against viruses. I’ve come across the following (caps for emphasis):
For example, NON-SECRETORS HAVE REDUCED INCIDENCE OF influenza A, influenza B, rhinovirus and respiratory syncytial virus infections,23 but increased incidence of Neisseria meningitidis, Streptococcus pneumoniae24 and Candida albicans25 infections, compared with secretors. In relation to chronic respiratory conditions, non-secretor asthma patients present with fewer exacerbations26 and non-secretor cystic fibrosis patients (with severe impairment of lung function) have prolonged time until P. aeruginosa colonisation;27 however, non-secretors with COPD have a lower FEV1%.28 https://thorax.bmj.com/…/08/thoraxjnl-2016-208775.full.pdf
Individuals homozygous for the FUT2 NONSECRETOR GENOTYPE APPEAR TO BE RESISTANT TO INFECTION WITH NOROVIRUS9, suggesting that individuals homozygous for nonsecretor status may be unable to mediate host-microbe interactions9.
Severe acute respiratory syndrome (SARS) is caused by the SARS coronavirus (SARS-CoV), an RNA virus. The original SARS outbreak in the winter of 2002 to 2003 infected >8,000 individuals worldwide, with a fatality rate of 10% (292). Like other human coronaviruses, SARS-CoV infects the mucosal epithelium, causing an acute respiratory illness often accompanied by gastroenteritis. In a Hong Kong outbreak, there was an apparent association between disease transmission and ABO type (293). An epidemiology study of 34/45 hospital workers who contracted SARS after exposure to a single index patient showed that most of the infected individuals (23/34) were non-group O individuals (groups A, B, and AB). Group O individuals were relatively resistant to infection, with an OR of 0.18 (95% CI, 0.04 to 0.81; P = 0.03).
LIKE HIV, CORONAVIRUS IS AN ENVELOPED VIRUS THAT TARGETS HOST CELLS VIA A VIRAL ADHESION GLYCOPROTEIN. The SARS-CoV spike (S) protein is a 210- to 230-kDa glycoprotein with 23 potential N-glycosylation sites (292). Glycan analysis shows a wide range of structures, including complex N-glycans with 2 to 4 antennae capable of supporting ABH epitopes (292, 294). Because the virus targets respiratory and gastrointestinal mucosa, it is highly likely that most human isolates express ABH antigens on the S protein and host envelope GSLs. Like the Env protein, S protein expressing A antigen can be blocked by monoclonal anti-A and human anti-A (292).
Nonsecretor status is associated with a decreased risk of several respiratory viral infections. By use of molecular genotyping, 2 populations of Senegalese women were examined for polymorphisms of the FUT2 gene. Among Senegalese commercial sex workers, absence of FUT2 (NONSECRETOR GENOTYPE) WAS ASSOCIATED WITH REDUCED RISK OF HUMAN IMMUNODEFICIENCY VIRUS (HIV).
Because various bacteria and viruses use attachment to cells as a means of causing infections, it has been determined that some NONSECRETORS have been found to have increased bacterial infections, but a DECREASED RISK IN RESPIRATORY AND GASTROINTESTINAL VIRAL INFECTIONS. Recent data from a study by Ali Suleman, et al1indicates that absence of this enzyme resulting in a nonsecretor status is associated with a reduced likelihood of infection after exposure and a greater chance of long-term nonprogression.
Extracellular superoxide dismutase [Cu-Zn] is an enzyme that in humans is encoded by the SOD3 gene. SOD3 is an antioxidant enzyme that catalyze the dismutation of two superoxide radicals into hydrogen peroxide and oxygen. This gene helps to protect the lungs from oxidative stress. Superoxide dismutase 3 helps to protect your DNA and cells from damage.
SOD3 is located in the extracellular matrix but it is also found in the cell junctions of airway epithelial cells and around the surface of vascular and airway smooth muscle cells (Oury et al., 1996,1994). SOD3 is involved in redox mediated signal transduction and in regulation of nitric oxide-mediated signaling across extracellular spaces (Folz and Crapo., 1994). In humans, SOD3 polymorphisms have been also associated with lung function decline and increased risk for COPD (Young et al., 2006, Wilk et al., 2007).
With the ongoing COVID-19 virus many researchers are seeing that zinc is a really important factor in the outcome of how people will recover from many types of coronaviruses. Zinc is being suggested as a nutraceutical to help protect the body from COVID-19. With this in mind, we must not offset our copper.
Foods that contain zinc:
- Whole grain
- Pumpkin Seed
- Cheddar cheese
- Red meat
- Potatoes regular and sweet
- Green Beans
Foods that contain copper:
- Shiitake Mushrooms
- Leaf vegetables
- Dark Chocolate
- Sesame Seeds
- Firm Tofu
- Sweet Potatoes
When wanting to get some of these in your diet, work with your doctor to see which ones would be healthiest for you and it is always wise to eat organic and not to microwave your food.
The HFE gene which is the homeostatic iron regulator provides instructions for producing a protein that is primarily located in the liver and intestines and is also found in some immune system cells. It interacts with other proteins to detect the amount of iron in the body. Some people with HFE mutations in the COVID-19 report may have trouble with their HFE organic instruction manual. When this happens there can be excessive amounts of iron in the intestines, liver and immune system cells and even other organs. This can lead to a cytokine storm.
Many who have ended up in critical care from COVID-19 are in a cytokine storm. So what can you talk to your doctor about if you are concerned about having excessive amounts of unusable iron? Getting an iron panel done including ferritin.
If you have elevated ferritin what should you avoid:
- Ascorbic acid
- Animal organ
- Elderberry syrup
- And other foods rich in iron your doctor may suggest to avoid
Types of vitamin C that are better for people with elevated ferritin:
- Ascorbate, meaning food based vitamin C vs the ascorbic form
What can your doctor suggest for lowering iron:
- Eating iron rich foods away from C rich foods Remember you must have C in your diet which is a powerful antioxidant to fight viruses.
- A cup of dandelion root and stinging nettles has helped people with elevated ferritin remove excessive iron from the liver.
- Vitamin B1 deficiency has been related to iron overload so your doctor may want to check your vitamin B1 and adjust to your daily dosage requirement.
When wanting changes in your diet, work with your doctor to see which would be the healthiest for you and it is always wise to eat organic and not to microwave your food.
This gene is also known as inflammatory bowel disease protein 1 gene. NOD2 gene plays a role in the immune system and recognizes bacteria and stimulates an immune reaction when working. Mutations in this gene have been related to Crohn’s disease, IBD, pulmonary sarcoidosis and the way you will react to viruses. When NOD2 is working your cells use this protein to surround bacteria, viruses and other harmful invaders to destroy them. This gene has been shown to bind in response to viral RNA treatment. NOD2 acts as a pattern-recognition receptor for viruses.
Support for people with NOD2:
- S boulardi
- B coagulins
- B subtilis
- Bone broth
- Slippery elm bark
- Mullein leaf
- Prickly pear
Always talk to your medical provider before doing anything listed here.
The COX2 enzyme takes arachidonic acid and converts it into prostaglandin 2. COX2 is involved in fever, pain and antibody production. So NSAIDs known as COX2 inhibitors can reduce fever and pain when they are used. What it can also do is halt antibody production. Antibodies are made by B cells. These antibodies go out into the blood and attack viruses like COVID-19. So are NSAIDs slowing down antibody production? This could be a high risk and why reports are coming out that some of these doctors on the front lines are correlating that NSAIDs may be injuring people infected with COVID-19 more. The oldest NSAID out there is aspirin. During the 1918 Spanish flu aspirin was used at very high doses and caused toxicity and was found to kill up to 3% of those with the 1918 Spanish flu. It has been found that salicylates (COX2 inhibitors) increase lung fluid and protein levels and impair mucociliary clearance. ACE2 receptors are abundant in the kidney and that is where NSAIDs are cleared. Could this be the reason why? Could we be seeing toxicity once the ACE 2 receptors lures the virus to attach itself to the copy instead of the actual cell? So once ACE2 has COVID-19 in the kidney could this be the reason for toxicity and the reports that doctors are seeing with those on non steroidal anti inflammatories.
We will keep PTGS2/COX2 in secondary and will move it up to primary when more information becomes available. If you have any concerns because you are on daily aspirin therapy or are on other NSAIDs, please consult your physician before getting off of your medications.