What do we know about Covid-19, Corona Virus, SARS, MERS and Immunity?
Who are most at Risk?

People of all ages exposed to the virus can be infected, however Immune compromised individuals, especially in their senior years, diabetics, asthmatics or anyone with an underlying pre-existing medical condition are at higher risk of contraction. Symptoms include fever, coughing, dry throat and shortness of breath. People who smoke cigarettes and VAPE are also in the high risk category

What do we know about the immune system?

The immune system is a network of special cells, tissues, proteins and organs that work together to protect the body from potentially damaging foreign invaders and disease.

Our immune system comprises the innate and the adaptive or acquired system which contains complexes that work in harmony and together make up a multilayered immune system to keep us healthy.

Amongst these complexes are cytokines which are molecules that are used in cell signalling or cell-to-cell communication that arises in the event of an infection and activate an immune response.

Other complexes, such as phagocytes, mast cells, macrophages, T-Cells & B-Cells, all form an army that mobilises action in response to infection.


A DNA polymorphism is nothing but a mutation (or in layman’s term, a change) that occur in a segment of a DNA or RNA molecule (introns) which does not code for proteins and interrupts the sequence of genes and hence, do not get expressed in the next generation. A “mutation” occurs when a nucleotide sequence within a gene is removed by RNA splicing during maturation of the final RNA product.

These changes keep accumulating and form the basis of DNA fingerprinting. (The process that forms a person’s DNA)

MTHFR is an example of a polymorphism which we have discussed at length in previous live telecasts and group sites. This variant effects methylation, a process that we use in every cell in your body, probably a billion times or more a day.

Methylation is used in liver detoxification, making processing and getting rid of neurotransmitters, changing and turning on & off bits of DNA, making, utilising and removing excess hormones, making & changing proteins, processing amino acids.

It aids in detoxification & clearance of

Heavy metals


Environmental toxins…more on this shortly!

What does this have to do with Immunity, Covid-19, Corona Virus, SARS and MERS?

Research has shown that SARS-CoV-2 infects alveolar endothelial cells and/or macrophages. Subsequently, the immune system mobilises a response including the generation of various pro-inflammatory cytokines (e.g., IL-1, IL-6, TNF, and IFN-γ).

Recall that our immune system mobilises Cytokines in response to an infection.

In some, this immune system mobilisation is “overexpressed”, and can result in a severe and highly lethal respiratory disease. This severe respiratory disease is characterised by a prominent pro-inflammatory response (cytokine storm), and has been referred to a bilateral pneumonia.

Research into the association of polymorphisms in inflammatory Cytokine-derived polymorphisms revealed that there may be different immune responses towards a severe outcome. For instance, this study demonstrated that influenza A- (H1N1) and B-infected patients and also IL-I controls have different profiles of immune parameters, and individuals carrying the specific cytokine-derived polymorphisms may show different immune responses towards severe outcome.


As we delve deeper and deeper into the world of epigenetics and nutrigenomics, we learn that an individual’s DNA mutation in immune response cells, such as IL-6 for instance, is associated with the susceptibility to viral and other infections. IL-6 (Interleukin 6) is a well­known pro-inflammatory cytokine produced by macrophages and fat cells. Interleukin 6 (IL-6) plays a crucial role in both adaptive and innate immunity. (Recall, SARS-CoV-2 infects macrophages) Individuals with a mutation in this gene may find themselves more susceptible to COVID-19. (1)

It should be noted that pro-inflammatory cytokines are a double-edged swords that not only mobilise a human immune system defence but can also drive pathological inflammation, and therefore can play both anti-viral and pro-viral roles during a SARS-CoV-2 infection.

Post-mortem data from fatal cases of the 2002-2003 SARS-CoV out-break showed diffuse alveolar damage including collapse and fibrous tissue in the alveolar spaces, significant monocyte–macrophage infiltration, and elevated serum cytokines.


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.

Scientists speculate that HIV patients’ weakened immune systems may put them at a lower risk of developing the disease, because death due to SARS may be the result of an overactive immune system response. (3)

Simplistic view of the sequence of effects of Sars-Co-V-2

The Sars virus docks onto ACE-2 receptors, mostly in the gastro-intestinal tract and the lungs via virus cell membrane fusion (via TMPRSS2 and FURIN,) which in turn, mobilises the immune response we have discussed previously. The virus then replicates in the lung. (3)

Why is this important?

A March 2020 article in the Lancet 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) are at higher risk for severe COVID-19 infection and, therefore, should be monitored for ACE2-modulating medications, such as ACE inhibitors or ARBs. (3)

Interestingly, scientists Liu Wenzhong, Li Hualan noted in a recent study that there was a massive demand of porphyrins for viruses to survive.

“Porphyrin test is a powerful biomarker of environmental toxicity. “

“The porphyrin test is a powerful biomarker of environmental toxicity. Porphyrins are intermediate products in the production of haem, which involves at least eight enzymes which are highly sensitive to toxins. When certain chemicals are present in the body these enzymes are inhibited, particular porphyrins build up and a distinctive pattern of porphyrins specific to each toxin is produced. These patterns of porphyrin production can therefore be used to analyse the presence of environmental toxins in the body and therefore of chemical exposure. Several health disorders have abnormal porphyrin levels associated with chemical exposure including chronic fatigue, multiple chemical sensitivities, learning and behavioural disorders as well as mental health conditions.

Multiple studies have recently revealed that autism spectrum disorder (ASD) is also associated with abnormal patterns of porphyrin production. It was suggested by these investigators that porphyrins should be routinely clinically measured in ASDs and potential ASD treatments should consider monitoring porphyrin levels.” (4)

Heme has a variety of functions. As a cofactor, it allows for the following]:

Oxygen transport in haemoglobin

Storage in myoglobin

A prosthetic group for cytochrome p450 enzymes

A reservoir of iron

Electron shuttle of enzymes in the electron transport chain

Cellular respiration

Signal transduction-heme regulates the antioxidant response to circadian rhythms, microRNA processing

Cellular differentiation and proliferation

Clinical significance

Heme synthesis is a biochemical pathway which requires a number of steps, substrates, and enzymes. A deficiency in an enzyme or substrate leads to accumulation of intermediates of heme synthesis in blood, tissues, and urine leading to a clinically significant outcome of a group of disorders called porphyrias. Porphyrias are hepatic or erythropoietic. They can be acute or chronic, lead to neurologic dysfunction, mental disturbance or photosensitivity. Defects of heme synthesis after formation of hydroxymethylbilane leads to photosensitivity of patients. Other symptoms include a change in urine colour, abdominal pain, abdominal colic, highly agitated state, tachycardia, respiratory problems, nausea, confusion, weakness of lower extremities.

Porphyrias are acute intermittent, congenital erythropoietic porphyria, porphyria cutanea tarda, hereditary coproporphyria. (5)

Furthermore, the novel coronavirus targeted haemoglobin, attacked heme and hunted porphyrins. This attack results in less and less availability of haemoglobin that can carry oxygen and carbon dioxide. The lung cells become extremely intensely poisoned and inflamed due to the inability to exchange carbon dioxide and oxygen frequently, which eventually results in ground-glass-like lung images. This concurrently reduces the availability of heme for the rest of the body, resulting in hypoxia and chronic organ failure.

The authors noted that depending on the computational simulation and discussion analysis of their study, we speculated the main pathogenic mechanism of this virus as thus:

“The virus may first infect cells with ACE2 receptors, including immune cells. Immune cells produced antibodies and viral proteins. Antibodies and red blood cells generated immune haemolysis. Haemoglobin was infected and then attacked. The virus captured porphyrin and inhibited heme metabolism. Therefore, we believe that the damage of the virus to the human body is systemic, not confined to the respiratory system.” (6)

In the meanwhile, the condition multiplies in the lung then deteriorates to hypoxia.

SNP’s and Covid-19

As we discussed earlier, deficiencies in SNP’s result in reduced function of various body processes that are essential in our day to day function. Various SNP’s are co-dependent and here we will discuss some SNP’s implicated in Covid-19.


However, a separate gene (FUT2) actually interacts with your blood type gene, and determines your ability to secrete your blood type antigens into body fluids and tissues. A person can be either a Secretor or a Non-secretor. This is completely independent of whether you are a blood type A, B, AB, or O. This means that someone can be an A Secretor or an A Non-secretor, a B Secretor or a B Non-secretor etc. (7)

Dr. Andrew Rostenberg DC tells us

“FUT2 genetic issues deplete the body of L-lysine. Without L-lysine we cannot use our body’s supply of B6 and that creates additional biochemical problems. In short, we need Vitamin B6 and L-lysine to kill viruses so if you are fighting a chronic virus, make sure you support those pathways with additional supplementation.”

Also, those individuals with slow MTHFR pathways or those who may be folate deficient due to chronic stress.

Our approach is to ensure that your whole body is supported to ensure that you are able to cope with increased methylation processes without suffering from unwanted side effects. A sudden increase in methylation may result in a rapid increase in detoxification, when your body is not ready.

Recent research has found that blood group A had a significantly higher risk for COVID-19 compared with non-blood group A groups (albeit modest effect size OR = 1.20, p = 0.02), whereas blood group O had a significantly lower risk for COVID-19 compared with non-O blood groups (OR = 0.67, p < 0.001). (8) What we do know is FUT2 expresses in the small intestine, mouth, colon, and lungs, is involved in the formation of an immune complex, H antigen and that carriers of mutations of the FUT2 genes have been shown to have lower concentrations of the gut microbe, Bifidobacterium, affects the Lewis blood group system, which is a classification of human blood based on the expression of glycoproteins called, Lewis (Le) antigens, on the surfaces of red blood cells or in body fluids, or both and gene (FUT2) gene actually interacts with blood type gene, and determines the ability to secrete the blood type antigens into body fluids. (9) G6PD Glucose-6-phosphate dehydrogenase deficiency (G6PD deficiency), also known as, favism (after the fava bean), is an X-linked recessive genetic condition that predisposes to haemolysis (spontaneous destruction of red blood cells (RBC)) and resultant jaundice in response to a number of triggers, such as certain foods, illness, or medication. It is particularly common in people of Mediterranean and African origin. The condition is characterized by abnormally low levels of glucose-6-phosphate dehydrogenase, an enzyme involved in the pentose phosphate pathway that is especially important in the RBC. G6PD deficiency is the most common human enzyme defect. A G6PD deficiency is the most common human enzyme defect, affecting more than 400 million people worldwide. G6PD is negatively regulated by acetylation on lysine. G6PD is a key enzyme in the pentose phosphate pathway and plays an essential role in the oxidative stress response by producing NADPH. G6PD Folks with G6PD deficiency typically have too much iron in their blood. http://g6pddeficiency.org/wp/faq/good-bad-iron/ In addition, iron overload may occur. In one study, the iron status of fifty Sicilian patients with G6PD deficiency under steady-state conditions was studied and compared to results with those for fifty control patients. Haemolysis and iron indices were considered to evaluate the iron balance. These patients could be considered to be at risk of iron overload as a result of increased bone marrow activity. HFE HFE is responsible for regulating the absorption of iron,;HFE; may confer a difficult time in metabolizing iron (hereditary hemochromatosis). HFE is related to positive regulation of T-cell mediated cytotoxicity. (recall our previous live immunity chat regarding our innate immunity, T-cells and lymphocytes) We need our army of lymphocytes marching into battle to contain attacks by foreigners, such as viruses, bacteria and other intermediate hosts that thrive in a compromised environment. C282Y A -Key gene This deficiency prevents the altered HFE protein from reaching the cell surface, so it cannot interact with Hepcidin and transferrin receptors. -Increased risk of Porphyria cutanea tarda. (recall our recent notation of porphyria, iron robbing by Covid-19 and hypoxia being a magnified risk in all organs! -Increased risk of Sideroblastic anaemia when SNPs in ALAS2. HFE H63D G -Works with HFE C282Y to increase risk. RAB6B Some HFE SNPs in combination with RAB6B SNPs have been associated with elevated serum transferrin saturation. Possible treatments Higher oxalate diet (Oxalates bind with iron. When treating someone with a vitamin B-6 deficiency, low lysine, pyroluria, calcium oxalate stones, elevated oxalates, and the patient has a hereditary hemochromatosis SNP compromised, you may then start seeing an elevation in ferritin Some genetic mutations to look at in association with HFE SNPs: SOD2 A16V (SOD 2 is iron binding) and HFE together can cause a tenfold increase for heart disease. SOD2 A16V; SOD2 is iron binding, and therefore, when down-regulated, may contribute to an iron overload condition. (9) 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 health care practitioner. Rather, our goal is to educate with current researched information that may be relevant to your personal health. Conti P, Ronconi G, Caraffa A, Gallenga CE, Ross R, Frydas I, et al. Induction of pro­inflammatory cytokines (IL-1 and IL-6) and lung inflammation by Coronavirus-19 (COVI-19 or SARS­CoV-2): anti-inflammatory strategies. J Biol Regul Homeost Agents. 2020;34(2). Gu J, Korteweg C. Pathology and Pathogenesis of Severe Acute Respiratory Syndrome. The American Journal of Pathology. 2007;170(4):1136-47. COVID-19 – MTHFR Support.pdf [Internet]. 2020 [cited 13.04.2020]. Available from: https://mthfrsupport.com/covid-19/[13/04. NUTRIPATH. PORPHYRINS. NUTRIPATH; 2020. Ogun AS VM. Biochemistry, Heme Synthesis - StatPearls - NCBI Bookshelf. 2020. hualan L, wenzhong l. COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism. ChemRxiv. 2020:31. McGovern DPB, Jones MR, Taylor KD, Marciante K, Yan X, Dubinsky M, et al. Fucosyltransferase 2 (FUT2) non-secretor status is associated with Crohn's disease. Human Molecular Genetics. 2010;19(17):3468-76. Zhao J, Yang Y, Huang H, Li D, Gu D, Lu X, et al. Relationship between the ABO Blood Group and the COVID-19 Susceptibility. medRxiv. 2020:2020.03.11.20031096. Sterling Hll Compiled by Cynthia Smith B, JD, With contributions by Sterling Hill Erdei and Carolyn Ledowsky N. SNPBit Compendium 2019.