James Odell, OMD, ND, L.Ac.
Many believe viruses to be harmful organisms that invade, infect, and even kill. In truth, the two dozen or so viral types that potentially wreak havoc with the human body represent an infinitesimally small fraction of the 100 million viral types on earth. In fact, most viruses are vital to our very existence and the sheer number of ‘good’ viruses is astonishing. Countless viruses have incorporated themselves into the genome of our ancestors for hundreds of millions of years. They typically have gotten there by infecting eggs or sperm, inserting their DNA into ours. There are 100,000 known fragments of viruses in the human genome. Approximately 8% of the human genome is made up of endogenous retroviruses (ERVs), which are viral gene sequences that have become a permanent part of the human lineage after they infected our ancient ancestors. Beneficial viruses attack pathogenic bacteria and assist in cellular detoxification. In short, numerous endogenous retroviruses have been essential for human survival.
Viruses are powerful, ancient, and vital to our existence, but they are extremely simple constructions. They tend to be nothing more than a few pieces: a protein capsid, which is a simplistic and protective shell; a protein called a polymerase, which carries out most of the functions related to replicating the viral genome; and a sequence of nucleotides — either RNA or DNA — that encode for the viral proteins. Thus, they are simply bits of genetic material (DNA or RNA) covered in protein. They attach to their target cell (the host), inject their genetic material, and replicate themselves using the host cells’ metabolic pathways. Then the new viruses break out of the cell, the cell explodes (lyses), releasing hundreds of viruses.
Viruses are very picky about whom they will infect. Each viral type has evolved to infect only one host species. Viruses that infect bacteria dominate our world and help control the many diverse microbiomes. A virus that infects one species of bacteria will not infect another bacterial species. We have our own suite of a couple of dozen viral types that are associated with certain diseases, but infection depends on our biological terrain and the strength of our innate and adaptive immunity.
The Syncytin Gene and its Proteins
Of the many beneficial viruses that have become part of our human genome, science is now looking to one in particular that has been credited with making human life possible. While examining the human genome, scientists encountered a curious gene creating a protein known as the syncytin gene, or more technically called ERVW-1 gene (endogenous retrovirus group W envelope member 1). This syncytin gene serves to encode the proteins (called syncytin-1 and syncytin-2) that are found in several bodily tissue types, but are particularly important to placenta-based cells. Cells that create syncytin are located at the point where the uterus and placenta meet and fuse to form a layer of cells known as the syncytiotrophoblast. This epithelial covering establishes nutrient circulation between the embryo and the mother and thus is critical for the development of the human fetus. Syncytin-1 mediates the fusion of cytotrophoblasts. Cytotrophoblast is the inner layer of the trophoblast, interior to the syncytiotrophoblast, and external to the wall of the blastocyst in a developing embryo. It functions for placental development and therefore is essential for fertility. Cell-cell fusion of trophoblasts is essential for the formation of the multinucleated syncytiotrophoblast layer during human placental development. In fact, syncytin 1 is known to be involved in the fusion of mononuclear cytotrophoblasts into a multinucleated syncytiotrophoblast layer because antisense oligonucleotides targeting syncytin 1 block trophoblastic fusion and differentiation.1, 2
Hence, syncytin is produced as a precursor to the formation of the cellular layer that allows for a fusion of the placenta and uterus. The placenta facilitates the exchange of nutrients, gases, and metabolic end products between mother and fetus. It also produces hormones regulating fetal and maternal physiology and provides immunotolerance toward the paternal component of the embryo.
Again, what makes syncytin even more incredible is the finding that it did not arise from a mammalian gene: syncytin arose from a virus. The gene encoding the protein syncytin is the envelope gene of a recently identified human endogenous defective retrovirus, HERV-W. HERV-W makes up about 1% of the human genome and is part of a superfamily of repetitive and transposable elements. It is speculated that the syncytin gene was incorporated into the primate genome more than 24 million years ago through viral infection. After millions of years of evolution, it has gained vital functions in human biology. Important to note, because it originated from a virus, syncytin shares amino acid sequences with certain viruses. So, what originally started as a viral gene designed to produce proteins that would fuse the host’s cells together, thereby allowing the virus to spread with greater ease, now serves to connect mother and child. Quite simply, syncytin is critical and without it, human life could never form.
Following the discovery of syncytin-1, French virologist Thierry Heidmann went on to discover another syncytin protein called syncytin 2. This viral-derived protein serves to suppress the mother’s immune system to prevent her body from attacking and rejecting her baby’s tissues as it would a foreign body. Thus, syncytin-1 plays a critical role in placental trophoblastic formation, and syncytin-2 is involved in the maternal immunosuppressive effect on the fetus.2
Abnormal Syncytin Expression and Disease
The reduced levels of syncytin expression in trophoblast cells cause various placental pathologies and can result in infertility. Bear in mind any foreign toxin or synthetic man-made or chimeric viral particle that causes an overexpression or underexpression of the syncytin gene and its proteins can cause infertility as well as other syncytin-related tissue dysregulation. When syncytin-1 is overexpressed in cells expressing the receptors, massive homotypic cell fusion is induced in cells that otherwise do not fuse. Cell fusion is a well-orchestrated process known to be mediated by the interaction between syncytin-1, and its receptor, ASCT2, both located on the cell membrane.3, 4
Over the years, it has been shown that abnormal increased and decreased expression of syncytin-1 results in numerous inflammatory and neurological illnesses. In neuropsychological diseases, syncytin-1 mediates the chronic inflammation in the nervous system, which can cause neuronal injury and/or damage to the brain microvasculature, cerebral blood flow, and the blood-brain barrier. Abnormalities in syncytin-1 have been particularly implicated in preeclampsia, a common pregnancy disorder with poor trophoblast differentiation and vascular dysfunction in placenta.5, 6, 7 It has also been shown that abnormally increased expression of the syncytin-1 protein was detected in brain tissues from multiple sclerosis patients and in endometrial carcinoma.8, 9, 10, 11, 12 Syncytin-1 shares high sequence similarity to the multiple sclerosis retrovirus-like particle envelope protein that is involved in the development of multiple sclerosis.
Additionally, studies demonstrate that various cancer cells express syncytin and/or syncytin receptors and can fuse with normal healthy cells. The results of such fusions differ between cell types and are either beneficial (suppression of tumorigenicity) or detrimental (increased proliferation activity, genetic instability, and malignant transformation). For example, the level of syncytin expression in breast cancer patients is a positive prognostic indicator for recurrence-free survival. It is believed that the syncytin-mediated fusion between the healthy endothelial cells and breast cancer cells suppresses the proliferation potential of the latter. In contrast, the fusion between spleen cells and myeloma cells results in the formation of hybrid cells with an unlimited proliferative ability, and the fusion between melanoma cells and macrophages enhances malignant phenotype 13, 14
Creating a Contraceptive Vaccine to Suppress Syncytin-1
In 2005 it was proposed that a targeted synthetic Syncytin-1 vaccine could be developed as a contraceptive that would work to produce antibodies against human Syncytin-1. Essentially, this project was aimed at the immunological inhibition of syncytial trophoblast fusion as an immunological approach to contraception. The authors wrote, “These synthetic peptides mimic trophoblast epitopes essential for syncytial fusion and are, therefore, considered specific immunogens for the generation of antibodies that will inhibit implantation.”15
The fact that pharmaceutical manufacturers have explored using a synthetic syncytin to create anti-syncytin antibodies as a form of contraception is alarming considering the importance of syncytin to human physiology.
SARS-CoV-2 Vaccine Types and Spike Proteins
The entry of the SARS-CoV-2 virus (causing the COVID-19 ‘pandemic’) is facilitated by the spike protein on the surface of the virus. Thus, the viral spike protein has been the primary target antigen for manufacturers of SARS-CoV-2 ‘vaccine’. Though there are more than a hundred SARS-CoV-2 ‘vaccines’ in development, currently, there are two types approved for Emergency Use Authorization (EUA): nucleic acid (mRNA,) and viral vector. The currently experimental Moderna and Pfizer–BioNTech products EUA approved use of synthetic mRNA coding for the spike protein enclosed within the nanolipid particles, while the Johnson and Johnson and Oxford–AstraZeneca vaccine uses a replication-deficient adenovirus with inserted SARS-CoV-2 spike protein sequences. However, both Johnson/Johnson and AstraZeneca shots carry a snip of double-stranded DNA (dsDNA) [transgene] wrapped in an adenovirus outer “shell”. 50-billion particles are injected with each injection. dsDNA-antibodies are diagnostic of a long list of autoimmune disorders.16
Johnson/Johnson and AstraZeneca shots release a transgene that can lead to potentially deadly side effects from injecting raw genetic material that can induce anti-DNA antibodies and can integrate into human DNA. Essentially, all the COVID shots lead to the creation of a spike protein through a process called translation.
Though this article focuses on how spike proteins derived from the mRNA ‘vaccines’ may adversely affect syncytin and cause infertility, there are other concerns associated with the creation of spike proteins in the body:
The spike protein behaves as a hapten, a small molecule that binds to the surface of organs, leading to an autoimmune response and possible antibody dependent enhancement (ADE).17 ADE is a phenomenon occurs when a person is exposed to a circulating coronavirus after being vaccinated. ADE was discussed in the last two BRMI E-Journal articles on COVID Vaccines.18, 19
The anti-S-Ab enhances the entry of the SARS-CoV-2 virus into the cell (usually macrophages) and accelerates its replication, causing more severe illness than they would have experienced if they had not been vaccinated.
The spike protein can damage organs directly by promoting cardiovascular complications, damaging blood vessels in the lungs, and breaking through the blood-brain barrier (BBB), important for protecting the brain. Breaking down the BBB means many particles can pass directly into brain tissue. This explains the VAERS reported neurological conditions associated with the SARS-CoV-2 spike protein: loss of smell, loss of taste, headache, seizures, and uncontrolled tremors.
The spike protein can incorporate into human DNA through a process called transfection.
The spike protein evokes the release of destructive anti-spike-antibodies. Anti-spike-antibodies [anti-S-Ab] can cause significant organ damage, specifically to the lungs. The antibodies can also cross-react with 28 different human tissue types, establishing a mechanism for multi-system autoimmune disorders and multi-organ failure.20
The spike protein can bind to the ACE2 receptor on the surface of sperm and ovaries causing a risk of miscarriage and infertility. ACE2 receptors are expressed on lung, intestine, and kidney tissues and the testis, sperm, ovaries, uterus, and vagina.21, 22
The reproductive consequences of the spike protein whether from the virus or because of being injected with one of the COVID shots – such as infertility and the risk of sexual transmission, are c`urrently unknown.23
mRNA Coronavirus (synthetic spike protein) ‘Vaccines’ and Syncytin
It has been observed that syncytin-1 shares high sequence similarity to the spike protein of coronavirus. Several scientists worldwide have voiced extreme concern that the Pfizer and Moderna mRNA COVID product designed to create a spike protein in the cellular ribosomes may elicit an antibody response against syncytin-1. This of course could result in infertility, miscarriages, and both male and female reproductive disorders of unknown duration. Because syncytin shares a similar amino acid sequence to the spike protein of SARS-CoV-2 there is valid and serious question as to its detrimental effect on the placenta. This is not surprising since the syncytin gene is of retroviral origin. Technically speaking, the syncytin protein has 538 amino acids. Recently studies showed that the regions of N- and C-terminal heptad repeats NHR (41 aa) and CHR (34 aa) in the S2 domain of the SARS coronavirus (SARS-CoV) spike protein and syncytin share similarities. 24
On December 1, 2020, the ex-Pfizer head of respiratory research Dr. Michael Yeadon and Dr. Wolfgang Wodarg, pulmonary specialist and Director of the Public Health Department in Flensburg, Germany filed an application with the European Medicine Agency responsible for EU-wide drug approval, for the immediate suspension of all SARS CoV 2 vaccine studies, in particular the BioNtech/Pfizer study on BNT162b.
This is an excerpt from Drs. Yeadon and Wodarg’s petition:
Syncytin-1, which is derived from human endogenous retroviruses (HERV) and is responsible for the development of a placenta in mammals and humans and is, therefore, an essential prerequisite for a successful pregnancy, is also found in a homologous form in the spike proteins of SARS viruses. There is no indication whether antibodies against spike proteins of SARS viruses would also act like anti-Syncytin-1 antibodies. However, if this were to be the case this would then also prevent the formation of a placenta which would result in vaccinated women essentially becoming infertile. To my knowledge, Pfizer/BioNTech has yet to release any samples of written materials provided to patients, so it is unclear what, if any, information regarding (potential) fertility-specific risks caused by antibodies is included.
According to section 10.4.2 of the Pfizer/BioNTech trial protocol, a woman of childbearing potential (WOCBP) is eligible to participate if she is not pregnant or breastfeeding and is using an acceptable contraceptive method as described in the trial protocol during the intervention period (for a minimum of 28 days after the last dose of study intervention). This means that it could take a relatively long time before a noticeable number of cases of post vaccination infertility could be observed.25
Thus, the claim is made that because of a similar or shared amino acid sequence in the spike protein of SARS-CoV-2 and the syncytin-1 placental protein, this can potentially mount an antibody response to syncytin and result in male and female infertility, miscarriages and reproductive dysregulation.
When this disturbing similarity was revealed, pharmaceutically sponsored fact-checkers and virologists were quick to discount such an idea as unlikely. They counter-claimed that human syncytin-1 and SARS-CoV-2 spike protein share only a few amino acid sequences.26 Thus, it has been presumed or assumed that this similar amino acid sequence is probably ‘too short’ for the immune system to meaningfully confuse it with this important placental protein. However, if this sequence similarity later does prove to create anti-syncytin antibodies then it will be too late to reverse the course of mass infertility. Tens of millions of women, men, and children will have been inoculated worldwide with this experimental synthetic pathogen creating a pathogenic spike protein for an unknown duration. This human experiment is truly beyond risky and may prove to have dire consequences on the entire human race and future generations.
VAERS Reports and the Clinical Appearance of Miscarriages, Stillbirths, and Menstrual Disturbances
Hundreds of COVID-19 vaccines associated miscarriages and stillbirths have been reported to the Vaccine Adverse Event Reporting System (VAERS), a national vaccine safety monitoring program co-sponsored by the Food and Drug Administration (FDA) and the Centers for Disease Control and Prevention (CDC).
It is becoming more clinically evident that the mRNA injections have a strong potential to cause miscarriages and stillbirths.
We are at a critical juncture in time for all of humanity on a lot of different levels. The experimental mRNA ‘vaccines’ are a serious existential threat and may result in mass infertility and millions of deaths in the next two to three years. The time is now past for being careful to not offend anybody by speaking frankly about the alarming adverse reactions daily being reported to the CDC-VAERS and EudraVigilance in Europe. Hundreds, if not thousands, of women are reporting miscarriages, stillbirths, and menstrual irregularities after receiving the mRNA injection.
This article has outlined how the human placenta formation relies on the interaction between fused trophoblast cells of the embryo with uterine endometrium. The fusion between trophoblast cells, first into cytotrophoblast and then into syncytiotrophoblast, is facilitated by the all-important fusogenic protein syncytin. Syncytin derives from an envelope glycoprotein of retroviral origin and plays a critical role in human placentation. This protein is also expressed in other tissues such as sperm and is involved in normal menstruation, inflammatory response, cancer as well as brain functioning. The syncytin gene has a retroviral origin and has been shown to have a similar amino acid sequence to the spike protein expressed on the surface of SARS-CoV-2. This similarity between sycytin-1 and SARS-CoV-2 spike protein has a questionable potential to result in antibodies that could attack syncytin and result in female and male infertility, miscarriages, and menstrual dysregulation.
We know there has been a dark history of pharmaceutical projects developing a synthetic syncytin-1 vaccine that could be used as a contraceptive due to its potential ability to produce antibodies against human syncytin-1. The mRNA vaccines create a spike protein that is in some ways are like these early synthetic vaccine contraceptive products. The bottom line is that any antibodies raised against this protein can potentially cause infertility in women and men and can trigger systematic dysregulation.
The role of retroviral proteins, especially syncytins, in the trophoblastic fusion process and placental morphogenesis were only identified and hypothesized about 20-years ago. There is still much to learn, and much we still do not know about similar amino acid sequences and their effect on human physiology. Thus, this issue warrants further research, and until then we should immediately stop all experimental coronavirus vaccines.
Mi, Sha, Xinhua Lee, Xiang-ping Li, Geertruida M. Veldman, Heather Finnerty, Lisa Racie, Edward LaVallie et al. "Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis." Nature 403, no. 6771 (2000): 785-789. https://www.biologicalmedicineinstitute.com/articles-aluminum1
Blaise, Sandra, Nathalie de Parseval, Laurence Bénit, and Thierry Heidmann. "Genomewide screening for fusogenic human endogenous retrovirus envelopes identifies syncytin 2, a gene conserved on primate evolution." Proceedings of the National Academy of Sciences 100, no. 22 (2003): 13013-13018. https://www.pnas.org/content/pnas/100/22/13013.full.pdf
Blond, Jean-Luc, Dimitri Lavillette, Valérie Cheynet, Olivier Bouton, Guy Oriol, Sylvie Chapel-Fernandes, Bernard Mandrand, François Mallet, and François-Loïc Cosset. "An envelope glycoprotein of the human endogenous retrovirus HERV-W is expressed in the human placenta and fuses cells expressing the type D mammalian retrovirus receptor." Journal of virology 74, no. 7 (2000): 3321-3329. https://jvi.asm.org/content/jvi/74/7/3321.full.pdf
Lavillette, Dimitri, Mariana Marin, Alessia Ruggieri, François Mallet, François-Loïc Cosset, and David Kabat. "The envelope glycoprotein of human endogenous retrovirus type W uses a divergent family of amino acid transporters/cell surface receptors." Journal of virology 76, no. 13 (2002): 6442-6452. https://jvi.asm.org/content/76/13/6442.full
Knerr, Ina, Ernst Beinder, and Wolfgang Rascher. "Syncytin, a novel human endogenous retroviral gene in human placenta: evidence for its dysregulation in preeclampsia and HELLP syndrome." American journal of obstetrics and gynecology 186, no. 2 (2002): 210-213. https://www.sciencedirect.com/science/article/abs/pii/S0002937802112282
Lee, X., J. C. Keith Jr, N. Stumm, I. Moutsatsos, J. M. McCoy, C. P. Crum, D. Genest et al. "Downregulation of placental syncytin expression and abnormal protein localization in pre-eclampsia." Placenta 22, no. 10 (2001): 808-812. https://pubmed.ncbi.nlm.nih.gov/11718567/
Chen, C‐P., K‐G. Wang, C‐Y. Chen, C. Yu, H‐C