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 mult