When we hear the word retrovirus, we think: Aids. The Human Immunodeficiency Virus or HIV is a retrovirus. HIV is what mainstream medicine tells us causes a number of different illnesses and weakening of immune defenses - Aids.
Retroviruses kick into action when pregnant and are involved in creating the blood supply to the fetus so if they are not working properly the blood flow is less and the fetus can starve from lack of nutrients.
|Trophoblasts and the uterine epithelium|
Downregulation of placental syncytin expression and abnormal protein localization in pre-eclampsia
"Furthermore cell fusion and differentiation of these normal trophoblastic cells are markedly inhibited by specific HERV-W antisense oligonucleotides."
Expression of HERV-W Env Glycoprotein (syncytin) in the Extravillous Trophoblast of First Trimester Human Placenta
Increased risk of pre-eclampsia and fetal death in HIV-infected pregnant women receiving highly active antiretroviral therapy
The Trophoblasts are part of the Placenta and have HERV-W retroviruses that are needed right throughout pregnancy.
This is an abstract giving an overview of how trophoblast cells cause angiogenesis or arterial remodeling for fetal blood supply.
"One of the most important local adaptations to pregnancy is the change in maternal blood flow to the implantation site. In rodents and primates, new blood vessels form through angiogenesis, dilate and then become modified such that the blood enters into trophoblast cell-lined sinuses (hemochorial). Evidence from gene knockout mice suggests that factors from the placenta regulate the uterine vasculature. Consistent with this, trophoblast giant cells produce a number of angiogenic and vasoactive substances that may mediate these effects. Teratocarcinomas containing large numbers of trophoblast giant cells (derived from Parp1 gene-deficient ES cells) show similar 'hemochorial' host blood flow, implying that the effects are not specific to the uterine vascular bed. As in primates, murine trophoblast cells also invade into the uterine arteries of the mother."
Cancer cells behave in a similar way to trophoblast cells and this is also why cancer is a disease where retroviruses HERV-W and HERV-K appear and also cause angiogenesis (angiogenesis is new arterial formation) but in the case of cancer cells they divert blood supply to tumours instead of a fetus.
I'll put the entire abstract from one of the early studies to sum up.
"We recently demonstrated that the product of the HERV-W env gene, a retroviral envelope protein also dubbed syncytin, is a highly fusogenic membrane glycoprotein inducing the formation of syncytia on interaction with the type D mammalian retrovirus receptor. In addition, the detection of HERV-W Env protein (Env-W) expression in placental tissue sections led us to propose a role for this fusogenic glycoprotein in placenta formation. To evaluate this hypothesis, we analyzed the involvement of Env-W in the differentiation of primary cultures of human villous cytotrophoblasts that spontaneously differentiate by cell fusion into syncytiotrophoblasts in vitro. First, we observed that HERV-W env mRNA and glycoprotein expression are colinear with primary cytotrophoblast differentiation and with expression of human chorionic gonadotropin (hCG), a marker of syncytiotrophoblast formation. Second, we observed that in vitro stimulation of trophoblast cell fusion and differentiation by cyclic AMP is also associated with a concomitant increase in HERV-W env and hCG mRNA and protein expression. Finally, by using specific antisense oligonucleotides, we demonstrated that inhibition of Env-W protein expression leads to a decrease of trophoblast fusion and differentiation, with the secretion of hCG in culture medium of antisense oligonucleotide-treated cells being decreased by fivefold. Taken together, these results strongly support a direct role for Env-W in human trophoblast cell fusion and differentiation."
"A retroviral envelope protein also dubbed syncytin is a highly fusogenic membrane glycoprotein"
"In addition, the detection of HERV-W Env protein (Env-W) expression in placental tissue sections led us to propose a role for this fusogenic glycoprotein in placenta formation."
"We observed that in vitro stimulation of trophoblast cell fusion and differentiation by cyclic AMP is also associated with a concomitant increase in HERV-W env and hCG mRNA and protein expression."
"Finally, by using specific antisense oligonucleotides, we demonstrated that inhibition of Env-W protein expression leads to a decrease of trophoblast fusion and differentiation."