What do retroviruses do when pregnant?
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.
We test for the presence of this retrovirus, or rather for the "signature" of its proteins, and when we find those signatures we declare that the person suffers from Aids and better start treatment as soon as possible.
Pregnant mothers are tested with special attention. And where they are found to be positive, they are told that a course of anti-retroviral drugs will be needed to try and protect the baby from becoming infected as well.
Now this all seems very logical, until you find out that in the normal course of every pregnancy, retroviruses are activated and that those retroviruses have an active role in the construction of new blood vessels that are needed to allow the growing fetus to survive and develop.
A fertilized ovum attaches itself to uterine tissue
A monstrous thought...
Could we be killing unborn babies by giving the mothers anti-retroviral drugs?
Is perhaps the whole idea that Aids is caused by a retrovirus to be put in question? Some would tell you yes, that is the case. But let's take this one step at a time. Here is what Cal Crilly has found in the scientific literature regarding retroviruses in pregnancy...
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What Retoviruses Do When Pregnant?
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.
Around the year 2000 a few studies came online about a so called retrovirus called HERV-W.
HERV-W or Syncytin was found to be a part of the trophoblast cells that surround fetal cells in pregnancy. The trophoblast cells do amazing things where they remodel arterial walls and divert blood from the mother's spinal artery and feed the baby with the blood supply.
These researchers found HERV-W which acted in similar ways to other retroviruses was doing cell to cell fusion. You could call these things RNA strands that do things if retrovirus is a loaded word. The amazing thing was that they didn't try to make out this was an infectious retrovirus and so published studies about what HERV-W actually did instead of the usual horror stories we get about HIV.
Trophoblasts and the uterine epithelium
Direct involvement of HERV-W Env glycoprotein in human trophoblast cell fusion and differentiation
http://www.ncbi.nlm.nih.gov/pubmed/12724415
Syncytin: the major regulator of trophoblast fusion?
http://humupd.oxfordjournals.org/content/10/6/487.full.pdf
So they have a mass of studies saying retroviruses are essential in pregnancy.
This was happening at the same time as the [HIV] Mother To Child Prevention drug campaign. No scientists mentioned what effects the drugs would have on babies. I was horrified and it is still a big part of why I've ended up speaking out.
Well people can still argue over what [retroviruses] are or what they do but some studies are indicators. The important thing to know is that if HERV-W stops working then arterial remodeling stops working and the baby loses blood supply and starves. This loss of blood supply is a condition called Preeclampsia. HERV-W or Syncytin is less active in Preeclampsia.
Downregulation of placental syncytin expression and abnormal protein localization in pre-eclampsia
http://www.ncbi.nlm.nih.gov/pubmed/11718567
If they deliberately switch off HERV-W the trophoblast cells don't work
"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
http://www.legs.cnrs-gif.fr/Partenaires/gdr2157/articlesgdr/2005/malassine2005.pdf
And if women are on antiretrovirals then they get preeclampsia as the drugs prevent the woman's retroviruses from successfully creating arteries for the fetus.
Increased risk of pre-eclampsia and fetal death in HIV-infected pregnant women receiving highly active antiretroviral therapy
http://www.ncbi.nlm.nih.gov/pubmed/16327320
This is because the HERV-W 'retrovirus', is needed to remodel the arteries so the blood supply can get to the baby.
This means that HIV+ women who don't take antiretrovirals are healthier and able to deliver a healthier baby because their retroviruses are working. That's how it looks to me. I'll emphasize some points in more detail.
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."
Trophoblast functions, angiogenesis and remodeling of the maternal vasculature in the placenta
http://www.sciencedirect.com/science/article/pii/S0303720701007031
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."
Direct involvement of HERV-W Env glycoprotein in human trophoblast cell fusion and differentiation
http://www.ncbi.nlm.nih.gov/pubmed/12724415
Because retroviruses are involved in arterial remodeling and cell to cell fusion it's easy to get this confused....
"A retroviral envelope protein also dubbed syncytin is a highly fusogenic membrane glycoprotein"
A retrovirologist sees this and defines it as an infection, but it really is sticking to cells and meant to.
"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."
This basically meaning placental formation is reliant on the retrovirus HERV-W functioning properly.
"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."
Trophoblast cell fusion as happens when pregnant is accompanied by an increase in retroviral HERV-W.
This is an important point because we give pregnant women the HIV test at a time when their retroviruses are high. The HIV antibody test was meant to be a blood screening test to be used by blood banks for all retroviruses so it's application to people is non-specific.
"Finally, by using specific antisense oligonucleotides, we demonstrated that inhibition of Env-W protein expression leads to a decrease of trophoblast fusion and differentiation."
And by switching off HERV-W expression they were able to decrease trophoblast fusion. This is of course what happens when taking anti-retrovirals.
Given simple nutrient problems in pregnant African women it seems to me a terrible waste of money to use anti-retrovirals when basic deficiencies are already causing childhood deaths and all these effects on mothers and children from the use of toxic anti-retrovirals are also never mentioned.
My thoughts.
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