Like a Virgin by Prasad, Aarathi (recommended reading txt) 📕

In primates, including humans, biologists believe that, over evolutionary time, the trophoblast gradually infiltrated the mother’s womb more and more deeply as the size of the foetal brain grows larger and larger. The brain, for instance, needs about sixty percent of the total nutrition supplied to a human foetus, compared with about twenty percent in non-primate mammal embryos. This may be why the human trophoblast invades the womb twice – something not seen in any other mammal.

The human placenta’s progressive and deep invasion into the womb poses a considerable challenge to the mother’s body. The mother’s immune system should protect her from infections and other foreign threats. But when she is pregnant, her immune system is forced to tolerate certain foreign material – the embryo and the placenta, both of which grow from that first cell that is half derived from the father’s DNA. From the body’s point of view, these growths are parasites, sucking life from the mother’s body for their own existence. Detection by the immune system of such foreign tissue would usually lead to organ rejection, and preventing rejection is a necessity when it comes to making babies.

To ensure their survival, the embryo and the placenta cannot simply suppress the mother’s immune system, as this would expose her (and her developing foetus) to the risk of infection – even possibly death. Instead, the trophoblast produces a special subset of MHC class I molecules that protect the foetus from natural killer cells in the mother’s womb. These particular molecules work only in the vicinity of the placenta – a neat biological trick. Still, these molecules are not all-important. If you were to destroy them, a mother would not immediately reject her foetus or its placenta. How could that be?

There must be at least one other strategy that prevents full-blown immunological warfare between mother and child. As it happens, the genetic compromise does not seem to have been developed specifically to adapt to life with a placenta. Instead, it depends on the fact that there is another, completely different source of DNA in the body. The cells that give rise to the placenta, and which protect the inner layer of cells destined to become the baby from attack by the mother’s immune system, are unique: not only do they exclusively come from the father, some of those genes are not even human. They are the DNA of ancient viruses.

Among egg-laying animals, which do not have placentas, contact between mother and foetus is very limited, of course. It is the shell that shields the embryo from the mother, and the mother from the embryo, and the shell is created entirely by contributions from the mother. The egg also does not stay inside the mother’s body for very long after it is fertilized. Incubating a fertilized egg inside the mother’s body required an ingenious ploy. In 1997, Luis Villarreal, a molecular biologist at the University of California, Irvine, wrote an article entitled ‘On Viruses, Sex, and Motherhood’ in which he recounted his theory of a very clever leap in evolution. In this article, published in the Journal of Virology, he proposed that viral DNA played an essential role in the evolution of mammalian pregnancy.

Viruses are among the oldest and most successful life forms on the planet, and Villarreal and others believe that the virus in question would have infected a distant ancestor in our primate lineage as far back as twenty-five million to forty million years ago. When you look at the genome of vertebrates, you find thousands of foreign elements that look a lot like the genetic information harboured in retroviruses, a form of virus that creates DNA out of RNA (opposite to most viruses, which make RNA out of DNA) and integrates this new DNA into its host. Indeed, nearly ten percent of human DNA today appears to be made up of old retroviruses. The most well-known retrovirus is HIV, the cause of AIDS, which shuts down the immune system, but other retroviruses have been linked to tumour cell growth.

Deploying some of the same tactics that viruses use to evade our immune system, the viral DNA in mammals allowed another invader into the body: the foetus. These genes, known as syncytin genes, allow the body to protect, nourish, and incubate the foetus, giving it time to mature without the threat of rejection by the ‘host’ immune system. Without viral DNA, humans and many other mammals might still be laying eggs. And syncytin genes are targeted on making the placenta, specifically at the level of the trophoblast ring of cells – exactly where exchanges between the foetus and the mother take place. Importantly, syncytin genes instruct cells to fuse with each other. That is, they are able to force cells from the lining of the mother’s womb, comprised solely of the mother’s DNA, to fuse with cells from the trophoblast, which is designed by DNA from the father alone.

It is important to note that syncytin genes work as diplomats rather than combatants in the war between different DNA: they do not affect the embryo’s development or the actions of the immune cells; instead, they temporarily cloak the embryo, keeping it from being recognized and destroyed by the mother’s immune system. When a particular syncytin gene, syncytin-A, is disabled in mice, the entire architecture of the trophoblast changes dramatically. Embryos begin to grow, but at a slow rate, and fewer blood vessels form to feed them. The pregnancies invariably end in miscarriage. A faulty placenta does not make for a healthy pregnancy, and this is exactly what the scientists attempting to create fatherless mice were fighting. Their early experiments kept showing that when they tried to produce offspring with DNA originating only from sperm, the embryo struggled to