Why We Don’t Lay Eggs

Among the many animals that live on land, and in the oceans, only the mammals don’t lay eggs.  They protect the developing fetus within the mother’s womb for lengthy periods, so that it is born into the world as a fully formed baby.  To achieve this, mammals have evolved a special organ capable of nourishing the foetus in the womb, and all the while protecting it from being attacked by the mother’s powerful immune system.  The organ that makes this possible is the placenta.   We humans have the most specialised placenta of all the mammals, more deeply penetrating into the mother’s womb, and with an exquisitely fine membrane, only a single cell thick – much finer than tissue paper – that separates the mother’s blood from that of the foetus, and through which nourishment and immunological protection takes place.  But here the wonder increases.  This ultra fine membrane is very unusual.  Its cells are fused together so their intervening membranes have dissolved away, making up a monolayer, known as a syncytium.  This helps protect the fetus from the mother's immune system, since half of the fetus's antigens are foreign to the mother, being derived from the father.  Animal genes cannot fuse cells in this way.  How then does our human placenta, vital to every human birth, manage to do this?

It does so with the help of very special types of viruses, which have been incorporated into our chromosomes.  The discovery of these viruses has shocked the world of science, since scientists are more familiar with viruses as the cause of infectious diseases, such as AIDS and flu.  But now we know that these viruses really are playing a key beneficial role in our human life history.  They are known as human endogenous retroviruses – in the scientific jargon, HERVs – and they have, in essence, become an integral part of us through an evolutionary mechanism known as genetic symbiosis.  More remarkably still, these viruses have a genetic make-up that is very similar to the virus HIV-1, notorious as the cause of AIDS.

How, you might well wonder, could a virus assist human reproduction in this way?

One of the genes of a HERV, known as HERV-W, codes for a protein called syncytin-1.  This protein changes the nature of the interface cells of the human placenta to allow them to fuse into the confluent monolayer.  This syncytium cannot be manufactured by our human cells, or genes, without the help of the viral gene.  Moreover, the viral gene responsible for the fusion, is regulated (promoted) by the viral regulatory region, known as an LTR, so that the viral genome works as a consistent functioning unit within our genome, and it has been tightly conserved by natural selection for millions of years as an integral part of us.  This is not a mutation -- mutations arise from copying errors during the reproduction of cells -- but in this instance the viral gene, and the viral promoter, arrived in the genome as pre-evolved genetic sequences.  Thus this evolutionary stop came about through the union of two quite different evolutionary lineages -- genetic symbiogenesis.

As a consultant physician, I have long had a special interest in how evolution applies to medicine.  I first defined the concept of viruses as examples of genetic symbiosis, and I have written a book, Virolution, and numerous scientific and medical papers, explaining this for lay readers and professional readers respectively.

The wonder of viruses and the human placenta doesn’t stop there.  Our human chromosomes are full of similar viruses, and genetic sequences that come from them.  They are an integral part of our genetic makeup.  We now know of eight separate viruses that play roles in human reproduction.  wo of the three placental viruses make proteins, known as syncytins, that enable the placental cells to fuse, and they also help the placenta to stop the mother’s immune system from damaging the foetus in the womb.  A Swedish pathologist, Erik Larsson, has recently discovered that these syncytins are also playing some important, but as yet unknown, function in the normal human brain.  Indeed, this viral part of our makeup is becoming very important to our understanding of human diseases.

For example, in multiple sclerosis, a slightly different form of syncytin-1 may be playing an important role in the inflammation that damages the insulation sheath around the nerve cells, known as myelin. 

I have written five linked review papers for the Journal of the Royal Society of Medicine, explaining how the evolutionary concepts are important to medical understanding.  I have also written a specific paper on the role of HERVs in MS, which has been accepted for publication in a pharmacological journal subject to slight revision.  This suggests ways in which the new knowledge might help with diagnosis, prognosis and even posssible therapy in the future.

Other studies, by doctors in Italy, have shown that our human viruses are playing a very important role in seven or eight of the common forms of cancer.

For more information about human endogenous retroviruses and Multiple Sclerosis see the more detailed article on this in my news collection.