Before I delve into this subject I must explain what exactly a retrovirus is. Most viruses (e.g. influenza) hijack the cell’s machinery (e.g. ribosomes) to self replicate after infection of a host cell. Retroviruses (e.g. HIV) instead insert their RNA into our genetic code using an enzyme called reverse transcriptase to convert its RNA into DNA for insertion into the host’s DNA. Once the genetic material has been integrated into the host cell’s DNA, the virus then uses the cell’s machinery to create the parts of the virus, which are assembled on the cell surface.
Where the retrovirus inserts its DNA into our genome is random. It then waits for the right moment to start virus production. This viral DNA can be copied along with the host’s (during cell replication), or it can be pasted into another random part of the genome. Over the course of millions of years, mutations cause the viral DNA to be unable to break free from the host cell’s DNA, however some of these endogenous retroviruses can still affect other parts of genetic code. This is because our cells use epigenetic marks to label and lock down the moving viral elements. But the viral genetic information can move with their marks, and so the viral sequences can spread to wherever they land.
About half of our genome comes from extinct viruses, which are collectively known as transposable elements, but are degraded beyond being virus-like.These large parts of repetitive and virus-derived DNA was thought to be rubbish, and some of it is almost certainly not much more than that, but other parts can form key triggers or serve key functions in the modern human and other spices too.
Professor Didier Trono and his team at the University of Lausanne, Switzerland believes that our bodies can harness the genetically embedded viral DNA toward our advantage is to do with the main group of special silencer molecules: KRAB Zinc Finger Proteins (KRAB ZFPs). They lock down viral sequences in our DNA. There are over 300 different types of these molecules in our genome, each individual prefers a different virus-derived DNA target. It used to be believed that they killed these rouge viral elements, but Trono belives that once attached to the viral sequence they suppress them and then eventually overpowers them. This idea is a bit controversial.
Some modern mammals have a syncitium (a special layer of tissue formed by fusing placenta cells). The molecule that does this is produced by a syncitin gene, which is very similar to the gene of a retrovirus. Another syncitin was later discovered, again it plays a part in forming the placenta, as well as this it also prevents the mother’s immune system from trying to attack the fetus in the womb. Humans, mice, cats and dogs all have their own two syncitin genes that do the same job, but that look as if they’re sourced from very different viruses. Horses and pigs don’t have a syncitium, nor do they have any syncitin genes from viruses; so they probably never caught one of the fusing viruses.
The University of Utah found an endogenous retrovirus in our genome that infected us 45-60 million years ago. This viral DNA has been used to help us fight other viruses. It does this by turning on the AIM2 gene when it detects an interferon molecule (the danger signal of a present viral infection). AIM2 then triggers the infected cells to self-destruct, preventing it spreading.
The PRODH gene is present in our brain cells, mainly in the hippocampus is also activated by the switch made from a long dead retrovirus. Chimpanzees share this gene and switch, although it is less used by them. Disfunctions of the PRODH gene have been linked to several mental disorders, so it is a key part of the brain. On the subject of chimpanzees, the genes that form and grow both our and their faces are nearly identical, so it is the switches (from viral infections) that are active in cells involved in this process that make the difference.