Do you know that actually 8% of our genome is viral? This fact has been elucidated in recent discoveries, however the impact of our co-evolution is yet to be determined.
Retroviruses can integrate permanently fragments of their own genome into the host’s DNA by infecting germ cells (sperm or eggs). In consequence, the viral genomic information can be potentially passed on to the human offspring. These viral DNA fragments that prevail are known as human endogenous retrovirus (HERVs). So far, more than 30 different HERV species have been identified in our genome.
Growing evidence suggest that some HERV proteins that are expressed are involved in human developement. Our story as human beings starts when we are just an agglomeration of cells. During this stage, some proteins of HERV are required to keep the pluripotent state in human embryonic stem cells. Furthermore, they play a role in human pre-implantation during embryonic development.
One example is the viral Syncytin protein, which is expressed at high levels in the multinuclear cell layer that is critical for implantation and embryo development, called the syncytiotrophoblast. This HERV envelope protein originally mediates viral cell entry by fusing the viral particle with the host cell. In humans, it helps the feto-maternal exchange and the trophoblast cell fusion that is critical for the formation of the placenta. Knocking down the Syncytin gene, which leads to depletion of the corresponding protein, results in miscarriage and growth retardation, a decrease in vascularization, and a reduction in placental transport function. This means that without usurping Syncytin, we would probably never have evolved a placenta to carry and nourish the fetus through its development.
Another important viral fragment is called Rec. This protein is functionally analogous to the REV protein in HIV which is responsible for the export of unspliced and partially spliced messenger RNAs out of the nucleus. This HERV gene encodes for the Rec protein, which is important to stimulate the immune response in early embryonic cells. The recognition of increased Rec protein levels on the cell surface triggers the expression of interferon, which is an unspecific viral defence mechanism and might prevent new viral infections in the embryonic state.
The co-evolution of humans and HERVs demonstrates that symbiotic interactions and cooperation can drive evolution of species. It does not need to stand in opposition with the more frequently mentioned competitive or natural selection. Actually, an organism might save a lot of time and effort if it uses a readily available feature developed by another species instead of evolving its own - so why not take advantage of viruses that are there anyway?!
Humans share about 99% of their genomic DNA with chimpanzees. HERV sequences are one of the elements that distinguish us from them. As the term evolution clearly suggests we are not only human but a jigsaw of our ancestor species and we have incorporated some genes from our greatest threats too: the viruses.