Proteins like APOBEC 3 disable endogenous retroviruses, but they don’t eliminate them. Overmillions of years, our genomes have picked up a vast amount of DNA from dead viruses. Each of us
carries almost a hundred thousand fragments of endogenous retrovirus DNA in our genome, making up
about 8 percent of our DNA. To put that figure in perspective, consider that the twenty thousand
protein-coding genes in the human genome make up only 1.2 percent of our DNA. Scientists have also
observed millions of smaller pieces of “jumping DNA” in the human genome. It’s possible that many
of those pieces evolved from endogenous retrovirus, having been stripped down to the bare essentials
required for copying DNA.
Endogenous retroviruses may be dangerous parasites, but scientists have discovered a few that we
have commandeered for our own benefit. When a fertilized egg develops into a fetus, for example,
some of its cells develop into the placenta, an organ that draws in nutrients from the mother’s tissues.
The cells in the outer layer of the placenta fuse together, sharing their DNA and other molecules.
Heidmann and other researchers have found that a human endogenous retrovirus gene plays a crucial
role in that fusion. The cells in the outer placenta use the gene to produce a protein on their surface,
which latches them to neighboring cells. In our most intimate moment, as new human life emerges
from old, viruses are essential to our survival. There is no us and them—just a gradually blending and
shifting mix of DNA.