In tomorrow’s New York Times, I dig up some of the fossil viruses that have been buried in our genome for tens of millions of years.
This is a subject I’ve explored here on the Loom before (1, 2), but now is a great time to stop and take stock of just how much progress scientists have made in exhuming the ancient invaders that helped make us what we are.
There was one dimension of this research that I didn’t have space to describe, but it’s too cool to let go unmentioned. In the article, I describe a virus protein called syncitin that is essential for placentas to develop. Cells push the protein to their surface, where it lets them latch onto other cells, fusing together to create a special layer through which nutrients can pass from mother to child. The protein got its start on viruses, which use it to latch onto host cells and fuse to them, allowing their genes to slip in.
But recent research has revealed an intriguing new twist to our viral legacy. It turns out that the viral surface protein in question has a second job. It also tamps down the immune system of its host. If the protein is altered to make it unable to suppress the immune response, viruses cannot successfully infect their hosts.
Thierry Heidmann, a leading paleovirologist whom I spoke to for the article, suspects that this second function may have been critical in the evolution of the placenta. That’s because there are two major challenges to being a placental mammal. First off, mothers need to be able supply their embryos with lots of nutrition for a long time through their circulatory system. Second, they have to cool down their immune systems. A baby’s tissues would otherwise look to the mother’s immune system like foreign tissue and be quickly rejected. So it’s possible that viruses not only let mothers feed their babies, but not kill them either.
This is a story that’s just going to get cooler, so expect updates as necessary.