chemicals, and extreme temperatures. But eventually the top layer of epithelial cells dies off, and the
next rising layers of epithelial cells take its place.
This arrangement means that HPV has to try to live on a conveyor belt. As HPV-infected cells
reproduce, they move upward, closer and closer to their death. The viruses sense when their host
cells are getting close to the surface and shift their strategy. Instead of speeding up cell division, they
issue commands to their host cell to make many new viruses. When the cell reaches the surface, it
bursts open with a big supply of HPV that can seek out new hosts to infect.
For most people infected with HPV, a peaceful balance emerges between virus and host. Fast-
growing infected cells don’t cause people harm, because they get sloughed off. The virus, meanwhile,
gets to use epithelial cells as factories for new viruses, which can then infect new hosts through skin-
to-skin contact and sex. The immune system helps maintain the balance by clearing away some of the
infected cells. (Dede’s tree-like growths were the result of a genetic defect that left his body unable to
rein in the virus.)
This balance between host and virus has existed for hundreds of millions of years. To reconstruct
the history of papillomaviruses, scientists compare the genetic sequence of different strains and note
which animals they infect. It turns out that papillomaviruses infect not just mammals, such as humans,
rabbits, and cows, but other vertebrates as well, such as birds and reptiles. Each strain of virus
typically only infects one or a few related species. Based on their relationships, Marc Gottschling of
the University of Munich has argued that the first egg-laying land vertebrates— the ancestor of
mammals, reptiles, and birds—was already a host to papillomaviruses three hundred million years
ago.
As the descendants of that ancient animal evolved into different lineages, their papillomaviruses
evolved as well. Some research suggests that these viruses began to specialize on different kinds of
lining in their hosts. The viruses that cause warts, for example, adapted to infect skin cells. Another
lineage adapted to the mucosal linings of the mouth and other orifices. For the most part, these new
papillomaviruses coexisted peacefully with their hosts. Two-thirds of healthy horses carry strains of
papillomavirus called BPV1 and BPV2. Some strains evolved to be more prone to turn cancerous
than others, but researchers can’t say why.
For thousands of generations, papillomaviruses would specialize on certain hosts, but from time to
time, they leap to new species. A number of human papillomaviruses are most closely related to
papillomaviruses that infect distantly related animals, like horses, instead of our closest ape relatives.
Nothing more than skin contact may have been enough to allow viruses to make the jump.
When our own species first evolved in Africa about two hundred thousand years ago, our ancestors
probably carried several different strains of papillomaviruses. Representatives of those strains can
be found all over the world. But as humans expanded across the planet—leaving Africa about fifty
thousand years ago and reaching the New World by about fifteen thousand years ago—their
papillomaviruses were continuing to evolve. We know this because the genealogy of some HPV
strains reflect the genealogy of our species. The viruses that infect living Africans belong to the oldest
lineages of HPV, for example, while Europeans, Asians, and Native Americans carry their own
distinct strains.