A Planet of Viruses - Carl Zimmer [10]
Many types of cells grow quickly in childhood and then slow down or stop altogether. Epithelial cells, the cells that HPV infects, continue to grow through our whole life. They start out in a layer buried below the skin’s surface. As they divide, they produce a layer of new cells that pushes up on the cells above them. As the cells divide and rise, they become different than their progenitors. They begin to make more of a hard protein called keratin (the same stuff that makes up fingernails and horse hooves). Loaded with keratin, the top layer of skin can better withstand the damage from the sun, 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