patterns that were similar to sexually transmitted diseases. Nuns, for example, get cervical cancer
much less often than other women. Some scientists had speculated cervical cancer was caused by a
virus spread during sex. Zur Hausen wondered if cancer-causing papillomaviruses were the culprit.
Zur Hausen reasoned that if this were true, he ought to find virus DNA in cervical tumors. He
gathered biopsies to study, and slowly sorted through their DNA for years. In 1983 he discovered
genetic material from papillomaviruses in the samples. As he continued to study the biopsies, he
found more strains of papillomaviruses. Since zur Hausen first published his discoveries, scientists
have identified one hundred different strains of human papillomavirus (or HPV for short). For his
efforts, zur Hausen shared the Nobel Prize for Physiology or Medicine in 2008.
Zur Hausen’s research put human papillomaviruses in medicine’s spotlight, thanks to the huge toll
that cervical cancer takes on the women of the world. The tumors caused by HPV grow so large that
they sometimes rip the uterus or intestines apart. The bleeding can be fatal. Cervical cancer kills over
270,000 women every year, making it the third leading cause of death in women, surpassed only by
breast cancer and lung cancer.
All of those cases got their start when a woman acquired an infection of HPV. The infection begins
when the virus injects its DNA into a host cell. HPV specializes in infecting epithelial cells, which
make up much of the skin and the body’s mucous membranes. The virus’s genes ends up inside the
nucleus of its host cell, the home of the cell’s own DNA. The cell then reads the HPV genes and
makes the virus’s proteins. Those proteins begin to alter the cell.
Many other viruses, such as rhinoviruses and influenza viruses, reproduce violently. They make
new viruses as fast as possible, until the host cell brims with viral offspring. Ultimately, the cell rips
open and dies. HPV uses a radically different strategy. Instead of killing its host cell, it causes the cell
to make more copies of itself. The more host cells there are, the more viruses there are.
Speeding up a cell’s division is no small feat, especially for a virus with just eight genes. The
normal process of cell division is maddeningly complex. A cell “decides” to divide in response to
signals both from the outside and the inside, mobilizing an army of molecules to reorganize its
contents. Its internal skeleton of filaments reassembles itself, pulling apart the cell’s contents to two
ends. At the same time, the cell makes a new copy of its DNA—3.5 billion “letters” all told,
organized into 46 clumps called chromosomes. The cell must drag those chromosomes to either end
of the cell and build a wall through its center. During this buzz of activity, supervising molecules
monitor the progress. If they sense that the division is going awry—if the cell acquires a defect that
might make it cancerous, for example—the monitor molecules trigger the cell to commit suicide. HPV
can manipulate this complex dance by producing just a few proteins that intervene at crucial points in
the cell cycle, accelerating it without killing the cell.
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,