The virus may use the same method to silence distress calls sent by infected cells to summon help from the immune system.
The findings could lead to new ways to treat the infection, blamed for most cases of cervical cancer and other cancers such as anal cancer.
Dennis McCance and colleagues at the University of Rochester Medical Center in New York have been studying the virus in cultures of human skin grown in the laboratory.
Human papilloma virus (HPV) infects more than half the adult population. There are many different strains, but two, HPV-16 and HPV-18, are strongly linked to cervical cancer and other cancers of the anal and genital regions.
HPV-16 is implicated in between 60 and 70 percent of cervical cancer cases in North America and and Europe. In industrialized countries most cases of cervical cancer are caught, by the Pap smear, before they start.
But there are still more than 370,000 new cases of cervical cancer worldwide every year, and more than half of all patients will die of it.
Many companies are working on both vaccines and treatments for the virus.
Writing in the Journal of the European Molecular Biology Organization, McCance said his team had broken down just how the virus disrupts a cell's function.
It uses a protein called E6 to block the cell's ability to differentiate -- to grow normally -- and to call for help.
Specifically it blocks two proteins that the cell uses for these functions, McCance found. The proteins fit together like a lock and key, and E6 blocks the keyhole.
"These proteins control the production of several cellular proteins," McCance said.
Normal cells replicate and differentiate into different kinds of cells, then die. Cancerous cells all look the same and grow out of control into a tumor.
A cell growing normally is of little use to a virus trying to replicate itself, McCance said.
"A differentiating cell is a terminally dead cell, and it won't contain the replicative enzymes that the virus needs. So what the virus needs to do is stimulate the replication. It does that with great success."
Cells usually shut down and kill themselves in a process known as programmed cell death when something like this happens to them. Or they may signal for help from the immune system.
But the immune system does not seem to attack HPV.
"One common thing about these viruses is they persist for many months and even years in the host without the immune system even recognizing that there is an invader there," McCance said.
He thinks the HPV's E6 protein blocks the signals. "We have to prove that now," he said.
McCance stressed the HPV alone does not cause cancer.
"HPV infection is most frequent in the most sexually active individuals -- the 16- to 30-year-olds," he said. "Howver, malignant disease tends to be in a higher age group. Only a very few women will carry the virus and develop malignancy."
Experts think genes play a role, as well as outside factors such as smoking. The virus may weaken the cells, but something else has to send them over the edge into cancer.
Written By By Maggie Fox