Throughout much of the 20th century, scientists suspected that sexually transmitted infections cause cancer of the cervix. But the guilty party remained hidden until 2 decades ago, when scientists isolated human papillomavirus (HPV) DNA from cervical tumors. That discovery is now paying dividends. In the Nov. 21 New England Journal of Medicine, a team of U.S. scientists reports that a vaccine produced from an HPV protein protects women from long-term viral infections that can lead to cervical cancer.
Responsible for roughly 250,000 worldwide deaths every year, cervical cancer kills more women than any other cancer in developing countries where Pap smears are infrequent. In contrast, it is only the 12th-most-lethal malignancy in U.S. women because most cases are detected and treated. There are more than 60 types of HPV, and at least 20 of which are linked to cervical cancer. After HPV-16, the most common type found in tumors is HPV-18. Some other HPV types, notably HPV-6 and -11, cause genital warts but haven't been linked to cancer.
Approximately 20 percent of adults become infected with human papillomavirus type 16 (HPV-16). Although most infections are benign, some progress to anogenital cancer. A vaccine that reduces the incidence of HPV-16 infection may provide important public health benefits.
In this double-blind study, we randomly assigned 2392 young women (defined as females 16 to 23 years of age) to receive three doses of placebo or HPV-16 virus-like–particle vaccine (40 µg per dose), given at day 0, month 2, and month 6. Genital samples to test for HPV-16 DNA were obtained at enrollment, one month after the third vaccination, and every six months thereafter. Women were referred for colposcopy according to a protocol. Biopsy tissue was evaluated for cervical intraepithelial neoplasia and analyzed for HPV-16 DNA with use of the polymerase chain reaction. The primary end point was persistent HPV-16 infection, defined as the detection of HPV-16 DNA in samples obtained at two or more visits. The primary analysis was limited to women who were negative for HPV-16 DNA and HPV-16 antibodies at enrollment and HPV-16 DNA at month 7.
The women were followed for a median of 17.4 months after completing the vaccination regimen. The incidence of persistent HPV-16 infection was 3.8 per 100 woman-years at risk in the placebo group and 0 per 100 woman-years at risk in the vaccine group (100 percent efficacy; 95 percent confidence interval, 90 to 100; P<0.001). All nine cases of HPV-16–related cervical intraepithelial neoplasia occurred among the placebo recipients.
Administration of this HPV-16 vaccine reduced the incidence of both HPV-16 infection and HPV-16–related cervical intraepithelial neoplasia. Immunizing HPV-16–negative women may eventually reduce the incidence of cervical cancer.
Source: New England Journal of Medicine