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Study evaluates the effectiveness of HPV vaccine for the prevention of oral HPV infection with encouraging results

July 23, 2013

On July 18th the NYTimes.com reported that a vaccine developed to protect women against cervical cancer appears to also protect them from throat cancer, based on the findings of a study published in PLOS One.

Most oral and pharyngeal cancers are caused by tobacco and alcohol use; however, a subset of oropharyngeal cancers are caused by human papillomavirus (HPV) infection.1 These “high-risk” HPV types cause cervical cancers and are also responsible for a high proportion of other anogenital and oropharyngeal cancers. HPV types 16 and 18 are associated with about 70 percent of cervical cancers. HPV type 16 is also associated with about 90 percent of HPV-positive oropharyngeal cancers.1

In 2006, a quadrivalent vaccine to protect against HPV types 6, 11, 16 and 18 was released (Gardasil, Merck, White-house Station, N.J.). At the time, the Centers for Disease Control and Prevention recommended the vaccine only for girls and young women. In 2009, the recommendation was expanded to also include boys and young men. The vaccine is intended to protect against genital warts, cervical cancer and precancerous lesions, vaginal and vulvar cancer, and anal cancer and precancerous lesions. A bivalent vaccine was released in 2009 to protect against HPV types16 and 18 (Cervarix, Glaxo-SmithKline, Brentford, England). Information about the safety of these vaccines is summarized on the CDC website.2

The PLOS One article reports the results of a randomized, controlled, blinded clinical trial evaluating the effectiveness of a HPV vaccine in the prevention of cervical HPV infection. The study included 7,466 women 18 to 25 years of age. The women were randomized to receive the bivalent HPV vaccine (Cervarix) or the hepatitis A vaccine (control). After 4 years the investigators added analysis of oral specimens. 5,840 women provided oral specimens to determine the presence of HPV types 16 and 18. The overall prevalence of HPV-positive oral specimens was low (only 1.7 percent of the study population). In the control group there were 15 HPV-positive oral specimens, compared to one in the Cervarix group. The authors concluded that the vaccine effectiveness in preventing HPV types 16 and 18 oral infections was 93 percent. The effectiveness in preventing cervical HPV infections was 72 percent. The vaccine did not prevent infections with other HPV types.


The study was initially set up to evaluate the vaccine effectiveness for preventing cervical infection with HPV types 16 and 18. Therefore, oral specimens were not collected at the beginning of the study and the oral HPV infection status at baseline is unknown. However, this was a randomized trial and inclusion of women who were HPV-positive at baseline would likely increase the observed effectiveness of the vaccine. For example, the authors reported that excluding women who were HPV-positive at enrollment increased the vaccine effectiveness for preventing cervical HPV infection from 72 percent to 80 percent.

The New York Times article reported that the HPV vaccine developed to protect women against cervical cancer appears to also protect them from throat cancer. However, the outcome reported was the prevalence of HPV infection and not cancer diagnosis. It seems likely that preventing HPV type 16 infection will prevent HPV-associated oropharyngeal cancer, but this study does not provide conclusive evidence.

Another recently published observational study conducted by the Centers for Disease Control and Prevention reported a reduction in HPV prevalence among young women after the HPV vaccine was introduced in 2006.3 Data from the National Health and Nutrition Examination Surveys shows that the prevalence of HPV types 6, 11, 16 and 18 among females aged 14 to 19 years declined 56 percent in the time period 2007 through 2010 compared to 2003 through 2006. The decline was not seen in other age groups.

The findings from both of these studies are encouraging. However, currently, there are no surrogate clinical endpoints for oropharyngeal cancer as there are for cervical cancer. Therefore, it will likely be decades before the effectiveness of the HPV vaccine in preventing throat cancer is determined.

1Cleveland JL, Junger ML, Saraiya M, Markowitz LE, Dunne EF, Epstein JB. The connection between human papillomavirus and oropharyngeal squamous cell carcinomas in the United States: Implications for dentistry. JADA. 2011;142(8):915-924.

2Centers for Disease Control and Prevention. Vaccine Safety: Frequently Asked Questions about HPV Vaccine Safety. June 19, 2012. (accessed July 23, 2013)

3Markowitz LE, Hariri S, Lin C, Dunne EF, Steinau M, McQuillan G, Unger ER. Reduction in Human Papillomavirus (HPV) Prevalence Among Young Women Following HPV Vaccine Introduction in the United States, National Health and Nutrition Examination Surveys, 2003–2010. J Infect Dis. 2013;208(3):385-393. (published online June 19, 2013)

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