Human Papillomavirus (HPV) infection has been linked with cervical cancer. Some medical professionals see it as the determining causal agent and therefore promote vaccination as an effective prevention strategy. However, the biological plausibility of a causal theory requires that the incidence of the causal agent varies with the incidence and mortality of the disease. Yet the incidence and mortality of cervical cancer do not vary with the incidence of infection with HPV strains 16 and 18; the strains covered by the HPV vaccine. Though HPV infection is a necessary precursor to most cervical cancer, most high-risk HPV infections (with one of 15 or more high–risk strains) do not progress to cervical cancer and HPV infection with any strain is not sufficient on its own to induce cervical cancer. This evidence supports the conclusion that environmental and lifestyle factors are a determining cause in conjunction with HPV in the progression to cervical cancer.
Clinical trials for the HPV vaccine did not attempt to observe the vaccine preventing any cervical cancer. Instead the trials looked for pre-cancerous lesions in women 16 – 26 years of age. This was an inadequate surrogate for cervical cancer because studies show that most lesions in this demographic clear quickly without requiring treatment. Preventing infection from HPV strains 16 and 18 also assumes these women will not get cervical cancer from infection with one of the many other high risk strains that are prevalent. Therefore the decision to use an HPV vaccine to prevent cervical cancer was based upon circumstantial evidence: assumptions. HPV vaccines have been promoted to women on selective information. This vaccine is an HPV vaccine not a cervical cancer vaccine. There is inconclusive evidence it will reduce any cervical cancer and the long –term risks of using this vaccine have not been determined.