Cervical cancer is characterized by persistent human papilloma virus (HPV) infection. But, why, in some cases, is the immune system unable to reliably detect the HPV infection? For years, this has been a central question, which has yet to be fully answered. At present, it is well known that HPV has evolved a variety of mechanisms to evade the immune attack, and it is the success of these, which will be critical to determine whether the infection will be cleared or remain as a persistent infection. This review will be particularly focused on addressing some of the mechanisms used by HPV to avoid early recognition by the host innate immune system, which will then facilitate viral persistence with the consequent risk of eventual progression towards cervical cancer. Undoubtedly, an understanding of the balance between viral and immunological factors will provide crucial information that must to be taken into account for the design of prophylactic and therapeutic vaccines against HPV-associated cervical cancer.