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Proposed model for the association between HPV-16-specific T-cell immunity and the development of disease (adapted from [26]).
Abstract Cervical cancer is the second most common cancer of women worldwide and is the first cancer shown to be entirely induced by a virus, the human papillomavirus (HPV, major oncogenic genotypes HPV-16 and -18).
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Thick arrows represent the fate of the majority of HPV-16-infected individuals, in contrast to thin arrows that represent the fate of the minority of HPV-16-infected individuals.
The tumor microenvironment is composed of cells of the adaptive immune system (such as CD4 and CD8 T-cells, Treg) and cells of the innate immune system (such as DC, NKT, macrophages) and potentially other cells (Mast cells?

Two recently developed prophylactic cervical cancer vaccines, using virus-like particles (VLP) technology, have the potential to prevent a large proportion of cervical cancer associated with HPV infection and to ensure long-term protection. However, prophylactic HPV vaccines do not have therapeutic effects against pre-existing HPV infections and do not prevent their progression to HPV-associated malignancy.
In animal models, therapeutic vaccines for persisting HPV infection can eliminate transplantable tumors expressing HPV antigens, but are of limited efficacy in inducing rejection of skin grafts expressing the same antigens. In humans, clinical trials have reported successful immunotherapy of HPV lesions, providing hope and further interest. Overall, the ideal vaccine would activate effector killer T-cells while silencing regulatory factors.

This review discusses possible new approaches to immunotherapy for HPV associated cancer, based on recent advances in our knowledge of the immunobiology of HPV infection, of epithelial immunology and of immunoregulation, with a brief overview on previous and current HPV vaccine clinical trials.

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