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). 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. 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.
Highlights
Cervical cancer is the first cancer recognized by the World Health Organization (WHO) to be 100%attributable to an infection
Based on phase III clinical trial results [98], the Advisory Committee on Immunization Practices (ACIP) states that women should be advised that the vaccine will not have any therapeutic effect on existing infection or disease and they should continue to receive routine cervical cancer screening [99]
Another study conducted in South Africa with children aged between 1 and 12 years found that 4.5% of sera tested were positive for antibodies to HPV-16, with a prevalence decreasing with age
Summary
Cervical cancer is the first cancer recognized by the World Health Organization (WHO) to be 100%. Papillomaviruses are non-enveloped, double-stranded DNA viruses that infect the epithelium. Their genome encodes six non-structural proteins [Early 1 (E1), E2, E4–E7] and two structural proteins [Late 1 (L1) and L2]. Proteins control the DNA-replication machinery of the infected cells by altering cell cycling and promoting viral genome replication, while late proteins, which form the capsid, are involved in the packaging of the virion [1]. As long as the infected epithelial cells are dividing, the virus will remain in its free (non-integrated) episomal form and replicate using the cellular DNA-replication machinery. The HPV DNA is mostly found integrated in the cellular genome [1]
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