Therapeutic Vaccines

Infected basal epithelial cells and cervical cancer cells do not express detectable levels of capsid antigen. Thus, although L1 VLP and L2 vaccines may be protective, they are likely to be ineffective in the elimination of pre-existing infection and HPV-related disease. Currently there are more than 100 million infected women, 5% of whom are estimated to have persistent disease (80). Moreover, it is still possible that some viruses will breakthrough neutralizing antibodies induced by prophylactic vaccination and establish new infection. This is especially important because those VLP vaccines in the clinic are likely to protect against a limited number of HPV types. Given these potential shortcomings, additional measures to deal with established HPV infection and HPV-associated diseases are currently under investigation.

Neutralizing antibodies are found in patients with both regressing and progressing lesions suggesting that these antibodies do not play a role in the regression process (81). Regression of low-grade CIN (Grade I) has been associated with the presence of neutralizing antibodies, but humoral immunodeficiency does not increase susceptibility to development of HPV lesions. In contrast, patients with altered CD4 T cell function, such as organ transplant patients (82) and patients with HIV (83-85), have an increased prevalence of HPV infection and more severe HPV-related disease. Preclinical studies with agents that suppress cellular immunity have reduced rates of papilloma regression and more aggressive disease. Furthermore, infiltrating CD4+ and CD8+ T-cells are often observed in spontaneously regressing HPV warts whereas T cells are rarely seen in non-regressing warts (86). These clinical observations provide evidence that cell-mediated

Table 4

Comparison of Prophylactic HPV Vaccine Antigens

Table 4

Comparison of Prophylactic HPV Vaccine Antigens

Antigen

Approach

Advantages

Disadvantages

Clinical trial results

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