Some estimates indicate that several groups of viruses, including the Human papillomavirus are associated to 20% of all human cancers. Cervical cancer is the best example of how a viral infection may progress to cancer. The E2 gene is disrupted when the HPV genome integrates in the cellular DNA. This gene inhibits the expression of E6 and E7 genes. E6 protein leads to degradation of p53 (cellular suppressing tumour protein), while E7 binds to pRb (retinoblastoma susceptibility protein), which fails in negatively regulating the cell cycle (from G1 to S). Moreover, other viral protein, E5, seems to act sinergically with the epidermic growing factor. When expressed in many different systems, the L1 HPV protein is able to form icosahedral particles, VLPs, similar to viral capsids, but lacking the DNA genome. The discovery of this L1 property led to progresses in studies on HPV infection immunogenicity and to the perspective of developing vaccines against that virus. VLPs are highly immunogenic and when injected in rabbits may induce the production of high titers of specific antibodies. The choice of HPV types to be used for VLP production, still depends on describing the prevalence of genotypes in different non-symptomatic and symptomatic populations. Sorological surveys in women infected with HPV-16, indicates 50% to 60% soropositivety to antibodies against viral capsid proteins.
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