Final answer:
The late proteins of HPV, such as E6, lead to the inactivation of p53, a tumor suppressor protein, promoting uncontrolled cell division and oncogenesis, particularly in cervical cancer.
Step-by-step explanation:
The late proteins of HPV, notably the E6 protein, are associated with the inactivation of tumor suppressor proteins such as p53. When E6 binds to p53, it typically results in the degradation of p53, thereby hindering its normal function. p53 is known for its role in detecting DNA damage and initiating DNA repair or apoptosis to prevent the accumulation of mutations. In the context of high-risk HPV infection, such as with types 16 and 18 which are responsible for approximately 70% of cervical cancers, the inactivation of p53 allows for uncontrolled cell division and the potential accumulation of genetic mutations, contributing to oncogenesis. Regular Pap testing and vaccination, like Gardasil 9, can help detect and prevent high-risk HPV infections, respectively.