Final answer:
In HPV infections, p53 is inhibited by viral oncoprotein E6, and Rb is inhibited by viral oncoprotein E7, leading to loss of growth regulation and increased risk of cancer development.
Step-by-step explanation:
In HPV infections, p53 is inhibited by viral oncoprotein E6 and Rb is inhibited by viral oncoprotein E7. This manipulation leads to the loss of two critical cell cycle checkpoints.
The p53 protein has a crucial role in detecting DNA damage and preventing the progression of the cell cycle for DNA repair, or in inducing apoptosis to prevent the accumulation of mutations.
However, when HPV's E6 protein binds to p53, it leads to p53 inactivity, hampering the cell's ability to repair DNA damage or undergo apoptosis, which allows mutations to accumulate.
Concurrently, HPV's E7 protein binds to the Rb protein, also leading to its inactivation. This interferes with Rb's normal function to regulate cell cycle progression, ultimately encouraging cellular proliferation without the usual growth controls, setting the stage for cancer development, such as cervical cancer caused by high-risk types of HPV.