Final answer:
HPV integration into host cell DNA disrupts normal functions and can prevent apoptosis, leading to uncontrolled cell division. High-risk HPV types, such as HPV 16 and HPV 18, have the potential to cause persistent infections and invasive cervical cancer.
Step-by-step explanation:
Relationship Between HPV Integration and Invasion
The relationship between HPV integration and invasion is significant in the development of cervical cancer. When high-risk types of HPV infect cells, they can integrate their DNA into the host cell's genome. This process disrupts normal cellular functions, such as those controlled by tumor suppressor proteins like p53. Normally, p53 ensures that damaged DNA is either repaired or the cell is directed to undergo apoptosis to prevent mutations. The E6 and E7 proteins of high-risk HPV types can inactivate these tumor suppressor proteins, leading to rapid cell division and an accumulation of mutations. Ultimately, this can cause the cells to become cancerous, leading to an invasive form of cervical cancer.
While low-risk HPV strains can result in benign conditions like genital warts, it is the persistent infection by oncogenic HPV types such as HPV 16 and HPV 18 that contribute to the majority of cervical cancer cases. These oncogenic strains can bypass the immune system and allow cancerous cells to proliferate, invade deeper into tissue, and potentially spread to other parts of the body.