Abstract:

Immune evasion is one of the core pathogenic mechanisms for the persistent infection of human papilloma virus (HPV) and the progression of related malignancies such as cervical cancer. At the molecular biological level, the genomic regions of HPV play a crucial role in invading and infecting host cells. At the level of the host immune response, HPV inhibits the functions of innate immune core effector cells such as natural killer cells, macrophages, and dendritic cells, and at the same time interferes with the T -lymphocyte-mediated adaptive immune response, ultimately leading to the functional exhaustion of immune effector cells and inducing an immune tolerance state. Notably, HPV can also disrupt the local vaginal microecological balance, causing an interactive imbalance between immune regulation and microbial homeostasis, and creating an immunosuppressive microenvironment conducive to the persistence presence of the virus. In-depth anaysis of these mechanisms is of great significance for the development of effective prevention and treatment strategies for HPV, and is expected to provide new ideas and targets for the prevention, diagnosis, and treatment of HPV-related diseases.

Key words: Papillomaviridae, Tumor escape, Immunity, innate, Adaptive immunity, Lactobacillus, Persistent infection, Biological characteristics