Abstract
Persistent infection with high-risk human papillomavirus is considered one of the main causes of cervical cancer. In recent years, there has been increasing concern about the health problems associated with HPV infection. To better understand the mechanisms by which high-risk human papillomavirus infection leads to cervical cancer, many studies have begun to explore the role of the vaginal microenvironment in this context. The female vagina is an open cavity with a special anatomical structure, which constitutes the first barrier to protect the vaginal microenvironment. At the same time, the female reproductive tract is a typical micro-ecosystem with a wide variety of microflora, which maintains a dynamic and balanced relationship of symbiosis, coexistence, and mutual control with the external environment and the host. Hormonal changes during the physiological cycle, especially estrogen, have an important influence on the structure and stability of the vaginal flora. In addition, the vagina has an important role in immune homeostasis, where the immune system plays a crucial role in maintaining tissue homeostasis, eliminating pathogens, and avoiding barrier damage. When a pathogen such as human papillomavirus enters the vagina, the immune system initiates an associated immune response to clear the virus and restore tissue health. However, in some cases, the immune system may not be able to effectively respond to human papillomavirus infection, leading to the development of persistent infections. Dysregulation of vaginal microecology may be an important factor in persistent human papillomavirus infection. This review focuses on this topic by describing the vaginal microenvironment, human papillomavirus, and the mechanisms involved in influencing the vaginal microecology causing persistent human papillomavirus infection and thus accelerating cervical carcinogenesis.