Human papillomavirus (HPV) infection can cause cervical intraepithelial neoplasia (CIN) and cervical cancer, and there are differences in the pathogenic ability of different HPV types, and persistent infection with high-risk HPV types is the most important factor promoting the development of cervical cancer. HPV belongs to the genus Papillomavirus of the family Papillomaviridae, which is a circular double-stranded DNA virus with a closed circular double-stranded DNA containing genetic information composed of about 7800~7900 base pairs covalently bonded to the core and enveloped by 72 capsids, forming a symmetrical 20-sided body. The virus has no outer envelope, is about 55 mm in diameter, and has a molecular weight of about 5.4 KD. There are multiple genotypes of HPV, and more than 120 genotypes have been identified, of which about 30 are involved in genital tract infections. Different types of HPV infection can lead to different clinical lesions. Based on biological characteristics and oncogenic potential, HPV is classified into high-risk and low-risk types. High-risk types such as HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68 are associated with cancer and precancerous lesions, while low-risk types such as HPV 6, 11, 42, 43, and 44 are mainly associated with mild squamous epithelial lesions and genitourinary warts and recurrent respiratory polyps. High-risk HPV infection has been found in close to 90% of CIN and more than 99% of cervical cancer tissues, of which about 70% are associated with HPV types 16 and 18. High-risk HPV types produce viral oncoproteins, of which E6 and E7 act on the host cell oncogenes P53 and Rb to inactivate or degrade them, respectively, and subsequently cause carcinogenesis through a series of molecular events. HPV is highly host-specific, suitable for growth in warm and humid environments, and mainly infects the complex squamous epithelium of skin and mucous membranes in deliberate areas of the body. Sexual contact is the main route of infection, and those who have been ill for about 3 months are the most infectious. Other routes such as contact transmission or direct mother-to-child transmission cannot be ruled out. The prevalence of HPV infection depends mainly on the age and sexual habits of the population. HPV infection rates are highest in sexually active women, with peak infection ages ranging from 18 to 28 years. However, most women have HPV infection for a short period of time, 2 to 3 years, and it usually resolves on its own in 8 to 10 months, with only about 10% to 15% of women over 35 years of age having persistent infection. Such women with persistent HPV infection will have a higher risk of developing cervical cancer. HPV infection can occur repeatedly throughout a woman’s life, and can also occur simultaneously with many different types of HPV. HPV infection usually has no obvious clinical symptoms, so it is difficult to estimate the risk factors affecting HPV infection, including oral contraceptives, pregnancy, and cell-mediated impairment of immune function, in addition to sexual habits.