Journal of Vaccine Research, 2025, Vol.15, No.1, 23-33 http://medscipublisher.com/index.php/jvr 24 HPV-16 and HPV-18, are associated with the occurrence of various cancers, including cervical cancer, anal cancer, oropharyngeal cancer, and some oral squamous cell carcinomas (Tomaic, 2016; Binazhi Bhutto, 2019). Hpv-16 and HPV-18 are the most common high-risk types of viruses. Most malignant tumors caused by HPV are related to them, and their presence is a key factor in the onset of these cancers. HPV-16 and HPV-18 can cause cancer. The main reason is that these two viruses can integrate into the genetic sequences of human cells, allowing the viruses to produce proteins that cause cancer and thereby disrupt the normal operation of cells. Research results have shown that the E6 oncogenic protein of HPV-16/18 can be detected in the tissues of oral squamous cell carcinoma, which proves that they are directly involved in the process of oral cell carcinogenesis (Jiang, 2024). The discovery of these high-risk viruses that are prone to cause oral diseases highlights their significance in medical clinical practice and also indicates the necessity of formulating specific preventive measures against them. 2.2 Interference of E6/E7 tumor proteins and tumor suppressor factors The E6 and E7 oncogenic proteins of high-risk HPV play a key role in the process of cell malignancy. E6 will promote the decomposition of the tumor suppressor protein p53, which is an important substance for controlling cell growth and death. E7 will bind to retinoblastoma protein (Rb), rendering it inactive and thereby disrupting the normal regulation of cell growth, leading to uncontrolled cell proliferation (Tomaic, 2016). The dual destruction of p53 and Rb by these two proteins eliminates an important obstacle to cell carcinogenesis, making cells more prone to accumulate gene damage and eventually develop into malignant tumors (Yukawa and Kiyono, 2009; Estevao et al., 2019). The latest research shows that substances E6 and E7 not only affect p53 and Rb, but also act on many oncogenes and tumor-suppressing proteins, interfering with the processes of cell DNA repair, generating immune responses and cell differentiation (Dust et al., 2022; Fernandes et al., 2025). E6 and E7 work together and play a crucial role in the transformation of epithelial cells into cancer cells. They can disrupt the normal functioning of proteins in cells on a large scale, creating an environment conducive to cancer growth (Estevao et al., 2019). 2.3 Oral mucosa serves as a target for HPV infection and carcinogenesis The oral mucosa is highly susceptible to HPV infection, mainly due to tiny wounds or injuries, which give the virus the opportunity to enter the cells at the bottom of the mucosa. Once the virus infects these cells, it may persist, especially when the human body's immunity declines or when it is infected with high-risk HPV (Tomaic, 2016; Basukala and Banks, 2021). Persistent viral infection is the main cause of precancerous lesions and cancer in the oral cavity. The continuous action of E6 and E7 oncoproteins promotes HPV-induced oral mucosal carcinogenesis, disrupts the normal order of cell growth, and increases the risk of genetic variation. The special environment of the oral cavity, such as the chance of exposure to carcinogens and unique immune characteristics, may further affect the risk of developing HPV-related oral cancer and the progression of the disease. The detection of E6 oncogenic protein in patients with oral squamous cell carcinoma confirmed the role of HPV in oral carcinogenesis and also highlighted the importance of early detection and prevention (Tomaic, 2016). 3 Epidemiology of HPV-related Oral cancer 3.1 Global and regional incidence rates Mouth cancer related to human papillomavirus (HPV) is now a significant global health issue and is becoming increasingly serious. Each year, approximately 300 000 new cases of mouth cancer are discovered worldwide (Pirmoradi et al., 2024). Although the proportion of HPV infection among patients varies from place to place, on the whole, HPV can be found in as many as 72.8% of oral cancer cases. The most common one is HPV-16, followed by HPV-18 (Yete et al., 2017; Pirmoradi et al., 2024). In the United States, 4.62 out of every 100 000 people have been diagnosed with HPV-positive oropharyngeal squamous cell carcinoma (OPSCC), especially among white men under the age of 65, who have the highest incidence (Mahal et al., 2019).
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