MEDI 9331 Scholarly Activities Clinical Years
Document Type
Poster
Publication Date
Spring 2-2025
Abstract
Background: Human papillomavirus (HPV) is a sexually transmitted infection that causes HPV-associated diseases such as vaginal, penile, cervical, and oropharyngeal cancer. Each year in the United States, about 13,000 cases of cervical cancer develop, and an estimated 4,000 deaths are attributed to it. Approximately 35,000 of U.S. citizens develop an HPV-related cancer every year. There are disparities in the incidence and mortality of cervical cancer across ethnicities, socioeconomic statuses, and regions. In the United States, Hispanic individuals comprise only 18% of the population, yet Hispanic women have the highest incidence of cervical cancer. The Rio Grande Valley’s (RGV) cervical cancer incidence rate is 68% higher than the rest of the United States, and the death rate is approximately 55% higher than the rest of the state of Texas. This review aims to understand the pathophysiology of HPV and cervical cancer development.
Methods: We conducted searches in PUBMED, MEDLINE, and Google Scholar to identify studies discussing the pathophysiology of HPV with cervical cancer. We excluded studies not written in English and those where the full text could not be accessed. We did not have a date restriction. A total of twenty studies were reviewed.
Results: Our review found that HPV utilizes multiple mechanisms to establish a persistent infection and subsequently develops into cervical cancer. HPV interferes with the production of immune sensing genes by inducing heterochromatin formation at their promoter regions. This leads to epigenetic silencing and hides infected cells from recognition. HPV also downregulates the production of chemoattractants and promotes methylation of glycoproteins, such as E-cadherin, so that immune cells are not retained at the site of infection. The virus inhibits activation of T cells and downregulates receptors on NK cells. It also promotes angiogenesis by upregulating PDGF formation and FGF activation. HPV early-region oncoproteins, particularly E6 and E7, were also found to play a role in the pathogenesis of cervical cancer. These oncoproteins disrupt critical tumor-suppressing pathways through interactions with p53 and retinoblastoma (Rb), leading to uncontrolled cell proliferation and oncogenesis. An unbalanced cervical microbiota, also known as dysbiosis, was found to be an additional factor in the development of cancer. High levels of Atopobium vaginae, Porpyromonas spp., and Fusobacterium spp. along with low lactobacillus diversity promote carcinogenesis through mechanisms such as toxin production, DNA damage, immunomodulation, and inflammation.
Discussion: By understanding the role of HPV in the development of cervical cancer, this can help us educate people in the importance of HPV vaccination as well as aid with the development of therapeutic intervention.
Recommended Citation
Gonzalez, Yazeth; Lozano Bonilla, Maria F.; Gonzalez Tovar, Maria Camila; and Okere, Bria, "Unveiling the Pathophysiology of HPV and Cervical Cancer" (2025). MEDI 9331 Scholarly Activities Clinical Years. 93.
https://scholarworks.utrgv.edu/som9331/93
Academic Level
medical student
Included in
Community Health and Preventive Medicine Commons, Public Health Education and Promotion Commons
