IJCCR_2024v14n5

International Journal of Clinical Case Reports 2024, Vol.14, No.5, 242-252 http://medscipublisher.com/index.php/ijccr 242 Research Insight Open Access Genetic Mechanisms and Clinical Significance of HPV16/18 Specific Variants in Cervical Cancer Liting Wang Hainan Institute of Biotechnology, Haikou, 570206, Hainan, China Corresponding email: liting.wang@hibio.org International Journal of Clinical Case Reports 2024, Vol.14, No.5 doi: 10.5376/ijccr.2024.14.0025 Received: 13 Jul., 2024 Accepted: 19 Aug., 2024 Published: 18 Sep., 2024 Copyright © 2024 Wang, This is an open access article published under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Preferred citation for this article: Wang L.T., 2024, Genetic mechanisms and clinical significance of HPV16/18 specific variants in cervical cancer, International Journal of Clinical Case Reports, 14(5): 242-252 (doi: 10.5376/ijccr.2024.14.0025) Abstract This study explores the genetic mechanisms and clinical significance of HPV16- and HPV18-specific variants in cervical cancer. Studies have shown that different variants of HPV16 and HPV18 exhibit significant differences in oncogenic potential, manifested through gene mutations, integration patterns, and interactions with the host genome. These variants primarily promote carcinogenesis by altering the functions of viral proteins, such as E6 andE7, which impact cell cycle regulation, DNA damage repair, and immune evasion mechanisms. Furthermore, specific variants of HPV16 and HPV18 display distinct geographical and population distributions, potentially influencing the epidemiological characteristics of cervical cancer in various regions. Understanding the oncogenic mechanisms and distribution patterns of these variants is crucial for developing personalized diagnostic tools, therapeutic strategies, and effective vaccines. Future research should focus on new variant types, the integration of genomics and immunotherapy, and the development of next-generation vaccines to better manage and prevent cervical cancer and reduce the disease burden. Keywords HPV16; HPV18; Cervical cancer; Genetic variants; Personalized medicine 1 Introduction Cervical cancer is a significant global health issue, ranking as the fourth most common cancer among women worldwide. Human papillomavirus (HPV) types 16 and 18 are the most prevalent and high-risk strains associated with cervical cancer, accounting for approximately 70-80% of cases (Vidal et al., 2016; Chen et al., 2014). These HPV types are known for their ability to integrate into the host genome, a critical step in the progression from infection to malignancy (Lagström et al., 2020). Despite the widespread prevalence of HPV infections, only a small fraction progress to cancer, suggesting that additional genetic and environmental factors play a role in carcinogenesis (Lagström et al., 2020; Gameiro et al., 2023; Wang et al., 2024). The genetic variability within HPV16 and HPV18 significantly impacts their oncogenic potential. Variants within these types are classified into different lineages and sublineages based on single nucleotide polymorphisms (SNPs) and other genetic markers. For instance, HPV16 variants are categorized into lineages A, B, C, and D, with lineage A being the most common globally (Vidal et al., 2016). Similarly, HPV18 variants are divided into lineages A, B, and C, with distinct geographical distributions and oncogenic potentials (Chen et al., 2014). Studies have shown that specific variants of HPV16 and HPV18 are associated with different risks of cancer progression. For example, the T350G polymorphism in the E6 gene of HPV16 has been linked to variations in disease outcomes and immune responses (Gameiro et al., 2023). Additionally, the integration of HPV DNA into the host genome, particularly in or near cancer-related genes, is a critical event in cervical carcinogenesis. The APOBEC3 enzyme-induced mutations and chromosomal integration sites further contribute to the genetic diversity and oncogenicity of these HPV types (Lagström et al., 2020). This study elucidates the oncogenic mechanisms of HPV16 and HPV18 variants and their clinical significance in cervical cancer. By analyzing the genetic diversity, integration patterns, and mutation profiles of these HPV types, we seek to identify specific variants that confer higher risks of cancer progression. This knowledge is crucial for developing targeted diagnostic tools, personalized treatment strategies, and effective vaccination programs. Understanding the genetic variability and integration profiles of HPV16 and HPV18 will also provide insights into

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