Host and viral genetics and risk of cervical cancer: a review
Abstract
Infection with human papillomaviruses (HPV) is known to play a central role in the development of cervical cancer. Both host and viral genetic factors have been postulated to be important determinants of risk of HPV progression to neoplasia among infected individuals. In this report, we review epidemiological studies that have evaluated the role in cervical cancer pathogenesis of genetic variation in human leukocyte antigen (HLA) genes and in the HPV genome itself. A protective effect of HLA Class II DRB1*13/DBQ1*0603 alleles is the most consistent HLA finding in the published literature. A consistent association between HPV16 non-European variants and risk of disease is also evident from published work. These findings are discussed. Gaps in our understanding and future research needs are also discussed.
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The increase in HPV infection and multiple types with age is explained by cumulative lifetime exposure, relative incompetency in viral clearance, and insufficient adaptive immune responses at menopausal transition, contributing to HPV persistence or reactivation.
“The frequency of HPV infection and multiple types increases with age explains cumulative lifetime exposure [33], relative incompetency in viral clearance and insufficient adaptive immune responses at this age caused by hormonal changes at menopausal transition, contributing to HPV persistence or reactivation of latent HPV infections [34, 35].”
From HPV Genotypes distribution in Indian women with and without cervical carcinoma: Implication for HPV vaccination program in Odisha, Eastern India (2017) · cites this paper as [35]
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Senapati, R., Nayak, B., Kar, S. K., & Dwibedi, B. (2017) · BMC Infectious Diseases · doi:10.1186/s12879-016-2136-4 · Cited by 95 · see citing works
“Synergistic effect of multiple infections by HPV genotypes on carcinogenesis is supported by many studies [7–9, 17, 26], while contradicting studies [25, 29, 31, 32, 35] invoke confusion.”
BackgroundResult
- Authors
- Hildesheim, A., & Wang, S. S.
- Affiliations
- National Cancer Institute (US)
- Corresponding author
- Hildesheim, Allan
- ORCID
- Wang, Sophia S
- Venue
- Virus Research
- Publisher
- Elsevier BV
- Published
- 2002-11
- Volume
- 89
- Issue
- 2
- Pages
- 229-240
- ISSN
- 0168-1702 (ISSN-L)
- OpenAlex
- W2094529863
- Cited by
- 329
- References
- 0
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 2 · 2023: 7 · 2022: 4 · 2021: 8 · 2020: 16 · 2019: 10 · 2018: 13 · 2017: 17 · 2016: 8 · 2015: 16 · 2014: 22 · 2013: 24 · 2012: 17
- FWCI
- 2.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Virus Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Cervical Cancer and HPV Research
- Health Sciences › Medicine › Otorhinolaryngology › Head and Neck Cancer Studies
- Life Sciences › Immunology and Microbiology › Microbiology › Reproductive tract infections research
- Keywords
- cervical cancer, human papillomavirus, HPV16, HLA class II, HLA-DRB1*13, host genetic susceptibility, viral genetic variation, cancer risk
- MeSH terms
- Uterine Cervical Neoplasms, Female, Genes, MHC Class II, HLA-DQ Antigens, HLA-DR Antigens, Humans, Risk Factors, Tumor Virus Infections, Genetic Variation, Genetic Predisposition to Disease, Papillomaviridae, Papillomavirus Infections, HLA-DRB1 Chains
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