Abstract
Human papillomaviruses (HPVs) are the most common sexually transmitted pathogens worldwide and among the more than 200 identified HPV types, approximately 15 high risk (HR-HPV) types are oncogenic, being strongly associated with the development of cervical cancer, anogenital cancers and an increasing fraction of head and neck squamous cell carcinomas (HNSCC). HPV-associated cervix cancer accounts for 83% of HPV-attributable cancers, and more than two-thirds of those cases occur in developing countries. Despite the high frequency of HPV infections, in most cases, the virus is cleared by the host immune response and only a small proportion of infected individuals develop persistent infections that can result in malignant transformation, indicating that other elements, including biological, genetic and environmental factors may influence the individual susceptibility to HPV-associated cancers. Previous studies have quantified that heritability, in the form of genetic variants, common in the general population, is implicated in nearly 30% of cervical cancers and a large number of studies conducted across various populations have identified genetic variants that appear to be associated with genes that predispose or protect the host to HPV infections thereby affecting individual susceptibility to HPV-associated cancers. In this article, we provide an overview of gene association studies on HPV-associated cancers with emphasis on genome-wide association study (GWAS) that have identified novel genetic factors linked to HPV infection or HPV-associated cancers.
Highlights
Human papillomaviruses (HPV) comprise a family of DNA viruses that spread through direct contact and cause benign and malignant lesions of the skin and mucosa of the anogenital and upper aero-digestive tract
We provide an updated overview of gene association studies on HPV-associated cancers with emphasis on data provided from recent genome-wide association study (GWAS) that have identified novel genetic factors linked to HPV infection or
Given the reported higher production of interleukin 10 (IL10) associated with the IL10 GCC haplotype [26], these results suggested that IL10 variants influence the clearance of infection with high-risk HPV types because higher levels of IL10 may impair the production of inflammatory cytokines such as IL-2, TNF-α, IL-4, IL-6 and IL-12 that are involved in the TH1-TH2 immunoregulation and immunity against HPVs
Summary
Human papillomaviruses (HPV) comprise a family of DNA viruses that spread through direct contact and cause benign and malignant lesions of the skin and mucosa of the anogenital and upper aero-digestive tract. The infection with certain HPV types is strongly associated with the development of cervical cancer and can cause anogenital cancers (carcinoma of the anus, penis, vulva and vagina), as well as a considerable proportion of head and neck squamous cell carcinomas (HNSCC) [3]. The carcinogenic potential of HR-HPVs has been demonstrated by clinical/epidemiological and molecular studies, despite the extremely high frequency of HPV infections, where almost all sexually active adults becoming infected at some point of their lives with at least an HPV type, most infected individuals never develop cancer, suggesting that for the development of HPV-associated cancers, additional factors are necessary In this regard, several factors, including biological, genetic, environmental factors and other individual features have been investigated for their possible implication in the carcinogenic process triggered by HPVs [8,9]. We provide an updated overview of gene association studies on HPV-associated cancers (cervical cancer, HNSCC and anogenital cancers) with emphasis on data provided from recent GWASs that have identified novel genetic factors linked to HPV infection or
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