Abstract
The human papillomaviruses (HPV) are a group of double-stranded DNA viruses that exhibit an exclusive tropism for squamous epithelia. HPV can either be low- or high-risk depending on its ability to cause benign lesions or cancer, respectively. Unsurprisingly, the majority of epigenetic research has focused on the high-risk HPV types, neglecting the low-risk types in the process. Therefore, the main objective of this study is to better understand the epigenetics of wart formation by investigating the differences in methylation between HPV-induced cutaneous warts and normal skin. A number of clear and very significant differences in methylation patterns were found between cutaneous warts and normal skin. Around 55% of the top-ranking 100 differentially methylated genes in warts were protein coding, including the EXOC4, KCNU, RTN1, LGI1, IRF2, and NRG1 genes. Additionally, non-coding RNA genes, such as the AZIN1-AS1, LINC02008, and MGC27382 genes, constituted 11% of the top-ranking 100 differentially methylated genes. Warts exhibited a unique pattern of methylation that is a possible explanation for their transient nature. Since the genetics of cutaneous wart formation are not completely known, the findings of the present study could contribute to a better understanding of how HPV infection modulates host methylation to give rise to warts in the skin.
Highlights
Human papillomaviruses (HPV) are double-stranded DNA viruses that exclusively infect the squamous epithelial layers of the mucosa and skin [1]
Notable differences were seen during the assessment of the methylation level (β) distributions for the genome-tiling regions in wart and normal skin samples (Figure 2)
Of the top-ranking 100 Differential methylation (DM) genes in warts compared to normal skin, 55 were protein-coding genes
Summary
Human papillomaviruses (HPV) are double-stranded DNA viruses that exclusively infect the squamous epithelial layers of the mucosa and skin [1]. A number of communicable as well as non-communicable diseases have been associated with HPV infection, including various types of warts and cancers [3]. Hundreds of HPV types have been identified and classified as either low-risk or high-risk depending on their likelihood upon infection to cause malignant or benign symptoms, Genes 2020, 11, 34; doi:10.3390/genes11010034 www.mdpi.com/journal/genes. Genes 2020, 11, 34 respectively [4] Due to their greater carcinogenic potential, the majority of HPV research has centered around high-risk types such as HPV 16 and 18 [5]. Low-risk HPV infection often manifests in the form of cutaneous warts in otherwise healthy individuals, it can result in serious pathologies in immunocompromised populations [6]
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