Human papillomavirus-associated plantar epidermoid cyst related to epidermoid metaplasia of the eccrine duct epithelium: a combined histological, immunohistochemical, DNA-DNA in situ hybridization and three-dimensional reconstruction analysis

Egawa, Kiyofumi; Egawa, Nagayasu; Honda, Yasuhiro

doi:10.1111/j.1365-2133.2005.06562.x

Cited by 37 publications

(32 citation statements)

References 29 publications

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“…It is possible that distinct HPV types isolated from pilar and epidermoid cysts reflect the topographic infection preferences of specific HPV types, as has been reported for bacteria and fungi . Specifically, while HPV‐24 has been identified as a commensal resident of hair follicles, HPV‐57 and ‐60 have been identified in non‐follicular epithelia from glabrous skin . It remains unclear whether HPV infection of the follicular epithelium drives the formation of verrucous pilar cysts or whether verrucous pilar cysts represent secondary or passenger HPV infection of existing cyst epithelia.…”

Section: Discussionmentioning

confidence: 99%

Verrucous pilar cysts infected with beta human papillomavirus

et al. 2019

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Epidermoid cysts with histopathologic features of human papillomavirus (HPV) infection have been previously reported and are commonly termed verrucous cysts. We report a series of eight histopathologically distinct verrucous pilar cysts, distinguished from traditional verrucous epidermoid cysts by trichilemmal keratinization, as well as two verrucous hybrid pilar‐epidermoid cysts. These lesions contain characteristic stratified epithelial linings with abrupt transitions to compact eosinophilic keratin, as well as areas of papillomatosis, coarse intracytoplasmic keratohyalin granules, and vacuolar structures suggestive of HPV‐induced cytopathic change. HPV‐24, a β genus HPV species, was identified by degenerate polymerase chain reaction in DNA extracted from two of the lesions, and the presence of β‐HPV E4 protein was confirmed by immunohistochemistry. HPV‐60, the HPV species most commonly reported in verrucous epidermoid cysts, was not detected. Verrucous pilar cysts represent histopathologically and potentially etiologically distinct lesions which may be underrecognized.

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Section: Discussionmentioning

confidence: 99%

Verrucous pilar cysts infected with beta human papillomavirus

et al. 2019

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“…Immunostaining suggests that such lesions are distinct from the associated dermal eccrine duct, but have similarities with the suprabasal cells of the epidermis. It has been suggested that palmoplantar epidermoid cysts may in some instances arise as a result of epidermoid metaplasia of eccrine ducts following HPV infection . Skin cancer. Bowen's disease (BD) is a SCC in situ of the skin. In 3–5% of cases, it progresses to invasive carcinoma with the capability to develop metastasis.…”

Section: Human Papillomaviruses Infection and Clinical Manifestationsmentioning

confidence: 99%

Human papillomavirus molecular biology and disease association

Doorbar

Egawa

Griffin

et al. 2015

Reviews in Medical Virology

742

624

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SummaryHuman papillomaviruses (HPVs) have evolved over millions of years to propagate themselves in a range of different animal species including humans. Viruses that have co‐evolved slowly in this way typically cause chronic inapparent infections, with virion production in the absence of apparent disease. This is the case for many Beta and Gamma HPV types. The Alpha papillomavirus types have however evolved immunoevasion strategies that allow them to cause persistent visible papillomas. These viruses activate the cell cycle as the infected epithelial cell differentiates in order to create a replication competent environment that allows viral genome amplification and packaging into infectious particles. This is mediated by the viral E6, E7, and E5 proteins. High‐risk E6 and E7 proteins differ from their low‐risk counterparts however in being able to drive cell cycle entry in the upper epithelial layers and also to stimulate cell proliferation in the basal and parabasal layers. Deregulated expression of these cell cycle regulators underlies neoplasia and the eventual progression to cancer in individuals who cannot resolve high‐risk HPV infection. Most work to date has focused on the study of high‐risk HPV types such as HPV 16 and 18, which has led to an understanding of the molecular pathways subverted by these viruses. Such approaches will lead to the development of better strategies for disease treatment, including targeted antivirals and immunotherapeutics. Priorities are now focused toward understanding HPV neoplasias at sites other than the cervix (e.g. tonsils, other transformation zones) and toward understanding the mechanisms by which low‐risk HPV types can sometimes give rise to papillomatosis and under certain situations even cancers. Copyright © 2015 John Wiley & Sons, Ltd.

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“…For the high‐risk AlphaPVs, such ‘vulnerable’ sites include the cervical and anal transformation zones, where stratified and columnar epithelium abut, and the tonsillar crypts, which comprise a poorly structured epithelium . Eccrine sweat glands have been proposed as a site of infection for MuPV types , and the frequent detection of BetaPV on plucked hairs points to the hair follicle as an important site of infection for BetaPV (and possibly GammaPV) types . In general, HPV entry is thought to require the initial binding to heparan sulphate on the surface of basal cells and the basal lamina , which facilitates subsequent association with a specific secondary receptor to allow virus entry and viral genome replication.…”

Section: Human Papillomaviruses – Betapv Versus Alphapvmentioning

confidence: 99%