A novel approach to the classification of epidermodysplasia verruciformis

Abstract

The proposed categorization scheme provides a simple and logical way to organize the different cases of EV that have been described in the literature. This system organizes EV by its cause, allowing for a better understanding of the disease and helps differentiate EV from other causes of generalized verrucosis.

Diagnosis of epidermodysplasia verruciformis: Two cases highlighting the role of direct HPV L1 gene sequencing

“…The diagnostic classification of EV is evolving as new risk genes are identified and as genetic risk factors for acquired EV are investigated . There is growing evidence that beta‐HPV species play a broader role in promoting development of cutaneous SCC, although the mechanisms that drive transformation are heterogeneous and differ from mucosal‐associated alpha‐HPV .…”

What’s new in HIV dermatology?

“…It classically manifests with numerous hypopigmented macules and thin papules in sun-exposed areas and often fails to improve after initiation of HAART 8 . Persons with vertically acquired HIV infection may be more prone to developing EV than persons infected as adults and this is perhaps because their cell-mediated immune system is impaired prior to their first exposure to HPV 9 . Although the genetic form of EV is associated with an increased risk of developing SCC, the risk of developing SCC in those with acquired EV is not well established in the literature.…”

Verrucous lesions in an HIV-positive man

“…Epidermodysplasia verruciformis (EV) is a rare autosomal recessive, dominant, or X-linked genodermatosis characterized by abnormal susceptibility to cutaneous human β-papillomavirus (β-HPV) infections 1, 2, 3. Classic genetic EV manifests most commonly as flat, scaly, reddish hypo- and hyperpigmented macules, verruca-like papillomatous papules, seborrheic keratosis–like lesions, and pink-red pityriasis versicolor-like macules 1, 2, 3. Lesions develop in childhood and are highly resistant to treatment 2 .…”

“…Lesions develop in childhood and are highly resistant to treatment 2 . EV is associated with mutations in the EVER1/TMC6 and EVER2/TMC8 genes 1 . Both genes are thought to play a role in cell-mediated immunity against human papillomavirus (HPV) and are expressed in keratinocytes, immune cells such as B and T lymphocytes, and dendritic cells 1 .…”