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Chronic verrucous varicella zoster virus skin lesions: clinical, histological, molecular and therapeutic aspects
Author(s) -
Arjen F. Nikkels,
Robert Snoeck,
Bernard Rentier,
Gérald Pierard
Publication year - 1999
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1046/j.1365-2230.1999.00498.x
Subject(s) - varicella zoster virus , virus , medicine , acanthosis , virology , immunology , pathology , hyperkeratosis
The outbreak of HIV infection introduced a new phenomenon in varicella zoster virus (VZV) pathology, namely the long‐standing wart‐like skin lesions that are frequently associated with resistance to thymidine kinase (TK)‐dependent antiviral agents. This paper reviews the clinical, histological, and molecular aspects and the therapeutic management of these verrucous lesions. The majority of lesions are characterized by chronically evolving, unique or multiple wart‐like cutaneous lesions. The main histopathological features include hyperkeratosis, verruciform acanthosis and VZV‐induced cytopathic changes with scant or absent cytolysis of infected keratinocytes. The mechanism that establishes the chronic nature of the lesions appears to be associated with a particular pattern of VZV gene expression exhibiting reduced or nondetectable gE and gB synthesis. Drug resistance to TK‐dependent antiviral agents is a result of nonfunctional or deficient viral TK. This necessitates alternative therapeutic management using antiviral agents that target the viral DNA polymerase.