The outbreak of HIV infection introduced a new phenomenon in varicella test
er virus (VZV) pathology namely the long-standing wart-like skin lesions th
at are frequently associated with resistance to thymidine kinase (TK)-depen
dent antiviral agents. This paper reviews the clinical, histological, and m
olecular 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 feature
s include hyperkeratosis, verruciform acanthosis and VZV-induced cytopathic
changes with scant or absent cytolysis of infected keratinocytes. The mech
anism that establishes the chronic nature of the lesions appears to be asso
ciated with a particular pattern of VZV gene expression exhibiting reduced
or nondetectable gE and gB synthesis. Drug resistance to TK-dependent antiv
iral agents is a result of nonfunctional or deficient viral TK. This necess
itates alternative therapeutic management using antiviral agents that targe
t the viral DNA polymerase.