|Reference : Occult Herpes Simplex Virus Colonization of Bullous Dermatitides|
|Scientific journals : Article|
|Human health sciences : Dermatology|
|Occult Herpes Simplex Virus Colonization of Bullous Dermatitides|
|Nikkels, Arjen [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Anatomie et cytologie pathologiques >]|
|Delvenne, Philippe [Centre Hospitalier Universitaire de Liège - CHU > > Anatomie pathologique >]|
|Herfs, Michael [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Anatomie et cytologie pathologiques >]|
|Pierard, Gérald [Centre Hospitalier Universitaire de Liège - CHU > > Dermatopathologie >]|
|American Journal of Clinical Dermatology|
|Yes (verified by ORBi)|
|[en] Herpes simplex virus ; HSV ; Bullous Dermatitides|
|[en] Background: Acantholytic disorders, including pemphigus vulgaris, chronic benign familial pemphigus
(Hailey-Hailey disease), Darier disease, and Grover transient acantholytic dermatosis, as well as other vesiculobullous
disorders, including bullous pemphigoid, epidermolysis bullosa, and atopic dermatitis, are prone to florid
infections by herpes simplex virus (HSV)-I and -II, and, more rarely, by varicella-zoster virus (VZV). As these
infections are difficult to recognize clinically and histologically, their frequency remains unknown. A possible
occult viral colonization has never been documented in these disorders. The manner in which the primary bullous
disorders are contaminated by herpesviridae remains unclear.
Objective: To retrospectivally assess the possible presence of HSV and VZV in a series of biopsies of
acantholytic disorders and bullous pemphigoid.
Method: The typical a-herpesviridae-related cytopathic signs were searched for by conventional microscopy in
skin biopsies of patients with pemphigus vulgaris (n = 19), bullous pemphigoid (n = 20), Darier disease (n = 18),
Hailey-Hailey disease((Author: is this the same as superficial pemphigus, as mentioned in both Histology
sections?)) (n = 3), and Grover transient acantholytic dermatosis (n = 3). Immunohistochemistry (IHC) targeted
specific HSV-I, HSV-II, and VZV antigens. Polymerase chain reaction (PCR) was used for detecting HSV- and
VZV-specific DNA sequences.
Results: No cytopathic signs suggestive of HSV or VZV infection were detected. However, IHC revealed HSV
antigens in Darier disease (1/18, HSV-I), Grover transient acantholytic dermatosis (1/3, HSV-I), pemphigus
vulgaris (1/20((Author: 1/19 in the Immunohistochemistry section?)), HSV-I), and bullous pemphigoid (2/
20, HSV-I and HSV-II). In these IHC-positive cases, PCR amplified specific HSV primers in Darier disease (1/
18), pemphigus vulgaris (1/20((Author: 1/19 in the PCR section?))), and bullous pemphigoid (1/20). VZV
antigens and nucleic acids were never identified. The HSV antigens were ((Author: nearly always, as in the
Immunohistochemistry section?)) restricted to the upper part of the granular layer and thus differed from the
usual HSV distribution during cutaneous infection. Negative and positive controls yielded consistently positive
and negative results, respectively.((Author: OK?))
Conclusion: This report shows for the first time that clinically and histologically occult HSV colonization may
occur in Darier disease, Grover transient acantholytic disease, pemphigus vulgaris, and bullous pemphigoid.
Given the frequent use of immunosuppressive treatments for primary bullous disorders, greater awareness of
HSV colonization and infection is recommended in these patients.
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