Search Our Scientific Publications & Authors

Clin Exp Dermatol 2018 Aug 23;43(6):703-707. Epub 2018 May 23.

Department of Dermatology, Kyorin University School of Medicine, Tokyo, Japan.

Although numerous infective agents, including varicella zoster virus (VZV), have been described in association with pityriasis lichenoides et varioliformis acuta (PLEVA) and pityriasis lichenoides chronica (PLC), none has been identified consistently in these lesions. We sought to immunohistochemically identify VZV glycoprotein (g)E antigens in the vascular endothelium in PLEVA and PLC lesions, based on our previous observation that gE was detected in the vascular endothelium and eccrine unit up until 2 months and 2.5, respectively, years after herpes zoster (HZ) infection. Read More

Neurology 2013 May 1;80(22):2017-21. Epub 2013 May 1.

Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA.

Objective: To address the incidence of varicella-zoster virus (VZV) infection in patients with biopsy-negative giant cell arteritis (GCA), we examined archived biopsy-negative temporal arteries from subjects with clinically suspected GCA for the presence of VZV antigen.

Methods: Formalin-fixed, paraffin-embedded temporal arteries that were pathologically negative for GCA and normal temporal arteries were analyzed immunohistochemically for VZV and herpes simplex virus-1 (HSV-1) antigen.

Results: Five (21%) of 24 temporal arteries from patients who were clinically suspect but biopsy negative for GCA revealed VZV but not HSV-1 by immunohistochemical analysis. Read More

Neurology 2013 Jan 12;80(1):62-8. Epub 2012 Dec 12.

Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA.

Objective: Pathologic changes in varicella-zoster virus (VZV)-infected arteries include inflammation, thickened intima, and paucity of smooth muscle cells. Since no criteria have been established for early vs late VZV vasculopathy, we examined inflammatory cells and their distribution in 6 normal arteries, and 2 VZV-infected arteries 3 days after onset of disease (early) and 10 months after protracted neurologic disease (late).

Methods: VZV-infected temporal artery obtained 3 days after onset of ischemic optic neuropathy from an 80-year-old man, VZV-infected middle cerebral artery (MCA) obtained 10 months after protracted disease from a 73-year-old man, and 5 MCAs and 1 temporal artery from normal subjects, age 22-60 years, were examined histologically and immunohistochemically using antibodies against VZV and inflammatory cell subsets. Read More

Dermatology 2012 17;225(1):22-6. Epub 2012 Jul 17.

Department of Dermatology, Kyorin University School of Medicine, Mitaka, Tokyo, Japan.

Background: Distinctions between 'linear lichen planus' (LP) and 'zosteriform LP' are difficult to determine solely based on clinical findings.

Objective: The aim of this study is to determine whether the presence of the varicella-zoster virus (VZV) antigens could be used to differentiate the zosteriform LP from the linear LP.

Methods: We immunohistochemically investigated the presence of in vivo localization of VZV antigens in 8 LP lesions (zosteriform LP: n = 5, linear LP: n = 3). Read More

J Neurovirol 2012 Jun 28;18(3):172-80. Epub 2012 Apr 28.

Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands.

Varicella-zoster virus (VZV) causes chickenpox, establishes latency in trigeminal (TG) and dorsal root ganglia (DRG), and can lead to herpes zoster upon reactivation. The VZV proteome expressed during latency remains ill-defined, and previous studies have shown discordant data on the spectrum and expression pattern of VZV proteins and transcripts in latently infected human ganglia. Recently, Zerboni and colleagues have provided new insight into this discrepancy (Zerboni et al. Read More

Br J Dermatol 2011 Oct 15;165(4):802-7. Epub 2011 Sep 15.

Department of Dermatology, Kyorin University School of Medicine, Shinkawa, 6-20-2, Mitaka, Tokyo 181-8611, Japan.

Background: It is well known that varicella-zoster virus (VZV) exhibits tropism for the epidermis and follicular epithelium, while little attention has been paid to eccrine gland and duct involvement by VZV. The presence of herpetic syringitis in immunocompromised hosts suggested the possibility of eccrine gland and duct involvement by VZV.

Objectives: To determine whether VZV antigens could be detected in eccrine gland or duct epithelium of herpes zoster (HZ) lesions obtained at various intervals after the onset of a rash, and whether this expression could also be detected in eccrine units from other inflammatory disease lesions suggestive of VZV infection. Read More

J Neurovirol 2010 Oct;16(5):342-54

Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado 80045, USA.

Simian varicella virus (SVV) infection of primates resembles human varicella-zoster virus (VZV) infection. After primary infection, SVV becomes latent in ganglia and reactivates after immunosuppression or social and environmental stress. Herein, natural SVV infection was established in 5 cynomolgus macaques (cynos) and 10 African green (AG) monkeys. Read More

Acta Cytol 2008 May-Jun;52(3):337-43

Department of Pathology, Faculty of Medicine, Kuwait University, P.O. Box: 24923, Safat 13110, Kuwait.

Background: Fibroadenomas with stromal giant cell reaction have been described in the literature, but cytologic atypia including giant cell reaction due to chickenpox giving rise to suspicious cytology has not been reported.

Case Report: A 25-year-old woman, recovering from chickenpox, presented with a 1.5 x 1. Read More

Ophthalmology 2000 Apr;107(4):790-4

Department of Ophthalmology, Tokyo Medical University, Japan.

Objective/background: To identify the etiologic agent of rapidly progressive outer retinal necrosis (PORN) in a 32-year-old man with acquired immunodeficiency syndrome (AIDS), who had retinitis developed from cytomegalovirus (CMV). Multiple yellowish spots appeared in the deep retina without evidence of intraocular inflammation or retinal vasculitis, diagnosed clinically as PORN. Death occurred after failure of multiple organs. Read More

J Infect Dis 1997 Jul;176(1):261-4

Department of Dermatopathology, Institute of Pathology, University of Liège, Belgium.

The pathogenesis of chronic, verrucous varicella-zoster virus (VZV) cutaneous lesions in human immunodeficiency virus (HIV)-infected persons is unknown. It has been hypothesized that these lesions are due to an altered pattern of virus gene expression. Immediate early and late (L) gene expression in five chronic verrucous VZV lesions, four full-blown herpes zoster vesicular lesions in HIV-infected persons, and eight vesicular herpes zoster lesions in immunocompetent individuals was semiquantitatively assessed immunohistochemically using specific antibodies to the IE63, gE (L), and gB (L) proteins. Read More

Acta Derm Venereol 1997 May;77(3):194-7

Department of Dermatology, Catholic University Medical College, Seoul, Korea.

The characteristics rash of herpes zoster begins as erythematous macules and papules, progressing to vesicles within 12-24 h. Patients with persistent papules without vesicular change are occasionally found. Our aim was to elucidate differences in vesicular and papular types of herpes zoster. Read More

Virchows Arch 1996 Jul;428(4-5):275-80

Department of Dermatology, Kasumigaura National Hospital, Ibaraki, Japan.

Herpes zoster is caused by reactivation of varicella-zoster virus (VZV) persisting in dorsal root or trigeminal ganglia. To clarify the pathway of viral spread from the ganglia to skin, 16 biopsy specimens of early skin lesions of herpes zoster obtained from the face and trunk of 13 patients were studied histologically and immunohistochemically using monoclonal antibodies to the structural proteins of VZV. VZV-infected cells were detected in the hair follicles in 10 of the 16 specimens and in the epidermis in 2 specimens. Read More

Virchows Arch A Pathol Anat Histopathol 1992 ;420(1):71-6

Department of Dermatology, University of Tsukuba, Ibaraki, Japan.

Thirty-seven biopsy skin tissues of herpes zoster taken from 27 patients were analysed immunohistochemically using two monoclonal antibodies detecting either nucleocapsid or glycoproteins of varicella-zoster virus (VZV) on paraffin sections of formalin fixed tissues. Skin lesions of herpes zoster were divided clinically into four stages: erythematous, vesicular, pustular and ulcerative. In the erythematous stage, VZV antigens, if detected, were found only within ballooning cells in the lower epidermis or follicular epithelium. Read More