The Experts below are selected from a list of 75 Experts worldwide ranked by ideXlab platform
Shinichi Imafuku - One of the best experts on this subject based on the ideXlab platform.
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Loss of ATP2A2 Allows Herpes Simplex Virus 1 Infection of a Human Epidermis Model by Disrupting Innate Immunity and Barrier Function
The Journal of investigative dermatology, 2018Co-Authors: Emi Sato, Kenji Hiromatsu, Kunihiko Murata, Shinichi ImafukuAbstract:Destruction of epidermal barrier function associated with atopic dermatitis or Darier's disease often causes severe secondary skin infections. Patients with skin barrier disorders often repeatedly acquire Kaposi Varicelliform Eruption, which is caused by herpes simplex virus, but the underlying mechanisms and effective preventive methods have yet to be found. Viral infection through an impaired epidermal barrier can be prevented by enhancing innate immunity and/or inhibiting viral entry. In this study, we established a three-dimensional skin barrier dysfunction model by silencing ATP2A2, which is mutated in some Darier's disease patients. We confirmed the loss of desmosomes and presence of histopathological clefts in the suprabasal layer. Herpes simplex virus 1 applied to the stratum corneum infected the deep epidermis. An innate immune reaction was assessed by evaluating the expression of IFNB1 and related genes. Pretreatment with polyinosinic-polycytidylic acid alone or plus the antimicrobial peptide, LL37 enhanced IFN-β production and suppressed viral replication. Furthermore, topical application of a white petrolatum ointment containing heparin, which binds viral glycoproteins related to virus entry, strongly inhibited viral replication, probably by inhibiting invasion. Our human barrier-dysfunctional model will have future application for identifying the mechanism of Kaposi Varicelliform Eruption onset, preventive methods, and therapies.
M Selores - One of the best experts on this subject based on the ideXlab platform.
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712 Kaposi Varicelliform Eruption
Pediatric Research, 2010Co-Authors: Nunes C Azevedo, T Torres, S Machado, M SeloresAbstract:Kaposi Varicelliform Eruption or eczema herpeticum is a potentially life-threatening viral infection that arises in pre-existing skin conditions. The vast majority of cases is caused by herpes simplex viruses and occurs concomitantly with atopic dermatitis. We report the case of a 14 year-old adolescent, with atopic dermatitis, who presented with extensive vesicular Eruption of the head and neck. The diagnosis of Kaposi Varicelliform Eruption was made based on clinical features, tzanck smear examination and polymerase chain reaction assay of the vesicle content. The patient responded adequately to oral acyclovir therapy without any complications. Kaposi Varicelliform Eruption is a rare condition and the severity varies from mild transient disease to a fulminating fatal disorder involving the visceral organs. Mortality ranges from 1 to 9%, with reported rates as high as 75% before the advent of effective antiviral drugs. Antiviral treatment is very effective and should be instituted without delay to avoid significant morbidity and mortality. Thus, high clinical suspicion for Kaposi Varicelliform Eruption should be maintained in children with atopic dermatitis who have a vesicular Eruption.
Julia S. Lehman - One of the best experts on this subject based on the ideXlab platform.
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Kaposi Varicelliform Eruption in patients with autoimmune bullous dermatoses
International journal of dermatology, 2015Co-Authors: Julia S. Lehman, Rokea A. El-azharyAbstract:Background Viral superinfection of skin affected by preceding dermatosis has been studied extensively in eczema and reported anecdotally in pemphigus. Little is known about its involvement and complications in patients with other immunobullous diseases. Methods To investigate clinical features and complications of viral superinfection in patients with immunobullous diseases, we performed a retrospective chart review. Results We identified 12 patients with immunobullous diseases (linear immunoglobulin A bullous dermatosis, n = 2; pemphigoid, n = 3; pemphigus, n = 7) and superinfection by herpes simplex virus 1 (n = 9) or 2 (n = 3). Complications included inpatient hospitalization for intensive management of skin lesions during viral flare (n = 6), herpes keratitis (n = 1), and death due to sepsis (n = 1). Five patients previously had a skin swab negative for herpes simplex virus polymerase chain reaction before a positive test. Nine patients were taking systemic corticosteroids or corticosteroid-sparing agents at herpetic infection; two with linear immunoglobulin A bullous dermatosis and one with a new diagnosis of pemphigus vulgaris had not. Conclusions Viral superinfection is a potentially serious complication in patients with immunobullous diseases. Clinicians should have a high index of suspicion for this phenomenon, even when patients are not otherwise immunosuppressed or when previous viral skin assays have been negative.
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Kaposi Varicelliform Eruption in patients with Darier disease: A 20-year retrospective study
Journal of the American Academy of Dermatology, 2015Co-Authors: Kaitlin A. Vogt, Christine M. Lohse, Rokea A. El-azhary, Lawrence E. Gibson, Julia S. LehmanAbstract:Background Kaposi Varicelliform Eruption (KVE), or herpes simplex virus (HSV) superinfection of pre-existing skin lesions, may complicate Darier disease. Objective We sought to compare the clinical features and outcomes of patients with Darier disease who developed KVE superinfection with those who did not. Methods A 20-year retrospective analysis of 79 patients with Darier disease treated at our institution was performed. Results Eleven (14%) patients developed KVE, of whom 45% required hospitalization for their skin disease during the follow-up period. Patients with KVE had more severe Darier disease ( P = .030) and were more likely to be hospitalized ( P = .015). HSV was detected in erosions without concomitant vesicles or pustules in 64% of confirmed cases. In all, 23 (55%) patients with erosions had HSV testing pursued. Limitations Retrospective study design is a limitation. Conclusion The majority of KVE occurs in painless or painful erosions that may also appear impetiginized without vesicle or pustule formation. As HSV superinfection is correlated with severe Darier disease and risk for hospitalization, increased recognition of this phenomenon may lead to better patient outcomes.
Emi Sato - One of the best experts on this subject based on the ideXlab platform.
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Loss of ATP2A2 Allows Herpes Simplex Virus 1 Infection of a Human Epidermis Model by Disrupting Innate Immunity and Barrier Function
The Journal of investigative dermatology, 2018Co-Authors: Emi Sato, Kenji Hiromatsu, Kunihiko Murata, Shinichi ImafukuAbstract:Destruction of epidermal barrier function associated with atopic dermatitis or Darier's disease often causes severe secondary skin infections. Patients with skin barrier disorders often repeatedly acquire Kaposi Varicelliform Eruption, which is caused by herpes simplex virus, but the underlying mechanisms and effective preventive methods have yet to be found. Viral infection through an impaired epidermal barrier can be prevented by enhancing innate immunity and/or inhibiting viral entry. In this study, we established a three-dimensional skin barrier dysfunction model by silencing ATP2A2, which is mutated in some Darier's disease patients. We confirmed the loss of desmosomes and presence of histopathological clefts in the suprabasal layer. Herpes simplex virus 1 applied to the stratum corneum infected the deep epidermis. An innate immune reaction was assessed by evaluating the expression of IFNB1 and related genes. Pretreatment with polyinosinic-polycytidylic acid alone or plus the antimicrobial peptide, LL37 enhanced IFN-β production and suppressed viral replication. Furthermore, topical application of a white petrolatum ointment containing heparin, which binds viral glycoproteins related to virus entry, strongly inhibited viral replication, probably by inhibiting invasion. Our human barrier-dysfunctional model will have future application for identifying the mechanism of Kaposi Varicelliform Eruption onset, preventive methods, and therapies.
Michael S. Howard - One of the best experts on this subject based on the ideXlab platform.
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Junctional adhesion molecule overexpression in Kaposi Varicelliform Eruption skin lesions - as a possible herpes virus entry site
North American journal of medical sciences, 2010Co-Authors: Ana Maria Abreu-velez, A. Deo Klein, Michael S. HowardAbstract:Context: Herpes simplex virus (HSV) infection of the skin represents a common challenge in dermatology; however, currently the port of viral entry remains obscure. HSV is known to induce an immunoglobulin-binding cell surface receptor in infected cells that utilizes a non-immune mechanism. The replication of HSV in cultured cells is accompanied by the appearance of surface receptors with an affinity for the Fc region of immunoglobulin G. Case Report : We describe a 43 year old African American male who presented with a generalized rash, including intense pruritus and umbilicated vesiculopustules. The patient had been previously diagnosed and treated for psoriasis with methotrexate and prednisone. Methods : Hematoxylin and eosin demonstrated keratinocytes with ballooning degeneration within the epidermis. Direct immunofluorescence (DIF) results resembled the pattern of paraneoplastic pemphigus, with negative indirect immunofluorescence (IIF) results on rat bladder. Immunohistochemistry revealed deposits of the complement membrane attack complex within dermal sweat glands, as well as the presence of herpes simplex virus 1 on the skin. We report a case of Kaposi Varicelliform Eruption, a cutaneous Eruption caused by a virus infecting patients with pre-existing dermatoses. Conclusion: HSV virus infection with over-expression of the junctional adhesion molecule close to herpetic infection sites may preferentially increase viral entry through the skin, possibly triggering a Kaposi Varicelliform Eruption.
