Herpes simplex virus reactivation as a trigger of mucous lesions in pemphigus vulgaris. (26th July 2014)

• Record Type: Journal Article
• Authors: Kurata, M.; Mizukawa, Y.; Aoyama, Y.; Shiohara, T.
• Is Part Of: British journal of dermatology. Volume 171:Number 3(2014:Sep.)
• Page Start: 554
• Page End: 560
• Publication Date: 2014-07-26
• Subjects: Dermatology -- Periodicals; Skin -- Diseases -- Periodicals; 616.5
• DOI: 10.1111/bjd.12961
• Languages: English
• ISSNs: 0007-0963

Abstract

Abstract : What's already known about this topic? Although infectious agents have long been implicated in the induction or exacerbation of pemphigus vulgaris (PV), a convincing role for the agent in the aetiology of PV has not been established. What does this study add? We successfully detected high levels of herpes simplex virus (HSV) DNA in the saliva samples from six of 16 patients with PV at the earliest stage, who had no episodes of herpes simplex. These patients with PV have run a more complex, intractable course refractory to conventional therapy. Detection of HSV DNA in saliva will alert physicians to the possibility of greater risk of subsequently developing refractory PV. Summary: Background: Although infectious agents have long been implicated in the induction or exacerbation of pemphigus vulgaris (PV), a convincing role for the agent in the aetiology of PV has not been established. Objectives: To establish the association with PV and herpes simplex virus (HSV). Patients and methods: We examined saliva for the presence of HSV DNA after the onset of PV initially localized to the oral lesions in addition to conventional serological tests and immunohistochemistry. Results: We successfully detected high levels of HSV DNA in the saliva samples from six of 16 patients with PV at the earliest stage, who had no episodes of herpes simplex. The prevalence (37·5%) of detecting HSV DNA in the patients with PV was lower than that of eczema herpeticum (56·5%), but comparable to that in patients with herpes labialis (30·0%). Copy numbers of the HSV DNA were rather higher than those with herpes labialis and with eczema herpeticum. In general, detection of HSV DNA in saliva was transient and restricted to the earliest phase of the disease. In addition, anti‐HSV immunoglobulin (Ig) G titres in patients with PV were significantly higher than those in patients with virologically confirmed HSV‐induced disorders. All salivary HSV DNA‐positive patients with PV had run a more complex, intractable course refractory to conventional therapy. Conclusions: Detection of HSV DNA in saliva is a useful and noninvasive, quantitative method for establishing the role of HSV in the pathogenesis of PV and for identifying individuals at greater risk for subsequently developing refractory PV.