Incidence of herpes family viruses in skin lesions of pemphigus patients

Abstract

<span>Background: Pemphigus is a group of autoimmune blistering skin </span><span>diseases that is related to auto antibodies against desmoglein 1 </span><span>and 3. Many reports have shown that HSV1, HSV2, VZV, EBV, </span><span>CMV, HHV8, and HIV are triggering agents for the activation </span><span>and exacerbation of pemphigus. In this study, we decided to </span><span>evaluate the frequency of HSV1, HSV2, HHV8, and EBV in </span><span>paraffin-embedded specimens of the new cases of pemphigus </span><span>patients using immunohistochemical methods.</span><br /><span>Method: Thirty patients with pemphigus whose diagnosis was </span><span>proved with direct immunofluorescens studies (20 cases of </span><span>pemphigus vulgaris and 10 cases of pemphigus foliaceus) and </span><span>10 specimens from the free margins of excised melanocytic nevi </span><span>were collected. Immunohistochemical staining was performed </span><span>for HSV1 and EBV (using Novo Castra kit) and for HSV2 and </span><span>HHV8 (using Dako kit).</span><br /><span>Result: The results showed a significance difference in the frequency </span><span>of positive staining for HSV1 in skin lesions of pemphigus vulgaris, </span><span>foliaceus, and controls (P= 0.041), foliaceus group more positive </span><span>staining than vulgaris group and both more than controls, but </span><span>not for HSV2, EBV, and HHV8 markers. Positive staining for </span><span>HHV8 occurred in 30% of PF patients and 15% of PV patients</span><br /><span>but P value was not significant (0.171).</span><br /><span>Conclusion: Like previous studies, our research also indicated </span><span>significant prevalence of HSV1 in lesions of pemphigus patients, </span><span>especially in pemphigus foliaceus. We collected new cases of</span><br /><span>pemphigus before starting immunosuppressive therapy, so we </span><span>think that the presence of HSV1 in skin lesions of patients can </span><span>act as a triggering factor for the disease which could not be </span><span>attributed to the suppressive therapy.</span>