Detection of human herpesvirus 7 in pityriasis rosea by nested PCR

Background Clinical presentation, immunologic, light microscopic, and electron microscopic studies suggest a viral etiology for pityriasis rosea (PR). Objective To evaluate whether human herpesvirus 7 (HHV-7) is an etiologic factor for PR. Patients and methods Twenty-one PR patients (12 female, nine male) aged between 12 and 52 years, whose diagnoses were confirmed clinically and histopathologically, were included in the study. The duration of the disease was questioned. Tissue samples of 5-mm punch biopsy material were collected from the patients and from six healthy volunteers (three female, three male) as the controls. Nested polymerase chain reaction (PCR) with specific primers for HHV-7 DNA sequences (OPERON technologies Inc., HV-7S/HV-8A external sences and HV-10S/HV11A internal sences) was performed on each tissue sample. Polymerase chain reaction products were analyzed by electrophoresis on 2% agarose gels. After molecular weight markers (Haphi174) had been placed and visualized on an ultraviolet transilluminator, the gels were immersed and photographs were taken. Results The mean age was 29.86 +/- 11.77 for the PR patients and 25.33 +/- 11.69 for the controls. The mean duration of the disease was 16.28 +/- 15.74 days. Human herpesvirus 7 DNA sequences were detected in six of the PR patients (28.57%). The mean duration of the disease was calculated as 11.67 +/- 9.85 for the HHV-7-positive patients (patient nos. 3, 4, 5, 7, 8, 9) and 18.13 +/- 17.05 for the HHV-7-negative patients, and there was no statistically significant differences in either of the groups (U = 29.5, W = 50.5, P = 0.2241, using the Mann-Whitney U and Wilcoxon's rank sum W -tests). Nested PCR was negative for HHV-7 in all of the specimens from the controls. There was no statistically significant difference for the presence of HHV-7 DNA sequence between the PR patients and the controls (P = 0.2843, Fisher's exact two-tail analysis test). Conclusion Our results failed to support a possible role for HHV-7 in the pathogenesis of PR.