摘要
Background: Lichen planus (LP) is a common inflammatory skin disease of unknown aetiology. Viral causes have been suggested. Objectives: To find candidate viruses associated with LP.Methods: Lesional and nonlesional skin samples,peripheral blood mononuclear cells and serum were obtained from patients with LP. Ultrastructural, viral DNA, immunohistochemical and serological analyses were performed, and comparisons were made with psoriatic and normal skin. Results: Electron microscopy revealed typical 120-200-nm enveloped particles with a 100-nm nucleus resembling human herpesvirus (HHV) virions both in dermis and in epidermis of lesional LP tissue. HHV-7 DNA was found in 11 of 18 lesional LP samples, as opposed to only one of 11 nonlesional LP samples (P =0.06), two of 11 lesional psoriasis samples (P = 0.05) and none of four normal skin samples. No relation was found between LP skin and DNA of other known HHVs (HHV-1,-6 and 8). With immunohistochemistry, significantly more HHV-7+cells were found in lesional LP epidermis than in normal epidermis. Lesional LP dermis contained significantly more HHV-7+cells than nonlesional LP, psoriatic or normal dermis. Moreover, LP skin contained overwhelmingly and consistently more plasmacytoid dendritic cells (upregulated in virally induced conditions) than nonlesional LP samples. Conclusions: We conclude that HHV-7 replicates in LP lesions, but not in psoriasis, another inflammatory skin condition. HHV-7 is possibly involved in the pathogenesis of LP. These preliminary data make further research on this topic of interest.
Background： Lichen planus （LP） is a common inflammatory skin disease of unknown aetiology. Viral causes have been suggested. Objectives： To find candidate viruses associated with LP. Methods： Lesional and nonlesional skin samples, peripheral blood mononuclear ceils and serum were obtained from patients with LP. Uhrastructural, viral DNA, immunohistochemical and serological analyses were performed, and comparisons were made with psoriatic and normal skin. Results： Electron microscopy revealed typical 120- 200-nm enveloped particles with a 100-nm nucleus resembling human herpesvirus （HHV） virions both in dermis and in epidermis of lesional LP tissue. HHV -7 DNA was found in 11 of 18 lesional LP samples, as opposed to only one of 11 nonlesional LP samples （P = 0.06）, two of 11 lesional psoriasis samples （P = 0.05） and none of four normal skin samples. No relation was found between LP skin and DNA of other known HHVs （HHV - 1, - 6 and 8） With immunohistochemistry, significantly more HHV -7 ＋ cells were found in lesional LP epidermis than in normal epidermis. Lesional LP dermis contained significantly more HHV -7 ＋ cells than nonlesional LP, psoriatic or normal dermis. Moreover, LP skin contained overwhelmingly and consistently more plasmacytoid dendritic cells （up nonlesional regulated in virally induced conditions） than LP samples. Conclusions： We conclude that HHV- 7 replicates in LP lesions, but not in psoriasis, another inflammatory skin condition. HHV- 7 is possibly involved in the pathogenesis of LP. These preliminary data make further research on this topic of interest.
