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Psoriasis is a common inflammatory skin disease. Infectious models are considered to be of pathophysiological importance in psoriasis. The immunological profile of stable psoriasis plaques suggests that viral antigens may be important. Human parvovirus B19 (PVB19) is a single-stranded DNA virus that causes various clinical symptoms. Several case reports have suggested associations between PVB19 infection and various chronic autoimmune and dermatologic diseases. There has so far been no information regarding the role of PVB19 in psoriasis, except psoriatic arthritis. In this report, to investigate the role of PVB19 in psoriasis, we analyzed PVB19 DNA of peripheral blood from psoriatic patients (n = 47) in comparison with blood donors (n = 20). We also determined the presence of anti-PVB19 IgG and IgM antibodies by using enzyme-linked immunosorbent assay (ELISA). We found that the presence of PVB19 DNA in patients with psoriasis (38%) was significantly higher than in controls (0%, P < 0.01). Anti-PVB19 IgG antibodies were detected in 79% of the cases while only 6% had anti-PVB19 IgM antibodies. PVB19 DNA presence was associated with seropositivity for anti-PVB19 IgG (P < 0.05) but not with IgM antibodies, indicating subclinical activation of latent infection. No correlation was found between the presence of PVB19 DNA and a patient's age, sex, type of psoriasis, or psoriasis area and severity index. The data demonstrated a statistically significant association between psoriasis and PVB19. Therefore, we suggest that PVB19 infection may be of pathophysiological importance in psoriasis.

Although the effectiveness of methotrexate (MTX) in the treatment of psoriasis is very well established, the mechanism of action is poorly understood. It was suggested that the therapeutic effect of MTX in psoriasis might be mediated by inhibition of adhesion molecule expression. The aim of our study was to investigate the different effects of MTX treatment on cell proliferation, inflammatory infiltrate, adhesion molecules, and angiogenesis in psoriasis, and to clarify the mechanism by which MTX exerts its therapeutic effects. Clinical response, the morpho-phenotypic changes, epidermal thickness, and mitosis count were analyzed and the expression of CD31 and ICAM-3, proliferative markers such as Ki-67, PCNA, were evaluated by immunohistochemical techniques in lesional psoriatic epidermis, before and after the treatment with MTX in ten patients. In posttreatment biopsies a decrease in the degree of epidermal hyperplasia and a significant reduction in the severity of the inflammatory infiltrate (P<0.05) were observed. In addition, CD31 and ICAM-3 expression was significantly decreased on dermal cellular infiltrate, (respectively; P<0.05, P<0.01). Ki67 and PCNA expression were suppressed concurrently in about 90% of cases (P<0.01). We suggest that MTX may have an inhibitory effect on an initial integral component of the pathways that lead to psoriasis. Immunopharmacologic intervention in adhesion event has the potential to improve psoriasis. Inhibition of revascularization may be another mechanism of action of MTX.