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Prevalence of human parvovirus B19 component NS1 gene in patients with Henoch‐Schönlein purpura and hypersensitivity vasculitis

SIR, Human parvovirus B19 has been proposed as an aetiological agent of cutaneous vascular diseases including Henoch– Schönlein purpura (HSP) and vasculitis. In the present study, we investigated the prevalence of human parvovirus B19 component genes in skin tissues of HSP and hypersensitivity vasculitis. Thirty-two patients with HSP (11 males and 21 females; age range 10–77 years, mean 43Æ6) and 18 patients with hypersensitivity vasculitis (seven males and 11 females; age range 21–87 years, mean 51Æ7) were studied. For comparison, we included 97 healthy subjects (23 males and 74 females; age range 24–74 years, mean 55Æ3). HSP was clinically characterized by palpable purpura of the buttocks and lower extremities, abdominal pain, and haematuria. Hypersensitivity vasculitis was characterized by a reaction to a causative drug. Histologically, the diseases are characterized by a combination of vascular damage and an infiltrate composed largely of neutrophils. Immunofluorescence demonstrated the deposition in capillaries of IgA in HSP and of IgG in hypersensitivity vasculitis. Crude DNA was extracted from skin tissue specimens with a QIAmp DNA Mini Kit (Qiagen, Hilden, Germany). Polymerase chain reaction (PCR) amplification was performed in a buffer described elsewhere containing 1Æ25 U lL AmpliTaqGold polymerase (Applied Biosystems, Foster City, CA, U.S.A.) and 20 pmol of the respective primers. The skin tissue DNA was studied by nested PCR for human parvovirus B19 component genes VP1, VP2 and NS1. The PCR reaction was carried out using two kinds of specifically designed primer sets for human parvovirus B19. Ten-microlitre aliquots of the PCR products were fractionated by horizontal gel electrophoresis on a 1Æ0% agarose gel stained with ethidium bromide. The v test was used to evaluate differences in occurrence rate. The results of second-round PCR to detect VP1 DNA are shown in Figure 1. Positive signals (391 bp) were obtained in some, but not all, samples of HSP, hypersensitivity vasculitis and normal skin. Similar results were obtained after second-round PCR to detect NS1 DNA (437 bp) and VP2 DNA (387 bp). The occurrence rates of VP1 and VP2 DNA in patients with HSP (21 of 32, 66%; 19 of 32, 59%) and hypersensitivity vasculitis (13 of 18, 72%; 13 of 18, 72%) showed no significant difference compared with that in normal controls (51 of 97, 53%; 51 of 97, 53%) (Table 1). The occurrence rates of NS1 DNA, of which the product is cytotoxic, in HSP (21 of 32, 66%) and hypersensitivity vasculitis (13 of 18, 72%) were significantly elevated compared with that in normal controls (43 of 97, 44%; P < 0Æ05). Human parvovirus B19 has been proposed as an aetiological agent of cutaneous vascular diseases including HSP and vasculitis. A case representing the first example of HSP associated with human parvovirus B19 in an adult patient has been reported. A case of HSP associated with human parvovirus B19 primary infection was demonstrated with an enzyme linked immunosorbant assay test which was positive for antihuman parvovirus B19 IgM. A study using in situ hybridization identified human parvovirus B19 DNA in dermal and glomerular capillary endothelial cells and surrounding dermal inflammatory cells. The results of the present study confirmed that human parvovirus B19 DNA can be detected in the skin tissues of HSP. The nonstructural protein NS1 is produced during the infection. Few functions have been shown to be involved in the transactivation of the viral promoter and the induction of apoptotic processes. Mainly based on comparison with the functional activities of the NS1 proteins from animal parvoviruses, it is