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Prevalence of Kaposi's sarcoma‐associated herpesvirus infection in haemophilic patients

Kaposi’s sarcoma-associated herpesvirus (KSHV) is a gamma herpesvirus, the sequence of which was identified by representative differential amplification in the lesion of HIV-infected patients with Kaposi’s sarcoma (KS) in 1994 [1]. KSHV has also been found in classic Mediterranean KS and other tumours such as multicentric Castleman’s disease and primary effusion lymphoma [2]. Little is known about the precise way in which KSHV is transmitted. It is known that KSHV transmission occurs during sex in homosexual men [3]. In classic and endemic KS countries, KSHV seroprevalence is high in adults [4,5], but also occurs in children because of close contact within infected members of the families [6–8]. Although the presence of viral genome in peripheral blood mononuclear cells and CD19+ B cells has been demonstrated [9,10], various studies have shown that blood-borne transmission of KSHV in multitransfused patients receiving white blood cell-reduced components, if it exists, is rare [11,12]. Epidemiological studies, even before the discovery of KSHV, have confirmed that HIV-positive patients with haemophilia had a low incidence of KS compared with HIV-positive homosexual or bisexual men. It was concluded that the presumed infectious agent causing KS was not normally transmissible parenterally [13]. After KSHV identification, studies have failed to reach a definite conclusion whether the virus could be transmitted by coagulation factor concentrates. Two studies have reported a lower KSHV seroprevalence in patients with haemophilia than in blood donors [14,15], while another study has shown a significantly higher prevalence of KSHV in HIV-infected and non-HIV-infected haemophilic patients than in controls [16]. In view of this, we investigated the seroprevalence of KSHV in patients with haemophilia by serological methods (anti-KSHV antibodies) and detection of KSHV DNA in blood. We tested blood samples from 50 patients (39 with haemophilia A, three with haemophilia B and eight with von Willebrand’s disease), of whom 25 were HIVand 44 HCV-infected. All HIV-infected patients except two, and 16 of the 25 non-HIV-infected patients with haemophilia suffered from severe disease. All the haemophilic patients have received non-virus-inactivated factor VIII concentrates before routine viral inactivation techniques were implicated, i.e when the risk for viral contamination of the concentrates was high. We also tested samples from 50 ageand sex-matched controls (HIVand HCVnegative) obtained from the volunteer blood donors. Indirect immunofluorescence assay (IFA) was used to detect antibodies against the latent nuclear antigen (LANA) encoded by open reading frame 73 (ORF73). Briefly, the BCP-1 cell line was used [17,18]. The cells were washed twice in phosphate-buffered saline (PBS), fixed in 4% paraformaldehyde and permeabilized with 0.2% Triton-X-100. Cells were resuspended in PBS, spotted and dried on glass slides. Human sera were diluted (1:100) in PBS with 3% foetal bovine serum (FBS). The diluted sera (1:100) were added to the fixed BCP-1 cells and incubated for 45 min at 22 C. Slides were then washed in PBS with 3% FBS and fluorescein isothiocyanate-(FITC)-labelled rabbit anti-human IgG Ab (DAKO, High Wycombe, UK) diluted (1:60) in PBS and 3% FBS was added. After 20 min of incubation at 22 C, the slides were washed Correspondence: George Theodossiades, MD, First Regional Transfusion and Haemophilia Centre, Hippokration Hospital, Vassilissis Sophias 114, Athens 11527, Greece. Tel.: + 302 10777 4833; fax: + 302 1077