Abstract

Recent studies have suggested a pathogenic role of human parvovirus B19 (B19) in the development of acute fulminant liver failure in children. The hypothesis was based on the detection of B19 DNA in 8 of 10 explanted livers of children requiring liver transplantation. In the present study, explanted livers from 43 adults selected at random undergoing orthotopic liver transplantation for various reasons were examined. Pre-transplant sera were available from 40 patients of whom 35 (88%) were anti-B19 IgG-seropositive. All but one serum were negative for anti-B19 IgM antibody. By polymerase chain reaction, B19 DNA was detected in the livers of 15/35 (43%) anti-B19 IgG-positive patients, in 2/3 livers of patients with unknown anti-B19 antibody status, and in the initial transplant of an anti-B19 IgG-positive patient who underwent liver retransplantation, and whose own liver was negative for B19 DNA. In a second study group, liver and bone marrow samples from 23 autopsied adults selected at random were tested. Serum specimens were available from 22 individuals, of whom 17 (77%) were anti-B19 IgG-seropositive. All sera were negative for anti-B19 IgM antibody. B19 DNA was detected in the livers of 4/17 (24%) anti-B19 IgG-positive individuals, three of whom had also B19 DNA in their bone marrow. This is the first report demonstrating that B19 DNA is frequently present in livers of anti-B19 seropositive adults suggesting persistence of B19 in the liver. Further studies are needed to address whether B19 is an innocent bystander in the liver or whether the presence of B19 in liver is of biological and clinical significance.

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