Human parvovirus B19 infection in acute fulminant liver failure

Human parvovirus B19 infection in acute fulminant liver failure We previously reported detection of human parvovirus B19 DNA in livers from patients requiring transplantation for acute fulminant liver failure. In this study, we used immune adherence PCR (IA-PCR) to bind B19 virions in recipient native liver onto solid phase with specific monoclonal antibodies followed by PCR amplification of virion DNA. IA-PCR had sensitivity and specificity similar to conventional PCR. We examined liver tissue from 16 patients with non-A, non-B, non-C, non-E (NA-E) acute fulminant liver failure (AFLF) (6 of unknown etiology associated with aplastic anemia (AA), 4 of unknown etiology without AA; and 6 patients with AFLF of known etiology). IA-PCR detected B19 virions in 5 of 6 (83%) of livers from patients with idiopathic NA-E AFLF associated with AA and in 2 of 3 (75%) without AA, compared to 1 of 6 (17%) of livers from patients with AFLF of known etiology and to 6 of 34 (18%) of 34 control patients with chronic or neoplastic liver disease. Viral mRNA encoding the structural protein was detected in the liver tissue from three B19 IA-PCR positive patients with AFLF. Detection of B19 virions and mRNA for capsid proteins provided strong evidence for B19 infection during the course of NA-E AFLF and argues for involvement of B19 virus in liver injury. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Human parvovirus B19 infection in acute fulminant liver failure

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Publisher
Springer-Verlag
Copyright
Copyright © Wien by 1999 Springer-Verlag/
Subject
Legacy
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s007050050699
Publisher site
See Article on Publisher Site

Abstract

We previously reported detection of human parvovirus B19 DNA in livers from patients requiring transplantation for acute fulminant liver failure. In this study, we used immune adherence PCR (IA-PCR) to bind B19 virions in recipient native liver onto solid phase with specific monoclonal antibodies followed by PCR amplification of virion DNA. IA-PCR had sensitivity and specificity similar to conventional PCR. We examined liver tissue from 16 patients with non-A, non-B, non-C, non-E (NA-E) acute fulminant liver failure (AFLF) (6 of unknown etiology associated with aplastic anemia (AA), 4 of unknown etiology without AA; and 6 patients with AFLF of known etiology). IA-PCR detected B19 virions in 5 of 6 (83%) of livers from patients with idiopathic NA-E AFLF associated with AA and in 2 of 3 (75%) without AA, compared to 1 of 6 (17%) of livers from patients with AFLF of known etiology and to 6 of 34 (18%) of 34 control patients with chronic or neoplastic liver disease. Viral mRNA encoding the structural protein was detected in the liver tissue from three B19 IA-PCR positive patients with AFLF. Detection of B19 virions and mRNA for capsid proteins provided strong evidence for B19 infection during the course of NA-E AFLF and argues for involvement of B19 virus in liver injury.

Journal

Archives of VirologySpringer Journals

Published: Sep 1, 1999

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