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Persistence of hepatitis A virus in fulminant hepatitis and after liver transplantation
Author(s) -
Fagan Elizabeth,
Yousef Galal,
Brahm Javier,
Garelick Hemda,
Mann George,
Wolstenholme Adrian,
Portmann Bernard,
Harrison Tim,
Mowbray James F.,
Mowat Alexander,
Zuckerman Arie,
Williams Roger
Publication year - 1990
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.1890300210
Subject(s) - virology , fulminant hepatitis , persistence (discontinuity) , liver transplantation , fulminant , hepatitis , hepatitis a virus , medicine , virus , transplantation , viral disease , immunology , biology , geotechnical engineering , engineering
Abstract A peroxidase‐labelled, specific mouse monoclonal antibody to hepatitis A virus (HAV) and an in situ hybridization technique (streptavidin‐biotin‐horseradish peroxidase reaction) with an HAV‐specific cDNA probe (recombinant plasmid pAWHA comprising 1.8 kb of the HAV‐specific cDNA, located toward the 3′ end of the genome) were used to detect HAV in liver tissues in two patients with fulminant viral hepatitis type A treated by liver transplantation after a protracted (day 40: case 1) and relapsing (day 60: case 2) clinical course. HAV antigens and HAV‐specific genomic sequences were detected in the hepatectomy tissues and in serial biopsies of the liver grafts through to final follow‐up at 2 months (case 2) or death at 7 months after re‐grafting for chronic rejection (case 1). In the fulminant liver parenchyma, numerous degenerating and some surviving hepatocytes were positive and randomly scattered. The immunoperoxidase staining was predominantly cytoplasmic and often granular. The localization of the cDNA probe was predominantly nuclear/perinuclear but was occasionally cytoplasmic. High‐titre IgM‐anti‐HAV antibodies persisted until death (case 1) or resolution (5 months) of an acute hepatitis (case 2), which occurred at 2 months, accompanied by HAV antigen (ELISA), in stool. Intact replicating virus particles must have been present in one or more sites in each case, including extrahepatic locations, with a viraemia as the most likely explanation for subsequent reinfection of the grafts.