DEMONSTRATION OF DUCK HEPATITIS-B VIRUS IN BILE-DUCT EPITHELIAL-CELLS- IMPLICATIONS FOR PATHOGENESIS AND PERSISTENT INFECTION

Citation
Aj. Nicoll et al., DEMONSTRATION OF DUCK HEPATITIS-B VIRUS IN BILE-DUCT EPITHELIAL-CELLS- IMPLICATIONS FOR PATHOGENESIS AND PERSISTENT INFECTION, Hepatology, 25(2), 1997, pp. 463-469
Citations number
43
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
25
Issue
2
Year of publication
1997
Pages
463 - 469
Database
ISI
SICI code
0270-9139(1997)25:2<463:DODHVI>2.0.ZU;2-9
Abstract
Hepatitis B virus (HBV) has been demonstrated in bile duct epithelial cells (BDEC) during chronic infection, The persistence of virus in BDE C may play an important role in disease pathogenesis, and may be at le ast partly responsible for the relapse phenomenon observed in antivira l treatments using nucleoside analogues, The aims of this study were t o examine the morphological changes within the liver in the duck hepat itis B model following bile duct ligation (BDL), and to assess the eff ect of biliary hyperplasia upon viral DNA and proteins. Seven-day-old ducklings, congenitally infected with the duck hepatitis B virus (DHBV ), were subject to BDL, The pathological and virological changes were then followed at 5, 10, 15, and 20 days after ligation, All results we re compared with age-matched unligated control birds congenitally infe cted with DHBV, To assess the early morphological changes, additional animals were sacrificed at 1, 2, 3, and 4 days post-BDL, The proportio n of DHBV-infected BDEC, was examined by immunohistochemistry and in s itu hybridization. BDL induced rapid biliary hyperplasia, with a doubl ing time for BDEC of 1.3 days, The proliferated BDEC displayed immunoh istochemical features identical to resting BDEC, More than 50% of BDEC in unligated controls, and more than 46% of proliferated BDEC in liga ted animals were positive for DHBV DNA and structural proteins, The in tensity of immunohistochemical staining and in situ hybridization sign al in the BDEC was consistently greater than that of the hepatocytes, both before and after BDL, BDL in duces biliary hyperplasia in the duc k model, and BDEC division does not reduce the viral burden in infecte d cells.