Experimental duck hepatitis B virus infection: Pathology and evolution of hepatic and extrahepatic infection

Freiman, John S.; Jilbert, Allison R.; Dixon, Robert; Holmes, Mikaela; Gowans, Eric J.; Burrell, Christopher J.; Wills, E. J.; Cossart, Yvonne E.

doi:10.1002/hep.1840080313

Cited by 57 publications

(35 citation statements)

References 26 publications

(11 reference statements)

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“…The primary duck hepatocytes or primary IBDE cells at day 1 of culture were inoculated with 100 viral genome equivalents (vge)/ml of DHBV (Australia strain) derived from pooled duckling sera (4,12). The cells were incubated for 2 h with occasional rocking prior to the addition of growth medium.…”

Section: Methodsmentioning

confidence: 99%

Duck Hepatitis B Virus Replication in Primary Bile Duct Epithelial Cells

Lee

Culvenor

Angus

et al. 2001

J Virol

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Primary cultures of intrahepatic bile duct epithelial (IBDE) cells isolated from duckling livers were successfully grown for studies of duck hepatitis B virus (DHBV).The primary IBDE cells were characterized by immunohistochemistry using CAM 5.2, a cytokeratin marker which was shown to react specifically to IBDE cells in duck liver tissue sections and in primary cultures of total duck liver cells. Immunofluorescence assay using anti-duck albumin, a marker for hepatocytes, revealed that these IBDE cultures did not appear to contain hepatocytes. A striking feature of these cultures was the duct-like structures present within each cell colony of multilayered IBDE cells. Normal duck serum in the growth medium was found to be essential for the development of these cells into duct-like structures. When the primary cultures of duck IBDE cells were acutely infected with DHBV, dual-labeled confocal microscopy using a combination of anti-DHBV core proteins and CAM 5.2 or a combination of anti-pre-S1 proteins and CAM 5.2 revealed that the IBDE cell colonies contained DHBV proteins. Immunoblot analysis of these cells showed that the DHBV pre-S1 and core proteins were similar to their counterparts in infected primary duck hepatocyte cultures. Southern blot analysis of infected IBDE preparations using a digoxigenin-

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Section: Methodsmentioning

confidence: 99%

Duck Hepatitis B Virus Replication in Primary Bile Duct Epithelial Cells

Lee

Culvenor

Angus

et al. 2001

J Virol

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“…[1][2][3][4][5] In particular, the duck on liver histology and expression of viral markers of replication. model has facilitated the study of the basic molecular virology Nineteen animals underwent BDL and fourteen animals served as of the Hepadnaviridae, including the replication strategy 2,6 unligated controls.…”

Section: Materials and Methods Division Does Not Reduce The Viral Burmentioning

confidence: 99%

Demonstration of duck hepatitis B virus in bile duct epithelial cells: Implications for pathogenesis and persistent infection

et al. 1997

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ogy, genomic organization, and replication by means of reHepatitis B virus (HBV) has been demonstrated in bile verse transcription. 1,3 duct epithelial cells (BDEC) during chronic infection.The replication of human HBV has been extensively studThe persistence of virus in BDEC may play an important ied in hepatocytes, but comparatively less is known about role in disease pathogenesis, and may be at least partly HBV infection of nonparenchymal cells within the liver. Hepresponsible for the relapse phenomenon observed in adnaviral antigens have been shown in bile duct epithelial antiviral treatments using nucleoside analogues. The cells (BDEC) in both human 7,8 and animal 9,10 livers, but the aims of this study were to examine the morphological significance of these findings has not been fully determined. changes within the liver in the duck hepatitis B modelThe HBV life cycle is complex, and there is evidence that following bile duct ligation (BDL), and to assess the efit may vary depending on the cell type, such as lymphoid fect of biliary hyperplasia upon viral DNA and proteins.cells compared with hepatocytes. 11-15 Also, HBV replication Seven-day-old ducklings, congenitally infected with the appears to be cell-cycle dependent with enhanced viral repliduck hepatitis B virus (DHBV), were subject to BDL. The cation occurring in quiescent compared with proliferating hepathological and virological changes were then followed patocytes. 16 Recent studies have shown that HBV replication at 5, 10, 15, and 20 days after ligation. All results were is inversely correlated with cellular DNA synthesis with noncompared with age-matched unligated control birds cytolytic cell arrest resulting in increased viral expression. 1.3 days. The proliferated BDEC displayed immunohistoTherefore, the interaction of HBV with BDEC warrants more chemical features identical to resting BDEC. More than detailed investigation. The aim of the present study was to 50% of BDEC in unligated controls, and more than 46% characterize DHBV infection in BDEC of congenitally inof proliferated BDEC in ligated animals were positive fected animals, and to examine the effect of cell division on for DHBV DNA and structural proteins. The intensity of hepadnaviral proteins and DNA in proliferating BDEC using immunohistochemical staining and in situ hybridization immunohistochemistry and in situ hybridization, respecsignal in the BDEC was consistently greater than that tively. of the hepatocytes, both before and after BDL. BDL induces biliary hyperplasia in the duck model, and BDEC MATERIALS AND METHODS division does not reduce the viral burden in infected cells. (HEPATOLOGY 1997;25:463-469.)Animals and Experimental Strategy. One-day-old Pekin-Aylesbury ducklings, congenitally infected with an Australian strain of DHBV, were obtained from a commercial supplier.17 Viraemia was monitored by dot blot hybridization as previously described.9,18 Thirty-eight conInfection of Pekin-Aylesbury ducks with the duck hepatitis genitally infected ducklings aged between 7 and 9 ...

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“…These different outcomes are viral dose dependent; persistent infection in young ducks develops more frequently with higher doses of virus [92] . In some cases, dependent on age and infection with a given mutant, experimental infections can cause symptoms of a liver inflammation [93] . It has been shown that one genome equivalent is sufficient to infect a duckling and that spread of the virus within the liver is very efficient: 14 d after inoculation, virtually all hepatocytes were infected [94] .…”

Section: In Vitro Infectionmentioning

confidence: 99%

Avian hepatitis B viruses: Molecular and cellular biology, phylogenesis, and host tropism

Funk

Mhamdi²,

Will³

et al. 2007

WJG

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The human hepatitis B virus (HBV) and the duck hepatitis B virus (DHBV) share several fundamental features. Both viruses have a partially double-stranded DNA genome that is replicated via a RNA intermediate and the coding open reading frames (ORFs) overlap extensively. In addition, the genomic and structural organization, as well as replication and biological characteristics, are very similar in both viruses. Most of the key features of hepadnaviral infection were first discovered in the DHBV model system and subsequently confirmed for HBV. There are, however, several differences between human HBV and DHBV. This review will focus on the molecular and cellular biology, evolution, and host adaptation of the avian hepatitis B viruses with particular emphasis on DHBV as a model system.

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Experimental duck hepatitis B virus infection: Pathology and evolution of hepatic and extrahepatic infection

Cited by 57 publications

References 26 publications

Duck Hepatitis B Virus Replication in Primary Bile Duct Epithelial Cells

Duck Hepatitis B Virus Replication in Primary Bile Duct Epithelial Cells

Demonstration of duck hepatitis B virus in bile duct epithelial cells: Implications for pathogenesis and persistent infection

Avian hepatitis B viruses: Molecular and cellular biology, phylogenesis, and host tropism

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