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At least 19 recordsLinked to original sources

PubMed2000

A vestigial X open reading frame in duck hepatitis B virus.

Duck hepatitis B virus (DHBV) appears to lack a homologue of the X protein found in mammalian hepadnaviruses. By replacing stop codons in the corresponding region of the DHBV genome, a hypothetical protein which closely matches the hydrophilicity profile of X proteins can be predicted, despite limited sequence homology. We conclude that a full-length X protein was once a common feature of the hepadnaviruses, conserved in structure but not sequence.

Amino Acid Sequence↗

PubMed1986

In vitro experimental infection of primary duck hepatocyte cultures with duck hepatitis B virus.

Duck hepatitis B virus (DHBV) obtained from the serum of congenitally infected ducks was used to infect primary duck hepatocyte cultures 1 to 4 days after plating. Virus replication was demonstrated by the appearance, beginning at 2 days after infection, of intracellular covalently closed-circular and single-stranded DHBV DNA replicative intermediates which were not present in the inoculating virus preparation. With increasing time after infection there was further amplification of intracellular relaxed circular, covalently closed-circular, and single-stranded DHBV DNA. Cultures of primary duck hepatocytes are competent for infection with DHBV only during the first 4 days of culture. Synthesis of DHBV core antigen and DHBV surface antigen was detected by immunofluorescence in 10% of the hepatocytes in culture. De novo synthesis and release of infectious virus was also demonstrated. Therefore, all stages of viral replication were carried out by these experimentally infected primary hepatocyte cultures. This system makes it possible to study DHBV replication in vitro.

Animals↗

PubMed1997

Insertions within epsilon affect synthesis of minus-strand DNA before the template switch for duck hepatitis B virus.

Duck hepatitis B virus (DHBV) is a DNA virus that replicates via reverse transcription of a pregenomic RNA (pgRNA). Synthesis of the first strand of DNA (minus-strand DNA) for DHBV can be divided into two steps: (i) synthesis of the first four nucleotides of minus-strand DNA, which is primed by the viral polymerase (P) protein and copied from the sequence 5'-UUAC-3' within the phylogenetically conserved bulge in the encapsidation signal (epsilon) near the 5' end of pgRNA; and (ii) a template switch of the four-nucleotide minus-strand DNA from epsilon to an acceptor site near the 3' end of pgRNA and synthesis of a complete minus-strand DNA. To understand why only four nucleotides of minus-strand DNA were synthesized before the template switch, we introduced small insertions immediately 5' to the UUAC sequence in epsilon and determined whether these epsilon variants were competent for protein priming and whether minus strands longer than four nucleotides were synthesized. Then we determined, in cell culture, whether the longer minus-strand DNAs were competent to undergo a template switch. Also, we analyzed the structure of the epsilon variants, in solution. We found that the epsilon variants were functional for protein priming and RNA encapsidation and that the insertions were copied into minus-strand DNA. However, two mutant viruses that contained two different three-nucleotide insertions failed to synthesize minus-strand DNA efficiently from the acceptor site, even though seven nucleotides of the donor and acceptor sites were identical. These results suggest that the length and/or sequence of the minus-strand DNA copied from epsilon can be important for an efficient template switch. The RNA structural analysis of the epsilon variants indicated alteration in the position and size of the bulge. Overall, these results are consistent with the notion that the template within epsilon is limited to four nucleotides because the remaining two nucleotides located within the bulge are inaccessible for polymerization.

Animals↗

PubMed1994

Inhibitory effects of acyclic nucleoside phosphonates on human hepatitis B virus and duck hepatitis B virus infections in tissue culture.

The inhibitory effects of the 9-(2-phosphonylmethoxyethyl)adenine-related compounds (S)-9-(3-hydroxy-2-phosphonylmethoxypropyl)-adenine, (S)-9-(3-fluoro-2-phosphonylmethoxypropyl)adenine, (R)-9-(2-phosphonylmethoxypropyl)adenine, (R)-9-(2-phosphonylmethoxypropyl)-2,6-diaminopurine, and (S)-1-(3-hydroxy-2-phosphonylmethoxypropyl)cytosine on human hepatitis B virus replication in the human hepatoma cell line HepG2 2.2.15 and duck hepatitis B virus infection in primary duck hepatocytes were investigated. (R)-9-(2-phosphonylmethoxypropyl-2,6-diaminopurine had the lowest 50% inhibitory concentrations against hepatitis B virus and duck hepatitis B virus, 0.22 and 0.06 microM, respectively, i.e., two- to fivefold lower concentrations than required for (R)-9-(2-phosphonylmethoxypropyl)adenine and 9-(2-phosphonylmethoxyethyl)adenine. All compounds were not toxic in vitro at a concentration of 100 microM.

Adenine↗

PubMed2006

Identification of T-cell epitopes associated with immunity within the surface protein of duck hepatitis B virus.

Duck hepatitis is a convenient model of hepatitis B virus (HBV) infection, but the lack of immunological reagents hampers investigation of pathogenesis and vaccine development. The aim of this study was to define T-cell epitopes in the surface peptide recognized by vaccinated immune birds. Blastogenesis assays were used to test the proliferative response of spleen mononuclear cells to synthetic peptides spanning the pre-S/S region in 22 naïve and 13 immunized and challenged immune ducks. Roughly > or = 50% of the immune ducks responded to five immunodominant peptides eliciting a statistically greater proliferative response than in naïve birds. Fewer ducks responded to an additional six peptides. No statistically significant difference could be shown for the response to 11 peptides between the immune ducks and the naïve ducks. There was no clustering of the immunodominant peptides which were located throughout the surface antigen at sites of major swings in hydrophobicity. A number of peptides which induce lymphoblastogenesis in vaccinated immune ducks have been identified. Their role in spontaneous recovery from duck hepatitis B infection merits investigation.

Amino Acid Sequence↗

PubMed1993

[The effects of Ara-A on viral markers in duck hepatitis B virus carrier ducks].

Duck hepatitis B virus (DHBV) carrier ducks of one week old were injected with Ara-A (adenine arabinoside) of different dose including 2.5 (11 ducks), 5.0 (11), 10.0 (10) and 20.0 (10) mg/kg for 14 days. This antiviral effect showed dose-dependence up to 5.0 mg/kg and this dose seemed effective to obtain significant antiviral effect. Viral DNA and DNA polymerase activity were reduced significantly from the 1st week after starting the administration of Ara-A. This antiviral effect was maintained even at the 1st week after discontinuation of the drug. These findings were quite similar to those observed in HBV carriers. With the increasing necessity of Ara-A treatment in patients who will not respond to interferon therapy, DHBV seemed a suitable model for the investigation of the dose and antiviral effect of Ara-A treatment in humans.

Animals↗

PubMed1992

The sequential change of serum 2',5' oligoadenylate synthetase in different infectious patterns of duck hepatitis B virus in ducks in experimental transmission.

Duck hepatitis B virus (DHBV) shows clear age-dependent infectious patterns like that of Hepatitis B virus, and many factors have been assumed to have a role in the persistence of the infection. In the present study, the activities of the interferon-induced enzyme 2',5' oligoadenylate synthetase (2,5AS) were observed sequentially in the serum of ducks experimentally infected with DHBV on posthatch days 1, 7 and 14. These were compared with the infectious pattern to investigate whether the endogenous interferon response after infection in ducks of different ages has a major role in its determination. The infectious pattern of DHBV in 1-day-old ducks was persistent without hepatitis and the others were transient with hepatitis. Persistently infected ducks showed significantly lower activities of 2,5AS compared with those with transient hepatitis, which resulted in a rapid elimination of DHBV. Although 1-day-old ducks showed significantly high 2,5AS compared with non-infected ducks, interferon response alone appeared to be insufficient for the elimination of DHBV. The immune response seemed necessary for the complete elimination of DHBV by way of evoking hepatitis and stimulating more interferon response during the usual infectious course. The interferon system alone did not seem to have a critical role in determining the infectious pattern. Other factors, including the immune response to the virus, seemed to have a major role in this problem.

2',5'-Oligoadenylate Synthetase↗

PubMed1999

Cellular immune response of ducks to duck hepatitis B virus infection.

Duck hepatitis B virus (DHBV) has been a useful model for hepadnavirus infection. There have been few studies on immunity to DHBV and none describing the cell-mediated immune response by acute and chronically infected ducks. A duck hepatitis B antigen-specific blastogenesis assay was used to measure DHBV antigen-specific responses of duck peripheral blood (PBMC) and splenic mononuclear cells (SMCs) from uninfected control ducks, ducks acutely or chronically infected with DHBV, and ducks immune to DHBV. A comparison of the group mean responses by PBMC to DHBV surface antigen (DHBsAg) found that the immune group was significantly different to the other three groups (controls or unexposed, P < 0.0001; acutely infected, P< 0.01; chronically infected, P < 0.01). The responses to DHBsAg by PBMC of the acute group (P< 0.01) were significantly different also to that of the unexposed group. For DHBV core antigen (DHBcAg), significant differences in the responses were found between immune ducks and unexposed (P < 0.0005) and acutely infected (P < 0.05) groups. The SMC showed a significant difference between unexposed ducks and immune ducks (P< 0.05) in the group mean responses to DHBsAg. The responses to DHBcAg were significantly different between the immune group and the acute (P < 0.01) and unexposed (P < 0.01) groups. The group mean of unexposed ducks was also significantly different to that of acutely infected ducks (P < 0.01). This study indicates that the cellular immune response in immune animals differs from acutely and chronically infected ducks. Further studies of these differences may provide some explanations for the differing outcomes of DHBV infection.

Acute Disease↗

PubMed1988

The arginine-stimulated insulin response is impaired in congenital duck hepatitis B virus infection.

Duck hepatitis B virus (DHBV) infects both A (glucagon-containing) and B (insulin-containing) islet cells. To examine the effect of this infection on islet cell function, baseline and secretagogue-augmented plasma insulin and glucagon levels as well as the pancreatic content of insulin and glucagon were compared in congenitally DHBV- and noninfected ducks. No difference in baseline plasma levels or the pancreatic content of insulin or glucagon was detected. However, the magnitude of the second phase of the biphasic arginine-stimulated insulin response was markedly diminished in infected ducks.

Animals↗

PubMed1992

Ultrastructural study on extrahepatic infection of duck hepatitis B virus in ducks.

Kidney and pancreas tissues from congenitally infected Ma ducks with duck hepatitis B virus (DHBV) were examined by immunohistochemical staining technique and electron microscopy. The immunostaining showed that DHBV antigen was localized in the cytoplasm of tubular epithelial cells of kidney and acinar cells of pancreas of infected ducks. Under electron microscope, we found that complete and incomplete DHBV particles existed in the dilated cisternae of rough endoplasmic reticulum of both the cells. The size of complete and incomplete virus particles was nearly uniform in both the cells, 50-65 nm and 40-50 nm in diameter respectively. Therefore, extrahepatic infection and replication of DHBV were directly demonstrated ultrastructurally.

Animals↗

PubMedDate not supplied

In vitro transmission of duck hepatitis B virus to primary duck hepatocyte cultures.

An attempt was made to infect primary duck hepatocyte cultures with duck hepatitis B virus in vitro in order to clarify the biology of hepatitis B virus. Livers of ducklings, 0 to 17 days posthatch, without viremia were digested ex situ by perfusion of collagenase solution through the portal or hepatic vein. Homogeneous hepatocyte suspensions were seeded into plastic dishes in L-15 medium containing 10(-8) M insulin, 2 X 10(-8) M glucagon and 10(-8) M dexamethasone and were subsequently inoculated with sufficient numbers of duck hepatitis B virus. As a result, duck hepatitis B virus multiplication started weakly on Day 2, gradually increased and reached the maximum level approximately on Day 10 postinoculation. Viral replication was revealed by duck hepatitis B virus DNA in the cell pellet and in the culture medium and duck hepatitis B virus DNA-specific transcripts in the cell pellet. Immunostaining demonstrated duck hepatitis B virus core antigen in approximately 10% of cultured hepatocytes, and an increase in numbers of positive cells was not observed with time for up to 18 days of culture. Viral particles were found within the endoplasmic reticulum, and the inoculation of culture medium provoked viremia in the ducklings. The age of ducklings did not influence the numbers of cells infected. The in vitro infection system was similar to the in vivo one; however, the former seemed to be age-independent and to allow replication of duck hepatitis B virus in the limited number of hepatocytes.

Animals↗

PubMedDate not supplied

Experimental transmission of duck hepatitis B virus to Pekin ducks and to domestic geese.

We investigated experimental transmission of duck hepatitis B virus to its original host, the domestic Pekin duck, and to three other avian species. Intramuscular injection of a standard inoculum of duck hepatitis B virus into 2- to 5-day-old Pekin ducklings hatched from a duck hepatitis B virus-free flock resulted in viremia in 100% of 107 animals, indicating that duck hepatitis B virus infection of young progeny of a defined duck hepatitis B virus-free flock occurs reproducibly. When the same inoculum was injected into chicks and Muscovy ducklings of the same age, no evidence of viral infection was detectable. In contrast, hatchlings of two domestic breeds of geese were readily infected by duck hepatitis B virus, developing viremia at a slower rate than Pekin ducklings, but a higher average titer of viremia 4 weeks or more after injection. Neither the pattern of restriction enzyme sites in the viral DNA nor the susceptibility of ducklings to the virus were detectably altered after passage in geese. As in duck hepatitis B virus-infected young ducklings, most of the experimentally infected goslings appeared to be persistently infected and those eventually laying eggs transmitted virus to the progeny. While ducklings exhibited a fairly uniform inflammatory response to the virus, duck hepatitis B virus inoculation of the goslings resulted in both inflammation and an altered hepatocellular morphology not seen in uninjected controls. The host range of duck hepatitis B virus appears to be limited to the primary host and a close taxonomic relative, similar to other members of the hepadnavirus family, hepatitis B virus and ground squirrel hepatitis virus.

Animals↗

PubMed1990

Epitope-specific antibody response to the surface antigen of duck hepatitis B virus in infected ducks.

In order to investigate the immune response to duck hepatitis B virus (DHBV) infection, newly hatched DHBV DNA negative ducklings were injected with infectious serum of sufficiently low DHBV-DNA titer to allow clearance of viremia. Of 20 injected ducklings, 13 (65%) became viremic. Of these, 6 (46%) cleared virus from the serum 3 to 22 weeks postinjection. The convalescent sera of these 6 animals were tested for an epitope-specific antibody response in a highly specific competitive inhibition assay using a panel of monoclonal antibodies against duck hepatitis B surface antigen (DHBsAg) that had been well-characterized. All 6 animals recovering from DHBV infection developed antibodies to epitopes on the preS and S proteins of DHBV. Antibody responses were highly variable with marked differences between animals in the extent and specificity of the antibody response. The humoral response to DHBsAg was prolonged in some animals but transient in others. No antibody to preS or S was detected in either preimmune sera or sera of control animals from an uninfected flock. Infected animals that did not clear viremia also remained antibody negative. The humoral responses to neutralizing preS epitopes III and V were weak but antibodies to two immunodominant epitopes on the preS region (II and B) were present in all 6 animals. The humoral response to the two epitopes in the S region was transient and of lower titer when compared to the two immunodominant preS epitopes. The two immunodominant preS epitopes may play an important role in clearance of DHBV infection in ducks.

Animals↗

PubMed1991

A percutaneous liver biopsy technique in ducks (Anas platyrhynchos) experimentally infected with duck hepatitis B virus.

Aylesbury ducks (Anas platyrhynchos) chronically infected with the duck hepatitis B virus provide a useful model for studying hepadna-virus infection, replication and the effects of antiviral therapy. In these studies, it is necessary to have an effective method for obtaining repeat liver specimens for histological and molecular analyses. We have therefore developed a percutaneous liver biopsy technique which has a low rate of complications, can be performed at repeated intervals, and provides sufficient quantities of liver tissue for histological and nucleic acid hybridization analysis.

Animals↗

PubMed1992

Duck hepatitis B virus infection and duck hepatocellular carcinoma.

To study the relationship between duck hepatitis B virus (DHBV) infection and duck hepatocellular carcinoma (DHCC), histological examination and DHBV DNA hybridization were performed in 875 ducks from three flocks in Qidong County. Among them, 34 suffered from hepatoma, including 23 hepatocellular carcinoma, 8 cholangiocarcinoma and 3 hepatocellular-cholangiocarcinoma. Of the 34 ducks with hepatoma 27 were positive for DHBV DNA in the liver and/or serum. DHBV DNA was demonstrated in neoplastic nodules of 22 ducks. Southern blot analysis showed that 13 cases were of the integrated pattern of DHBV DNA in neoplastic nodules. The paratumor tissues of 14 ducks with massive tumor were analysed at the same time. Five cases showed integrated pattern, 4 cases free pattern and the other 4 cases both integration and free pattern of DHBV DNA. The hybridization pattern of DHBV DNA in tumor nodule was different from that in paratumor regions in 11 cases and identical in 3 cases. DHBV antigen was positive in 13 tumor nodules and 21 paratumor tissues in the 34 ducks with hepatic tumor by both victoria blue and orcein stain methods. Advanced liver diseases were found in 30 out of the 34 ducks with hepatoma, including 12 cirrhosis and 18 chronic active hepatitis. In southern blot analysis of 122 DHBV DNA positive Qidong ducks without hepatoma, only free pattern of DHBV was seen, while 44 control ducks from Changchun were negative for DHBV DNA. Neither hepatic tumor nor liver diseases were seen in the control ducks. The results suggest that hepatocellular carcinoma in ducks is similar to that in human HCC. They have a high frequency of viral DNA integrated into the host genome and a liver disease background.

Animals↗

PubMed1991

Natural and experimental infection of wild mallard ducks with duck hepatitis B virus.

Wild duck populations were investigated over a 4 year period for duck hepatitis B virus (DHBV) infection and liver disease. It appeared that DHBV is endemic in wild migratory mallards from France and the U.S.A., although neither hepatocellular carcinoma nor viral DNA integration could be detected in liver samples examined. The follow up of natural infection indicated that wild mallards developed significantly higher serum titres to DHBV DNA than Pekin ducks. The results of experimental transmission demonstrated that such differences in viraemia were not related to the breed of ducks but to the virus isolate, since the wild mallard-isolated DHBV (DHBV WM) induced significantly higher viraemia in both mallard and Pekin ducklings compared to the domestic Pekin DHBV (DHBVP) isolate. The naturally infected mallard and Pekin ducks had only minor histological lesions of the liver compared with experimentally infected birds. There was no correlation between the intensity of viraemia and the severity of liver lesions, suggesting that as for mammalian hepadnaviruses the hepatic injury in DHBV-infected ducks is probably immunologically mediated.

Animals↗

PubMed2003

[Sequence analysis of cloned duck hepatitis B virus genome from a Chongqing brown duck].

OBJECTIVE: To clone and analyze duck hepatitis B virus genome from Chongqing brown duck. METHODS: Duck hepatitis B virus (DHBV) DNA extracted from a Chongqing brown duck was amplified by PCR and cloned into PGEM-T vector using T-A clone method. The sequence of this DHBV genome was analyzed with some softwares after identified. RESULTS: The duck hepatitis B virus genome from Chongqing brown duck (DHBVcq), which was 3 024 nucleotides long, contained three ORFs whose onset and end nucleotides were in accord with those of HPUGA, encoding P, PreC/C and PreS/S protein respectively. Comparison of this strain with other DHBV reported in GenBank showed that the homology of DHBVcq and M32990 got the highest score of 94.9% at nucleotide level, while DHBVcq and DHBVCG got the least (89.8%). Most of the conserved regulation nucleotides and amino acids sequence found in other DHBV were also identified in DHBVcq. The epsilon region of DHBVcq, which was important for encapsidation of pgRNA and synthesis of minus-strand DNA, differed from that of most other DHBV strains, forming a stem-loop conformation with a three- nucleotides upper stem rather than a common nine-nucleotides one in free status. CONCLUSION: The successful clone and analysis of DHBVcq provide further studies with helpful information.

Animals↗

PubMed1989

Infection and uptake of duck hepatitis B virus by duck hepatocytes maintained in the presence of dimethyl sulfoxide.

Primary duck hepatocytes maintained in serum-free culture medium containing dimethyl sulfoxide support efficient replication of duck hepatitis B virus following infection in vitro. Cells remain susceptible to infection for at least 2 weeks after plating, allowing spread of virus via repeat cycles of infection. Up to 100% of cultured hepatocytes can be infected by prolonged exposure to high titer virus inoculum at 37 degrees. We have identified a fraction of infecting virus which binds tightly to cells at 4 degrees, presumably due to association with high affinity receptors on the hepatocyte membrane. The rate at which tightly bound virus is internalized at 37 degrees appears slow, with uptake occurring over a period of at least 16 hr.

Adsorption↗