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PubMed1988

Influence of aflatoxin B1 intoxication on duck livers with duck hepatitis B virus infection.

In an attempt to determine the effect of aflatoxin B1 (AFB) intoxication on livers with duck hepatitis B virus (DHBV) infection, domestic ducks were given 0.1 mg of AFB/kg body weight twice a week for a maximum period of 54 weeks employing various experimental designs. The ducks were infected with DHBV by i.v. inoculation of DHBV-positive sera within 24 h posthatch. The livers were examined histologically, immunohistochemically, and ultrastructurally, and the livers and sera were examined by molecular hybridization for DHBV DNA. AFB administration induced hepatocellular necrosis and marked biliary cell proliferation of the periportal areas, and finally liver cirrhosis. On short-term administration, the hepatocytes of DHBV-infected livers revealed a marked increase in incomplete particles of DHBV by immunostaining and electron microscopy, as compared to those without its administration. Long-term AFB administration provoked frequent nodular or cirrhotic changes. There was no significant increase in frequency of these changes in DHBV-positive ducks as compared to DHBV-negative ones. AFB administration induced hepatocellular carcinoma (HCC) in one DHBV-positive duck and in two DHBV-negative ducks. The HCC and cirrhotic livers revealed extrachromosomal but no integrated form of DHBV DNA by Southern blot hybridization analysis. Immunostaining demonstrated a heterogeneous distribution of DHBV from area to area in nodular and cirrhotic livers. Thus, AFB intoxication provoked various liver disorders independent of DHBV infection, and neither a cocarcinogenic effect of AFB and DHBV nor integration of viral DNA into the genome of neoplastic and nonneoplastic tissues was observed in the present experiments. Generally speaking, DHBV infection did not appear to accelerate hepatic disorders induced by AFB intoxication. However, AFB administration altered the DHBV in the liver in terms of its amount and distribution.

Aflatoxin B1↗

PubMed1980

Pituitary and adrenal control of pancreatic endocrine function in the duck. III. Effects of glucose, oleic acid, arginine, insulin and glucagon infusions in hypophysectomized or normal ducks.

The existence of plasma metabolites (glucose, free fatty acids [FFA[, aminoacids [AA])--pancreatic hormones (insulin, glucagon) feedback mechanisms and of insulin-glucagon relationships were studied in hypophysectomised ducks; the insulinogenic effect of glucagon was also studied in normal ducks in physiological conditions. Glucose infusion stimulated insulin secretion in hypophysectomised ducks; during oleic acid infusion, plasma IRI (immunoreactive insulin) was not modified whereas plasma GLI (glucagon like immunoreactivity) level drops slightly. Arginine induced insulin and glucagon secretion. Plasma GLI did not decrease during insulin infusion. In normal ducks glucagon was insulinogenic, hyperglycaemic and hypoaminoacidaemic. These biological properties of glucagon were lost in hypophysectomised ducks, except the effect on plasma aminoacids. It is concluded that the anterior pituitary and the adrenal cortex indirectly control the endocrine function of the pancreas, via the plasma metabolites and the insulin-glucagon interactions. In normal ducks, glucagon is probably insulinogenic in physiological conditions.

Adrenal Glands↗

PubMed1989

Prolonged duck hepatitis B virus replication in duck hepatocytes cocultivated with rat epithelial cells: a useful system for antiviral testing.

Duck cultured hepatocytes from Pekin ducks naturally infected by duck hepatitis B virus can remain functional twice longer if a coculture system with rat liver epithelial cells is used instead of ordinary primary culture. The use of a selective medium in which ornithine and lactate replaced arginine and glucose, respectively, allowed viral replication initiated in vivo to be maintained in the coculture for 2 months. Several antiviral compounds including the pyrophosphate analog (phosphonoformic acid) or nucleoside analogs (9 beta-arabinofuranosyl AMP, 1-(2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl)-5-iodocytosine, 1,2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl-5-ethyluracil and 1,2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl thymine) were studied in both culture systems for their ability to inhibit duck hepatitis B virus replication. Hepatocytes were treated for 7 days with 1,2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl-5-ethyluracil (10 microM) and 1,2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl thymine (0.5 microM) or for 14 days with 9 beta-arabinofuranosyl AMP (90 microM), phosphonoformic acid (100 microM) and 1-(2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl)-5-iodocytosine (6 microM). The effects of the drugs on viral replication were monitored by testing for duck hepatitis B virus DNA in the culture supernatant and in the cells by molecular hybridization.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Immunity in Pekin ducks experimentally and naturally infected with duck hepatitis B virus.

The immune response to duck hepatitis B virus (DHBV) had not been elucidated. An assay was therefore established to detect the presence of antibody to DHB surface antigen (anti-DHBs) in serum of experimentally inoculated and naturally infected ducks. Anti-DHBs in serum was detected by indirect RIA from the percentage inhibition of binding of rabbit anti-DHBs to purified DHBsAg. Specificity was confirmed by positive and negative controls, infected and noninfected sera, and a mouse monoclonal antibody to DHB core antigen (anti-DHBc). Serum and liver samples were tested for DHBV DNA by dot-blot hybridization assay. Adult ducks repeatedly inoculated with DHBV remained non-viraemic but developed anti-DHBs. This antibody activity neutralized the infectivity of DHBV, which was experimentally inoculated into 1-day-old ducklings. In naturally infected flocks anti-DHBs was detected in a proportion of noninfected adult ducks as well as 1-day-old hatchlings. Anti-DHBs activity in hatchlings neutralized the infectivity of experimentally inoculated DHBV. Pekin ducks can therefore mount a neutralizing antibody response to DHBV, and immunity may be transferred in ovo from dam to off-spring.

Aging↗

PubMed1993

Evaluation of anti-hepadnavirus activity of Phyllanthus amarus and Phyllanthus maderaspatensis in duck hepatitis B virus carrier Pekin ducks.

Extracts of the two traditional Indian herbs, Phyllanthus amarus (P. amarus) and Phyllanthus maderaspatensis (P. maderaspatensis), described by others as useful in the treatment of chronic hepatitis B virus infection were studied for antiviral properties on duck hepatitis B virus infection. One hundred and fourteen ducks infected posthatch with the duck hepatitis B virus (DHBV) were divided into groups at three months of age and treated intraperitoneally with the aqueous, butanol, and alcoholic extracts of these two plants at doses of 25, 50, or 200 mg/kg body weight. Saline-treated animals served as controls. In the ducks negative for DHBV in serum after treatment, we observed replicative intermediates in the liver. There was no definite antiviral property observed in the treated ducks.

Animals↗

PubMed1996

Kinetics of duck hepatitis B virus infection following low dose virus inoculation: one virus DNA genome is infectious in neonatal ducks.

Using pooled serum from congenitally duck hepatitis B virus (DHBV)-infected ducks as inoculum, we examined the effect of virus dose on the incubation period of infection and on the patterns of spread of virus infection in the liver. The pooled serum inoculum contained 9.5 x 10(9) DHBV genomes per milliliter and had an infectivity titre (ID50) in newly hatched ducks of 1.5 x 10(10) per milliliter with a 95% confidence interval of 3.0 x 10(9) to 6.3 x 10(10) ID50/ml, indicating the equivalence between one DHBV genome and one infectious unit within the limits of the assays. The incubation period of infection was inversely related to the dose of inoculum and the onset of viraemia ranged from Day 6 with the highest dose to Day 14 or 29 with the lowest dose inoculum. To study the spread of virus infection from a low percentage of initially infected cells we inoculated newly hatched ducks intravenously with sufficient DHBV (1.5 x 10(3) ID50) to infect only approximately 0.0001% of total liver cells. DHBV infection first reached detectable levels on Day 4 postinoculation (p.i.) and was detected in approximately 0.035% of hepatocytes, most of which occurred as single cells or pairs of cells, indicating that a number of rounds of infection had occurred with the spread of virus both to adjoining cells, i.e., by cell-to-cell spread, and to cells located in other parts of the liver lobule. Despite some bird-to-bird variation in timing, the percentage of infected hepatocytes increased exponentially with a mean doubling time of 16 hr from Day 4 to Day 14 p.i., by which time replication was seen in > 95% of hepatocytes. This rapid dissemination from a small number of infected hepatocytes suggests that, in neonatal ducks, there are no major delays in virus replication within the liver, that any innate and adaptive defence mechanisms operating during the first 10 to 14 days of infection are insufficient to contain virus spread, and that even a small number of infected hepatocytes produce enough progeny to rapidly infect the remaining hepatocytes.

Age Factors↗

PubMed1993

The use of ampligen alone and in combination with ganciclovir and coumermycin A1 for the treatment of ducks congenitally-infected with duck hepatitis B virus.

Ampligen, a known immunomodulator and interferon inducer, was used alone and in combination with other antiviral agents to treat ducks congenitally-infected with duck hepatitis B virus. These antiviral agents included the conventional nucleoside analogue ganciclovir and the prokaryotic DNA gyrase B inhibitor coumermycin A1. When used alone, ampligen decreased the amount of serum and liver viral DNA, but had no effect on circulating duck hepatitis B surface antigen (DHBsAg). In combination with ganciclovir, the antiviral effect appeared at least additive with a greater inhibition of viral DNA replication within the liver. The combination of ampligen with coumermycin A1 also resulted in inhibition of viral replication but to a lesser extent than ampligen alone. When all three agents were used together, viral DNA replication was again inhibited, but as with previous treatment regimes, serum DHBsAg levels remained unchanged. At the end of the treatment period for all regimes, analysis of viral DNA forms in the liver showed that the viral relaxed circular and supercoiled DNA forms had persisted. Within 1 week of cessation of therapy, viral replication had often returned to pre-treatment levels. Interferon-like activity was detected in the sera of the majority of the treated ducks during the ampligen therapy, but no clear relationship between the presence of interferon and antiviral effect could be established. These observations in the duck hepatitis B model may provide a rational basis for the use of combinations of antiviral and immunomodulatory regimes for the management of chronic hepatitis B infection in man.

Aminocoumarins↗

PubMed2000

Decrease of wild-type and precore mutant duck hepatitis B virus replication during lamivudine treatment in white Pekin ducks infected with the viruses.

BACKGROUND/AIMS: Lamivudine, an antiviral agent, has been used in the treatment of chronic hepatitis B, but little is known about its effect on intrahepatic replication of hepatitis B virus. We investigated the effect of lamivudine on the replication of wild-type and precore mutant duck hepatitis B virus (DHBV) in the liver and serum of DHBV carrier ducks. METHODS: Chronic carrier ducks with either wild-type or precore mutant DHBV were treated for 2 weeks with either low-dose (20 mg/kg, p.o., b.i.d.) or high-dose lamivudine (100 mg/kg, p.o., b.i.d.) or were untreated. Serum levels of DHBV DNA were examined serially by slot-blot hybridization. A second group of chronic carrier ducks was treated for 12 weeks with lamivudine (100 mg/kg, p.o., b.i.d.) or was untreated. The amount of DHBV DNA in serum and its various replicative intermediates in the liver were serially examined by slot-, Southern, and Northern blot methods. RESULTS: In the 2-week treatment study, concentration of DHBV DNA in serum treated with low- and high-dose lamivudine was reduced to 10.8% and 1.1% of the control level in wild-type DHBV carriers, and to 2.3% and 0.48% in precore mutant DHBV carriers, respectively. In the 12-week treatment study, concentration of DHBV DNA in serum at the end of treatment was reduced to <0.65% and <5.36% in wild-type and precore mutant DHBV carriers, respectively. Southern and Northern blot analyses revealed that the various replicative forms of DHBV DNA in the liver were decreased in all treated ducks, but, covalently closed circular DNA and RNA intermediates tended to remain unchanged. CONCLUSIONS: Our results showed that lamivudine could reduce both wild-type and precore mutant DHBV levels in the liver through inhibition of the reverse transcription step, but complete elimination of the viruses from liver is difficult even by relatively long-term lamivudine monotherapy, suggesting a need for some additional therapy to obtain complete clearance.

Animals↗

PubMed1999

Recombinant duck interferon gamma inhibits duck hepatitis B virus replication in primary hepatocytes.

Interferon gamma (IFN-gamma), which has been cloned in several mammalian species and recently in birds, plays a critical role in modulating immune system function. IFN-gamma and tumor necrosis factor alpha (TNF-alpha) have been shown to be crucial in the pathogenesis of viral hepatitis and in the transient disappearance of hepatitis B virus (HBV) from the liver after adoptive transfer of HBV-specific cytotoxic T lymphocytes into HBV-transgenic mice. Similar studies in the natural animal hosts of related hepadnaviruses have been limited because the corresponding probes and recombinant cytokines were not available. For this reason, we initiated studies to clone and characterize cytokines from the duck, the natural host of the duck hepatitis B virus (DHBV). We describe here the cDNA cloning and initial characterization of the IFN-gamma homologue of ducks (DuIFN-gamma). The DuIFN-gamma cDNA codes for a predicted mature protein of 145 amino acids with a molecular mass of 16.6 kDa. The precursor protein has 67% identity with the previously cloned chicken IFN-gamma and 21 to 34% identity with mammalian IFN-gamma. Recombinant DuIFN-gamma induces the transcription of several IFN-inducible genes including IFN regulatory factor 1 and guanylate-binding protein, and it exhibits antiviral activity that protects duck cells from vesicular stomatitis virus-mediated lysis. Importantly, treatment of primary duck hepatocytes with recombinant DuIFN-gamma inhibits DHBV replication in a dose-dependent fashion. Time course analysis revealed that IFN-gamma treatment does not affect initial covalently closed circular DNA (cccDNA) conversion but inhibits the synthesis of progeny cccDNA by amplification.

Amino Acid Sequence↗

PubMed1991

[Duck hepatitis B virus DNA in multiple primary cancers and metastatic tumors in duck liver].

Duck hepatitis B virus (DHBV) DNA was detected in both multiple primary cancers and intrahepatic metastatic tumors in duck liver by Southern blot technique. Among 7 ducks with multiple primary tumors in the liver, the banding pattern of integrated DHBV DNA in different tumors was identical in 3 animals but different in 2. One duck showed a similar hybridization pattern in different tumor nodules and the remaining one was negative for DHBV DNA. Integrated DHBV DNA was also identified in one duck with metastatic tumor in the lung, in which the hybridization pattern was the same as that of the primary hepatocellular carcinoma. The presence of the same distinct hybridization bands in various tumor nodules indicated that they may arise from the same clone of neoplastically transformed cell. Different hybridization bands showed that tumors may arise from different clones. The results suggest that hybridization pattern of hepatic carcinoma with viral DNA probe could be used as a clone marker of transformed cells to distinguish multiple primary hepatic cancers from intrahepatic metastasis.

Adenoma, Bile Duct↗

PubMedDate not supplied

Characterisation of the Indian strain of duck hepatitis B virus (DHBV) and development of a carrier duck colony for antiviral drug testing.

Duck hepatitis B virus (DHBV) infected carrier ducks serve as a useful model for testing anti-hepadnavirus drugs. This needs a well characterised duck hepatitis B virus strain. We cloned and sequenced the complete genome of duck hepatitis B virus strain of Indian origin. It was 3021 nucleotides in length and had all the recognisable open reading frames (Polymerase: 20-2530 nucletides, Surface: 693-1787 nucleotides and Core: 2518-412). Using an inoculum of 50 microliters serum containing 1 x 10(11) virus particles/ml, we could infect 80% of one day old ducklings and develop a duck colony.

Animals↗

PubMed1994

Characterization of the antiviral effects of 2' carbodeoxyguanosine in ducks chronically infected with duck hepatitis B virus.

This study was carried out to evaluate benefits and limitations of long-term therapy of hepatitis B virus infections with a nucleoside analog inhibitor of virus replication. The model we used was the domestic duck chronically infected with duck hepatitis B virus by in ovo infection. 2' Carbodeoxyguanosine was used as an inhibitor of viral DNA synthesis. In all animals examined there was a reduction in virus production during therapy. A dose of 2' carbodeoxyguanosine of 10 micrograms/kg every other day reduced the number of infected hepatocytes from greater than 95% to 25% to 50% in less than 3 mo, whereas a 10-fold higher dose produced a decline to less than 10%. Histological evaluation revealed mild to moderate liver injury in ducks receiving the higher dose of 2' carbodeoxyguanosine, suggesting that disappearance of infected hepatocytes may have been accelerated by a toxic effect of the drug. Drug treatment did not completely eliminate duck hepatitis B virus from any duck, and replication was restored in all hepatocytes within a few weeks to several months after antiviral therapy was terminated. Our results suggest that elimination of a chronic infection with a single inhibitor of replication may be difficult in a host that lacks an antiviral immune response capable of eliminating at least a portion of the infected hepatocytes and of ultimately producing antibodies capable of neutralizing residual virus.

Animals↗

PubMed1984

Viral antigen in endocrine cells of the pancreatic islets and adrenal cortex of Pekin ducks infected with duck hepatitis B virus.

Endocrine cells in the pancreas and adrenal glands of duck hepatitis B virus-infected ducks were examined for the presence of viral antigen. Analysis of pancreas tissue was based on double immunofluorescence assays in which anti-duck hepatitis B virus serum was used to detect viral antigen, and anti-glucagon and anti-insulin serum were used, respectively, to identify endocrine alpha and beta cells. Assays of pancreas from infected ducks ranging in age from 3 to 20 weeks indicated that subpopulations of both alpha and beta cells expressed viral antigen. A higher percentage of viral antigen-positive cells was observed in alpha-islets than in beta-islets. As assayed by immunofluorescence and immunoperoxidase staining with anti-viral serum, small clusters of viral antigen-positive cells were detected in the adrenal glands of young infected ducks. These cells were identified as cortical cells on the basis of histologic criteria.

Adrenal Cortex↗

PubMed1976

Duck plague in gnotobiotic ducks.

Four-week-old gnotobiotic and conventional ducks were inoculated orally with duck plague virus. Both groups of ducks died on the third and fourth day after inoculation. Gross and microscopic lesions of duck plague were similar in gnotobiotic and conventional ducks, indicating the synergistic action of species of Salmonella and Pasteurella was not essential for development of lesions.

Administration, Oral↗

PubMedDate not supplied

In vitro incorporation of 1-14C acetate by blood cells of normal ducks and ducks infected with Plasmodium lophurae.

Several investigations have been made, on a qualitative basis, of in vitro incorporation of 1-14C acetate into the lipids of whole blood from normal ducks and ducks infected with Plasmodium lophurae (1,3,4). It was found generally that the percent labeling in blood cells and plasma was higher for infected ducks than for normal ducks. The present study was concerned with quantitative determination of the incorporation of 1-14 C acetate into the lipids of purified erythrocytes (RBC) and leukocytes (WBC) of normal and infected ducks.

Acetates↗

PubMedDate not supplied

Occurrence of duck virus enteritis (duck plague) in Pennsylvania, 1968-74.

During the 7-year period 1968-74 cases of duck virus enteritis (duck plague) were diagnosed in waterfowl in Pennsylvania. Muscovy ducks were affected in 8 cases, geese in 3 cases, and mallard ducks in 1 case. In 5 of these cases either domestic or wild ducks were closely associated with infected waterfowl but were unaffected.

Animals↗

PubMedDate not supplied

Active and passive immunization of ducks against duck viral enteritis.

The newly isolated Sheridan-83 strain of duck enteritis virus (DEV) was apathogenic to ducks. Inoculation of ducks with this virus resulted in the production of antibodies that enabled the ducks to resist challenge with the virulent LA strain of DEV. The minimum protective dose of the Sheridan-83 virus was determined to be less than 10 TCID50. Solid immunity lasted 1-2 months. Passive transfer of antibodies to susceptible ducks also significantly protected them from lethal challenge.

Animals↗

PubMed1998

Biodistribution, stability, and antiviral efficacy of liposome-entrapped phosphorothioate antisense oligodeoxynucleotides in ducks for the treatment of chronic duck hepatitis B virus infection.

This study investigated the feasibility of using liposomes to increase the hepatic delivery and antiviral efficacy of phosphorothioate antisense oligodeoxynucleotides (PS-ODN) for the in vivo treatment of hepatitis B virus (HBV) infection. Ducks infected with duck hepatitis B virus (DHBV) were used as the model. We studied the stability of an antisense PS-ODN in duck plasma, its integrity during the process of liposome entrapment, its in vivo biodistribution, plasma clearance, and excretion. In addition, the intrahepatic distribution of a labeled free and liposome-entrapped ODN was also investigated. The results of our studies show that: 1) phosphorothioate ODN remain stable during the process of liposome entrapment; 2) are stable in duck plasma for many hours; 3) are rapidly cleared from the plasma when injected intravenously; 4) intravenous injection of antisense ODNs entrapped within liposomes enhances delivery of the ODN to the liver; and 5) inhibit DHBV replication. Serum DHBV DNA levels fell rapidly, with a corresponding decrease in intrahepatic viral replicative intermediates at the end of the 5-day study period. Although inhibition of viral replication and a fall in the target protein was observed, a marked inhibition of viral replication was also observed with high doses of a random-sequence ODN. Thus, it is not certain that inhibition of viral replication was entirely through an antisense mechanism. Therefore, liposomes may be effective vehicles to improve the delivery of antisense oligonucleotides to the liver for the therapy of hepatotropic viruses.

Animals↗