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At least 19 recordsLinked to original sources
PubMed1976

Oral immunization of ducklings with attenuated duck hepatitis virus.

Duck hepatitis, a highly fatal disease of ducklings, must be controlled in successful commercial duck enterprises. Several procedures which have been effective in controlling the disease are 1) vaccination of adult breeders with passive transfer of antibodies through the yolk to the duckling, 2) administration of antisera to ducklings at the onset of signs of disease, and 3) parenteral vaccination of ducklings with attenuated DH virus after the loss of passive immunity. However, in each of these procedures, some losses usually occur and the administration of antiserum or vaccine to 2- to 3-week-old ducklings is costly and involves physical stress. Experimental studies of oral immunization in ducklings from immunized and nonimmunized parents were conducted to determine the feasibility of a convenient control program with little stress to the ducklings. Ducklings immunized with attenuated live duck hepatitis virus by intramuscular method, oral instillation, and through the drinking water were challenged with virulent duck hepatitis virus either intramuscularly or orally. Intramuscular, oral instillation, and drinking water application all provided adequate protection on challenge with virulent virus. Rise in neutralizing antibody was detected following immunization especially in sera of ducklings from nonimmunized parents. On the basis of successful experimental results, over 350,000 ducklings from immunized parents on a commercial farm have been sucessfully vaccinated by the drinking water method.

Administration, Intranasal↗
PubMedDate not supplied

Effect of experimental duck virus hepatitis infection on some biochemical constituents and enzymes in the serum of white Pekin ducklings.

Experimental duck virus hepatitis infection of 11-day-old white Pekin ducklings having specific maternal antibodies revealed significant changes in some biochemical constituents and enzymes of the serum during the 3 weeks following exposure. These changes included a marked decrease in the total proteins and the albumin fraction, together with a significant elevation in levels of alkaline phosphatase, glutamic pyruvic transaminase, bilirubin, and creatinine. Most of these changes were attributed primarily to a deranged liver function associated with duck virus hepatitis infection.

Alanine Transaminase↗
PubMed1978

Active immunisation of ducklings against duck virus hepatitis.

Egg-attenuated duck hepatitis type (Rispens H55) was exhaustively tested as a potential vaccine under controlled conditions in ducklings fully susceptible to the disease at day 2 after hatching. Data are presented which indicate that this vaccine fulfils essential criteria of efficacy in terms of (a) the optimal age at which successful vaccination is practicable (day 2 or earlier), (b) the rapidity of onset of immunity (in 48 to 72 hours), (c) the high level of immunity induced (88.0 to 94.0 per cent), (d) the persistence of this degree of immunity in the individual bird throughout the period when it would otherwise be at risk (until the end of the fourth week of life) and (e) the consistency of the effects of the vaccine in successive groups of ducklings hatched over a four year period. Employed as a vaccine. H55 was completely innocuous to the vaccinated ducklings under laboratory conditions.

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↗
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↗
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↗
PubMedDate not supplied

Humoral immune response of the duck to duck hepatitis virus: virus-neutralizing vs. virus-precipitating antibodies.

Ducks were induced to develop high-level duck hepatitis virus (DHV)-neutralizing antibodies by inculation with a chicken-embryo-adapted DHV via subcutaneous, intramuscular, and intratracheal routes. Administration of the DHV orally in a gelatin capsule failed to stimulate immune response in the ducks. Contact controls of these ducks also remained negative for anti-DHV antibodies. These observations indicated that the DHV administered orally, in gelatin capsule, failed to infect the ducks. None of numerous duck anti-DHV immune sera, with virus-neutralizing activity in the range of 1.8 to 5.57 log10 median- embryo-infective-dose (EID50) neutralization index, developed precipitin lines against a variety of DHV preparations tested in low- and high-ionic-strength agar. The results suggest that the agar-gel immunodiffusion test is unsuitable for serologic testing of duck sera for anti-DHV antibody activity. Virus-neutralizing activity was revealed in both immunoglobulin M (IgM) and IgG classes of sera of actively immunized ducks. Immunodiffusion tests of Sephadex G-200 fractions of 1-day-old duckling sera with monospecific rabbit anti-duck IgM (DIgM) serum failed to detect DIgM. These results demonstrated that the IgM is not being transferred from the dam to the newly hatched ducklings. Seven- and 14-day-old ducks had DIgM in their sera. However, this IgM had no DHV-neutralizing activity, indicating that it was newly developed by the ducklings, which had no active DHV immune response, not having been exposed to DHV.

Animals↗
PubMed1977

Correlation of induced drug metabolism with titer of duck hepatitis virus in chickens.

While chickens infected with duck hepatitis virus showed no signs of clinical illness, their levels of hepatic cytochrome P-450 in response to phenobarbital induction and their microsomal aryl hydrocarbon hydroxylase activities in response to 3-methylcholanthrene induction were each found to correlate with the titer of virus recovered from the livers. These clear correlations indicate that avian hepatic drug metabolism is significantly modified during viral infection.

Animals↗
PubMed1977

Duck virus hepatitis.

The present report gives a survey of the occurrence in Denmark of DVH, its symptoms,the course of the disease, transmission of infection and the posibilities of prevention and control. As it appears from Figs. 2 and 3, DVH can cause considerable losses for the individual producers, for whom it is difficult to safeguard themselves against new infections because of the resistance and stability of the DVH virus in infected premises. Three possibilities of controlling DVH are pointed out: isolation of the flocks, serum therapy and vaccination.

Acute Disease↗