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PubMedDate not supplied

Immunization of broiler breeder chickens against Newcastle disease with an oil-emulsion vaccine.

Antibody response was rapid and high in broiler breeder chickens receiving 1 or 2 vaccinations with oil-emulsion vaccine against Newcastle disease at 23 or at 23 and 26 weeks old. The antibody titers remained high during the 41-week experimental period. At 64 weeks old, about 41 weeks after vaccination, the geometric mean hemagglutination-inhibition antibody titer was 67 from the single vaccination, and 103 from the double vaccination. The immune response to live-virus vaccine given at 2, 9, 20, 30, 42, or 54 weeks of age via the drinking water was high, but uniformity was lacking in the antibody response in the breeders and maternal antibody response in the progeny. Maternal antibody levels in one-day-old chicks were related to the titers of antibody in the dams. Maternal antibody titers of chicks originated from breeder flocks that were vaccinated with the oil-emulsion vaccine remained high for all hatches.

Administration, Oral↗
PubMed1989

Newcastle disease virus evolution. I. Multiple lineages defined by sequence variability of the hemagglutinin-neuraminidase gene.

We compared the hemagglutinin-neuraminidase gene sequence among 13 strains of Newcastle disease virus (NDV) isolated over the last 50 years. Although overall homology was remarkably high, the sequence variability demonstrated the existence of at least three distinct lineages, which must have co-circulated for considerable periods. The sequence variability also appears to reflect some accumulation of mutations over time. Strictly correlating with the lineages, the translation products could be classified into three size classes. One class lacked the interchain disulfide bond, and another represented unusual precursor protein of biologically inactive form. The lineages correlated to some extent with virulence and place of isolation of the strains. However, antigenic variations, which were neither cumulative nor progressive, did not correlate with the lineages. These analyses showing multiple lineages were greatly facilitated by a precise calculation of synonymous substitutions, which had been largely free from selective pressures and had occurred frequently and evenly throughout the coding region.

Amino Acid Sequence↗
PubMedDate not supplied

Isolation of a monoclonal antibody with specificity for commonly employed vaccine strains of Newcastle disease virus.

A monoclonal antibody, AVS-I, was produced from a hybridization of murine myeloma cells and splenocytes from mice immunized with the La Sota strain of Newcastle disease virus (NDV). The hybridoma producing AVS-I, selected from 184 NDV-positive supernatants, is one of two supernatants that reacted exclusively with lentogenic strains in an indirect enzyme-linked immunosorbent assay. AVS-I can also be assayed by hemagglutination-inhibition (HI), which was used to test selected reference avian paramyxovirus (PMV) strains of types 1 to 3. NDV vaccines La Sota and B1 and field isolates from chickens, turkeys, pigeons, and cockatoos were also used as antigens. AVS-I had a high binding affinity for all La Sota and B1 strains, including vaccines. The antibody bound with a lower titer to the Australian Queensland V4 and Ulster strains, but it did not bind to the F strain, a lentogenic strain from England. AVS-I was HI-negative against the other PMV reference strains. AVS-I may be valuable for identifying field isolates antigenically similar to La Sota and B1 and rapidly differentiate those vaccine strains from more virulent viruses.

Antibodies, Monoclonal↗
PubMed1995

Antiviral action of interferon-beta on Newcastle disease virus: selectivity to the hemagglutinin-neuraminidase gene expression.

Interferon-beta (IFN-beta) strongly inhibited the expression of the hemagglutinin-neuraminidase (HN) gene of Newcastle disease virus (NDV), a paramyxovirus, in HeLa cells under the conditions where it did not affect the expression of the four upstream genes encoding the nucleocapsid protein, phosphoprotein, membrane protein and fusion protein. Even the downstream gene, encoding the large protein as well as the genome replication, appeared to be less susceptible to IFN-beta than the HN gene. This selective action of IFN-beta did not appear to be attributable to its well characterized antiviral mechanisms such as acceleration of RNA decay and translation inhibition. No similar down-regulation of a particular gene expression was found with another paramyxovirus, Sendai virus, or with a rhabdovirus, vesicular stomatitis virus, or seems to have been reported previously with any negative-strand RNA viruses. This new effect of IFN-beta thus suggests gene expression mechanism unique to NDV and may further lead to the discovery of a novel biochemical effect of IFN-beta.

Animals↗
PubMed1994

Characterization of Newcastle disease virus envelope glycoproteins expressed in insect cells.

Recombinant baculoviruses carrying cDNAs of hemagglutinin-neuraminidase (HN) and fusion (F) glycoprotein genes of virulent and avirulent strains of Newcastle disease virus (NDV) were constructed to examine the contribution of the individual proteins in cell fusion. F proteins of both virulent and avirulent strains expressed by the recombinant viruses were glycosylated and translocated onto the cell surfaces and only the F protein of the virulent origin was proteolytically cleaved into F1 and F2 subunits and bound intermolecularly by disulfide bonds. HN proteins of virulent and avirulent strains expressed by the recombinant viruses showed both hemadsorption and neuraminidase activities. Single infection of the recombinant baculoviruses could not induce cell fusion; however, co-infection with the recombinant viruses of the F protein of virulent strain and HN protein of both strains gave clear syncytia in insect cells. The syncytium formation was much clearer in the cells co-infected with the recombinants of F protein of virulent strain and the HN protein of avirulent strain in comparison with those co-infected with F and HN recombinant viruses of virulent origin. The cell fusion was completely blocked by monoclonal antibodies against the F protein but not by those to the HN protein.

Animals↗
PubMed1986

Genetic variation within a neutralizing domain on the haemagglutinin-neuraminidase glycoprotein of Newcastle disease virus.

Previously, a panel of monoclonal antibodies recognizing epitopes in four antigenic sites on the haemagglutinin-neuraminidase (HN) glycoprotein of the Australia-Victoria strain of Newcastle disease virus were used in strain comparisons. Epitopes in three sites were found to be conserved while the epitope recognized by the single antibody to site 3 was not. A new panel of antibodies is described, two of which bind to epitopes in site 3 and six of which bind to a site (site 1,4) that overlaps with sites 1 and 4 as determined by analyses of variants, temperature-sensitive mutants, and strains by assays of neutralization of infectivity and binding in a radioimmunoassay. Neutralization of heterologous strains with the panel of antibodies revealed that both new site 3 epitopes are also highly divergent, while three additional epitopes outside site 3 (those in site 1,4) are highly conserved. The new site 3 antibodies can bind to virions of several heterologous strains without neutralizing infectivity. Thus, of the 10 epitopes we have now examined, all of three in site 3 are specific with respect to neutralization of infectivity for the homologous strain, while all of seven in other sites are conserved in heterologous strains. This suggests that the strain specificity originally described for a single site 3 epitope is, instead, a property of a much more extensive, poorly conserved domain on the HN molecule.

Antibodies, Monoclonal↗
PubMed1986

Molecular cloning of complementary DNA to Newcastle disease virus, and nucleotide sequence analysis of the junction between the genes encoding the haemagglutinin-neuraminidase and the large protein.

Complementary DNA clones to 90% of the Newcastle disease virus (NDV) genome have been produced and mapped. These clones cover the entire HN, F and M genes, most if not all of the L gene and parts of the NP and P genes. The map of overlapping clones gives the gene order 3'-NP-P-M-F-HN-L-5' for NDV, identical to the gene order of Sendai virus, on the assumption that the NP gene of NDV is at the 3' end of the genome as previously suggested by inactivation of NDV transcription by u.v. light. The nucleotide sequence of 453 bases covering the junction between the HN and L genes has been determined. There is nucleotide sequence homology to the consensus polyadenylation and mRNA start sites of Sendai virus and vesicular stomatitis virus. The deduced amino acid sequence of the C terminus of the HN protein of NDV shows homology to the C-terminal amino acid sequences of the HN proteins of simian virus 5 and Sendai virus. An explanation for the presence of HN0, the precursor to HN in some strains of NDV, is suggested by the presence of a long non-coding region at the 3' terminus of the mRNA encoding the HN protein of NDV that could, by mutation, allow synthesis of a larger polypeptide.

Base Sequence↗