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PubMed1983

Establishment and preliminary characterization of a cell line persistently infected with Newcastle disease virus.

A murine osteosarcoma (OGS) cell line was permanently infected with Newcastle disease virus (NDV). The presence of NDV in the subsequent passages was demonstrated by haemadsorption and by immunofluorescence. Compared to the uninfected OGS line the persistently infected cells had a slightly reduced growth rate and they had a reduced sensitivity to several viruses, shown by several different methods. Interferon sensitivity was considerably reduced in the OGS-NDV cells, both the antiviral activity and the cell multiplication inhibitory activity.

Animals↗
PubMed2001

Recombinant Newcastle disease virus as a vaccine vector.

A complete cDNA clone of the Newcastle disease virus (NDV) vaccine strain Hitchner B1 was constructed, and infectious recombinant virus expressing an influenza virus hemagglutinin was generated by reverse genetics. The rescued virus induces a strong humoral antibody response against influenza virus and provides complete protection against a lethal dose of influenza virus challenge in mice, demonstrating the potential of recombinant NDV as a vaccine vector.

Animals↗
PubMed1980

Location of post-translational cleavage events within F and HN glycoproteins of Newcastle disease virus.

The biologically active form of the fusion glycoprotein F from Newcastle disease virus (NDV) comprises two polypeptides, F1 and F2 (derived from a precursor polypeptide F0 by a post translational cleavage event), which are covalently linked together (F1,2) by disulphide bonds. This feature was exploited in a two-dimensional SDS-polyacrylamide gel electrophoretic analysis to orientate the position of the cleavage event within F0. Separation of proteins from NDV-infected CEF in the first dimension in the absence of reducing agent resolved F1,2 protein from all NDV-induced proteins other than F0. Reduction of the first dimension gel with 2-mercaptoethanol, followed by electrophoresis in the second dimension, resolved F1 (55K), F2 (12.5K) and F0 (64K) proteins. The only polypeptides other than F1 and F2 which fell below the diagonal, indicating the positions of the polypeptides from infected cells, were two minor glycoproteins designated HN1 (51.5K) and HN2 (27.5K) which took up positions vertically beneath the major haemagglutinin-neuraminidase glycoprotein HN (75K). Dual isotope labelling experiments with NDV-infected chick embryo fibroblasts, which had previously received a salt shock to effect synchronization of polypeptide initiation upon release of salt shock, revealed the following orientations within the parent molecules: NH2-F2-F1-COOH and NH2-HN1-HN2-COOH. The existence of intermolecular disulphide bonds, orientation and relative lengths of the two NDV HN fragments is analogous to the HA1 and HA2 proteins of influenza virus haemagglutinin.

Animals↗
PubMed1985

Cytochalasin D accelerates the release of Newcastle disease virus from infected cells.

The role of the cellular cytoskeleton in Newcastle disease virus (NDV) infection was explored in two ways. First, the extent of the association of viral proteins with the cytoskeletal fraction of chicken embryo cells was determined. NDV-infected cells, pulse-labelled with [35S]methionine with or without a subsequent chase, were fractionated into Triton X-100-soluble and cytoskeletal fractions. All NDV proteins become associated with the cytoskeletal fraction of cells subsequent to their synthesis. Mixing experiments provided evidence against nonspecific sticking of proteins with this cell fraction. Second, the functional significance of the cytoskeletal association was explored using the inhibitor cytochalasin D. In the presence of this inhibitor, the rate of release of radioactively labelled virions was accelerated 2.5-fold. Colchicine did not significantly alter the rate of virion release. Virus particles released from cytochalasin D-treated cells had the same density as virions released from untreated cells, but were slightly less infectious and contained less actin. These results suggest that functional microfilaments do not play an obligatory role in viral morphogenesis but rather function to slow virus particle release.

Animals↗
PubMed2005

[Construction of minigenome of Newcastle disease virus of goose origin and its preliminary application].

On the base of obtaining the full length genome sequence of a Newcastle disease virus (NDV) isolated from goose, the minigenome was constructed by replacing all the encoding region with the reporter gene of enhanced green fluorescent protein (eGFP), except the virus regulating sequences relating to replication, transcription and packing of virus genome. The reporter gene could be expressed after it was transfected into the HEp-2 cells infected with helper virus of NDV. This result indicated that the minigenome could be translated by the NDV NP, P and L proteins provided by helper virus. Furthermore, the support plasmids expressing NDV NP, P and L protein were constructed respectively and the function of these plasmids was identified using the minigenome. Additionally, the virus rescue system was optimized by changing the infection dose of the recombinant vaccinia virus expressing T7 RNA polymerase. The work mentioned above will accelerate greatly the rescue of NDV and other relative research.

Animals↗
PubMedDate not supplied

Response of congenitally immune chicks to viscerotropic velogenic Newcastle disease virus.

Separate groups of chicks of hen hyperimmune to viscerotropic velogenic Newcastle disease virus (VVNDV) were challenge-exposed to VVNDV by intraocular route at 1 day and 34 days old. Their response was evaluated by clinical symptoms, hemagglutination-inhibition (HI) titers, and virus isolations. Chicks exposed at 1 day old excreted VVNDV from the vent for up to 60 days; their active mean HI titers remained low (10-40); and deaths from VVNDV occurred early (5-16 days) and late (28-55 days). Chicks challenge-exposed at 34 days old excreted virus from the vent for 10 days; active HI titers developed quickly and remained high (891-1177); and deaths and signs of VVNDV occurred early (5-13 days).

Animals↗
PubMed1995

Catecholaminergic transmission in different brain regions of chick during Newcastle disease virus (NDV) infection.

Alterations in the catecholaminergic transmission during Newcastle disease virus (NDV) infection was studied in different brain regions of chick. The results obtained in the present study reveal that the epinephrine, norepinephrine, dopamine and 5-HT were decreased and monoamineoxidase activity was elevated during both the time periods of infection. The chickens after 72 h infection showed more depletion when compared to 24 h, indicating that the catecholaminergic activity was impaired during NDV infection.

Animals↗
PubMed1966

Topography and dynamics of synthesis of structural proteins of Newcastle disease virus.

Zhdanov, Victor M. (The D. I. Ivanovsky Institute of Virology, Moscow, USSR), Nonna B. Azadova, and Leonid V. Uryvayev. Topography and dynamics of synthesis of structural proteins of Newcastle disease virus. J. Bacteriol. 91:1902-1906. 1966.-Newcastle disease virus S and V antigens are synthesized in the cytoplasm, as revealed by the immunofluorescence method. In some experiments, S antigen was found also in the nucleoli. Actinomycin D moderately decreased the titer of infectious virus and V antigen and accelerated the time of appearance of mature virus. Proflavine sharply decreased the synthesis of both antigens and the release of mature virus.

Antigens↗
PubMed1994

Acquisition of pathogenicity of a Newcastle disease virus isolated from a Japanese quail by intracerebral passage in chickens.

Newcastle disease virus (NDV) was isolated from a Japanese quail (Cotornix cotornix japonica). The effect of intracerebral and intranasal passages of the NDV in chickens on the pathogenicity was studied. Pathogenicity of the viruses of different passage levels was compared with that of the original isolate by the mean death time with the minimum lethal dose in chicken embryos, intracerebral pathogenicity index in day-old chicks, intravenous pathogenicity index with 6-week-old chickens and the mortality rates of chickens and quails inoculated intravenously or intranasally. The original isolate from the quail did not kill chickens but only embryos and some one-day-old chicks, exhibiting a mesogenic character. Pathogenicity of the virus of the 10th intranasal passage was not different from that of the original isolate. The viruses passaged intracerebrally, on the other hand, killed chickens of all ages by either route of inoculation, showing a velogenic property. Virus recovery from the blood and the brain was positive only in the chickens infected with brain-passaged viruses by any route of inoculation. Virus titers in the tissues of chickens infected with the brain-passaged viruses were higher than those with the original isolate and the virus of the 10th intranasal passage. These results indicate that the enhanced pathogenicity of the mesogenic NDV isolate from the quail for chickens was induced by acquiring the properties of neurotropism and pantropism through intracerebral passage in chickens.

Animals↗
PubMed1981

The in vitro effects of Newcastle disease virus on the metabolic and antibacterial functions of human neutrophils.

Live Newcastle disease virus (NDV) was used to investigate the in vitro effects of a viral infection on phagocytosis, chemiluminescence generation, superoxide production, oxygen consumption, NADPH-oxidase activity, and intracellular killing of bacteria by Ficoll-Hypaque separated human neutrophils. Phagocytosis of oil red O particles by NDV-treated PMN was inhibited by 50%. Chemiluminescence by PMN was inhibited 79% after zymosan stimulation and 86% after tetradeconyl phorbol acetate stimulation. Superoxide generation was inhibited by 68%. Oxygen consumption was inhibited in the presence of NDV by 37% after stimulation with phorbol myristate acetate, while membrane-associated NADPH-enzyme activity was decreased by 19%. The percent of surviving intracellular S. aureus was significantly elevated in NDV-treated PMN after 60 and 120 min of incubation. Purified bacterial neuraminidase markedly suppressed chemiluminescence, while neuraminic acid blocked the effects of the virus. These observations suggest that infections with myxoviruses may suppress a number of vital neutrophil functions. It appears that the effects may be partly mediated by the interaction of viral neuraminidase with the external neutrophil membrane.

Adult↗
PubMedDate not supplied

Serological and pathological studies of Newcastle disease viruses isolated from caged birds from Southeast Asia.

Eleven isolates of Newcastle disease virus (NDV), from caged birds imported from or captured in Southeast Asia in 1979-80, were antigenically divided into five distinct groups. Most of them were distinguishable from more classical NDVs (vaccine B1 strain and Miyadera strain) on the basis of their reactivity to eight monoclonal antibodies against the HN molecule of NDV in hemagglutination-inhibition tests. However, when three representative isolates were evaluated for their biological properties and pathogenicity against 1-day-old chickens, all three were found to be velogenic types that could induce serious symptoms of Newcastle disease and which eventually killed all of the chickens, regardless of the route of infection. There was not any significant correlation between their reactivity patterns with the monoclonal antibodies and their virulence.

Animals↗
PubMed2006

[Characterization of a recombinant Listeria monocytogenes strain containing the fusion protein gene of Newcastle disease virus].

Homologous recombination was utilized for construction of a recombinant strain of L. monocytogenes carrying a gene from the Newcastle diseases virus by insertional mutation targeting its listeriolysin O gene (hly). The gene encoding fusion protein of the Newcastle disease virus (NDV-F) was used as the model heterologous gene. The F gene was inserted into hly downstream to its promoter and signal sequence by overlapping extension polymerase chain reaction, which was then subcloned into the shuttle plasmid pKSV7 for allelic exchange with L. monocytogenes chromosome. PCR amplification of the target genes indicated insertion of the F gene into the chromosome DNA of L. monocytogenes. RT-PCR showed transcription of F gene from the recombinant L. monocytogenes strain. Comparisons were then made between the recombinant strain and its wild parent strain in terms of the hemolytic activity, adhesion and invasiveness to cultured HeLa cells, virulence to mice and chicken embryos, and growth kinetics in broth medium as well as its stability upon repeated subculturing and serial passages in mice. The recombinant L. monocytogenes lost its hemolytic activity on the blood agar and had no hemolytic titer from its culture supernatants as compared with the titer of 24 in the supernatant from the wild parent strain. The recombinant strain also had lower adhesiveness (P > 0.05) and significantly lower relative invasiveness to the HeLa cells than its wild type strain (P < 0.05). Such insertional mutation resulted in reduced virulence, about 3.7 logs and 6.5 logs less than its parent strain L. monocytogenes 10403S as shown by the 50% lethal dose assays in the mouse and chicken embryonated egg models respectively. The recombinant strain was relatively stable as shown by amplification of the target gene NDV-F from its genomic DNA after subculturing in BHI broth or in mice for 5 times.

Animals↗
PubMed2005

Molecular characterization of virulent Newcastle disease virus isolates from chickens during the 1998 NDV outbreak in Kazakhstan.

Newcastle disease virus (NDV) infects domesticated and wild birds throughout the world and has the possibility to cause outbreaks in chicken flocks in future. To assess the evolutionary characteristics of 10 NDV strains isolated from chickens in Kazakhstan during 1998 we investigated the phylogenetic relationships among these viruses and viruses described previously. For genotyping, fusion (F) gene phylogenetic analysis (nucleotide number 47-421) was performed using sequences of Kazakhstanian isolates as compared to sequences of selected NDV strains from GenBank. Phylogenetic analysis showed that all newly characterized strains belonged to the genetic group designated as VIIb. All strains possessed a virulent fusion cleavage site (RRQRR/F) belonging to velogenic or mesogenic pathotypes with intracerebral pathogenicity indexes (ICPI) varying from 1.05 to 1.87.

Amino Acid Sequence↗
PubMed1982

UV irradiation analysis of complementation between, and replication of, RNA-negative temperature-sensitive mutants of Newcastle disease virus.

Random UV irradiation-induced lesions destroy the infectivity of Newcastle disease virus (NDV) by blocking downstream transcription from the single viral promoter. The nucleocapsid-associated polypeptides most likely to be involved in RNA synthesis are located at the extreme ends of the genome: NP and P are promoter proximal genes, and L is the most distal gene. We attempted to order the two temperature-sensitive (ts) RNA-negative (RNA-) mutant groups of NDV by determining the UV target sizes for the complementing abilities of mutants A1 and E1. After UV irradiation, E1 was unable to complement A1, a result compatible with the A mutation lying in the L gene. In contrast, after UV irradiation, A1 was able to complement E1 for both virus production and viral protein synthesis, with a target size most consistent with the E mutation lying in the P gene. UV-irradiated virus was unable to replicate as indicated by its absence in the yields of multiply infected cells, either as infectious virus or as particles with complementing activity. After irradiation, ts mutant B1 delta P, with a non-ts mutation affecting the electrophoretic mobility of the P protein, complemented E1 in a manner similar to A1, but it did not amplify the expression of delta P in infected cells. This too is consistent with irradiated virus being unable to replicate despite the presence of the components needed for replication of E1. At high UV doses, A1 was able to complement E1 in a different, UV-resistant manner, probably by direct donation of input polypeptides. Multiplicity reactivation has previously been observed at high-multiplicity infection by UV-irradiation paramyxoviruses. In this case, virions which are noninfectious because they lack a protein component may be activated by a protein from irradiation virions.

Genes, Viral↗
PubMed1982

The serological response of chickens to oil emulsion vaccines containing the V4 strain of Newcastle disease virus.

Experiments were conducted with vaccines containing the V4 strain of Newcastle disease virus (NDV). Both living aqueous vaccines and vaccines consisting of virus incorporated oil emulsion were used. The calculated dose of virus contained in the oil emulsion vaccine was 10(8.7) 50% embryo infectious doses (EID50) per bird dose. Haemagglutinin inhibition (HI) antibody levels of 8 are presumed protective. One-day-old chicks with low levels of maternal antibody were vaccinated intraocularly with 10(6.3)EID50 ol live vaccine, and concurrently with oil emulsion vaccine. Presumed protective levels of antibody were present at two weeks post vaccination and were maintained for at least seven weeks longer. When adult birds 15 weeks old with no previous exposure to NDV were vaccinated intraocularly with 10(6.7)EID50 per bird, protective levels of antibody were produced within a week. Unvaccinated birds put in contact with the vaccinated birds produced similar antibody levels within 14 days. Revaccination with oil emulsion vaccine after antibody levels had fallen resulted in a rapid response with high levels of antibody. When antibody-free adult commercial birds with an unknown history of exposure to NDV were vaccinated intramuscularly with oil emulsion vaccine, high antibody levels were produced for at least 21 weeks. Concurrent intraocular inoculation with 10(7.0)EID50 live virus did not enhance the response. Natural infection of unvaccinated birds occurred during the experiment. This was detected by the presence of HI antibody levels of short duration. When antibody-free commercial birds were inoculated intramuscularly with oil emulsion vaccine containing 10(6.0), 10(7.0), or 10(8.0)EID50 per bird dose, 100% of birds inoculated with the highest dose produced presumed protective levels of antibody within two weeks, as compared with a 5-week delay when using the 10(7.0)EID50 per bird dose.

Animals↗
PubMedDate not supplied

Hemagglutinating and fusogenic activities of Newcastle disease virus: studies on receptor binding specificity and pH-induced conformational changes.

Vaccinal and wild strains of Newcastle Disease virus (NDV) were analyzed for cell receptor binding and fusogenic biological properties associated with their HN (hemagglutinin-neuraminidase) and F (fusion protein) surface structures respectively. The evaluation of the biological activities of HN and F was carried out respectively by determination of hemagglutinating titers and hemolysis percentages, using erythrocytes from various animal origins at different pH values. Significant differences in hemagglutination titers for some strains of NDV were detected, when interacting with goose, sheep, guinea-pig and human "O" group erythrocytes at neutral pH. Diversity of hemolysis percentages was observed between different NDV strains at acid pH. These analysis were developed to evaluate particular aspects of the actual influence of the receptor specificity and pH on the receptor binding and fusogenic processes of Newcastle Disease viruses.

Animals↗
PubMed2006

Molecular epidemiological analysis of Newcastle disease virus isolated in China in 2005.

Eighty-three strains of Newcastle disease virus (NDV) were obtained from outbreaks in chickens, pigeons, geese, and ducks in China in 2005 and characterized genotypically. The main functional region of the F gene (535 nucleotides) was amplified and sequenced. A phylogenetic tree based on nucleotides 47-435 of the F gene was created using sequences from 83 isolates and representative NDV sequences obtained from GenBank. Phylogenetic analysis showed that all newly characterized strains belonged to six genetic groups: I, II, III, VIb, VIIc, and VIId. All the isolates belonging to groups I and II (14 total) were lentogenic according to the amino acid sequences of the fusion protein cleavage site, and either V4 or LaSota-type, depending on the vaccines that were used. Most isolates (64 total) were classified in group VIId, a predominant genotype responsible for most Newcastle disease outbreaks since the end of the last century. One strain, NDV05-055, was in group VIIc, three pigeon strains were in group VIb, and one isolate, NDV05-041, was in group III, and characterized as a velogenic strain. This study revealed that genotype VIId was the major NDV strain responsible for the 2005 ND epizoonosis that occurred in China.

Animals↗
PubMed1995

The Newcastle disease virus V protein binds zinc.

The V protein of Newcastle disease virus (NDV) is produced by the insertion of a single nontemplated G residue at a specific point during transcription of the phosphoprotein (P) gene, accessing a new reading frame upon translation. The V protein, in common with its counterpart in other paramyxoviruses contains a highly cysteine rich motif near the carboxyl terminus, suggestive of a zinc-binding domain. By constructing E. coli overexpression plasmids for the NDV P and V proteins, and monitoring the binding of 65ZnCl2 to proteins electroblotted onto nitrocellulose membranes, we have demonstrated that the V protein strongly binds zinc.

Animals↗