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PubMed1986

Nucleotide sequence analysis of the haemagglutinin-neuraminidase gene of Newcastle disease virus.

The nucleotide sequence of the haemagglutinin-neuraminidase (HN) gene of Newcastle disease virus (NDV) has been determined. The HN gene is 2031 nucleotides long, approximately 13.5% of the viral genome. The nucleotide sequence contains a single long open reading frame which would encode a protein of 577 amino acids, with a mol. wt. of 63,149. This is in good agreement with estimates of the molecular weight of the unglycosylated HN protein. Analysis of the amino acid sequence reveals six potential glycosylation sites and shows the major hydrophobic region to be close to the N terminus. This provides evidence for the N-terminal attachment of HN to the viral membrane. The hydrophilic nature of the extreme N-terminal amino acids suggests the absence of a cleaved signal sequence. Analysis of the long non-coding region at the 3' end of the mRNA encoded by the HN gene of NDV suggests a possible explanation for the origin of HN0 in extremely avirulent strains of NDV. There are regions of high homology between the deduced amino acid sequence of the NDV HN glycoprotein and the HN glycoproteins of two other paramyxoviruses, Sendai virus and simian virus 5 (SV5). An alignment of the HN amino acid sequences of these viruses shows 32% of amino acid residues are conserved between NDV and SV5, and 23% between NDV and Sendai virus. In contrast, only very limited homology is found between NDV HN and the influenza virus glycoproteins.

Amino Acid Sequence↗
PubMed2005

Identification and subgrouping of pigeon type Newcastle disease virus strains by restriction enzyme cleavage site analysis.

A host variant of Newcastle disease virus (NDV, genus Avulavirus, family Paramyxoviridae) is responsible for an autonomous disease in pigeons. It emerged in the late 1970s in the Mediterranean region. Despite great genetic diversity the vast majority of strains belong to a monophyletic group (sublineage VIb) within genotype VI of NDV strains that were indigenous in the region at that time. To date only a monoclonal antibody assay is available for the specific identification of pigeon type strains. A specific genetic assay is described suitable for the identification of pigeon isolates. Cleavage site analysis of a 1349 bp amplicon of the fusion protein gene was carried out using restriction enzymes (RE) HinfI, BstOI and RsaI. RE analysis of over 100 strains isolated between 1978 and 2002 deriving from 16 countries has revealed nine RE-patterns, which were progressive site variants of the parental (group VI) genotype. In spite of substantial site variation, extant pigeon viruses lacked a BstOI cleavage site at nucleotide 1601 shared by other NDV strains of chicken origin. RE analysis is a simple and reliable method both for the identification and subgrouping of pigeon type viruses.

Animals↗
PubMed1998

Phylogenetic relationships among highly virulent Newcastle disease virus isolates obtained from exotic birds and poultry from 1989 to 1996.

Newcastle disease virus [NDV (avian paramyxovirus type 1 [APMV1])] isolates were recovered from imported exotic birds confiscated following importation into the United States, from waterbirds in the United States, and from poultry. The exotic birds probably originated from Central and South America, Asia, and Africa. The NDV isolates were initially characterized as highly virulent because of a short mean death time in embryonated chicken eggs. The isolates were typed as neurotropic or viscerotropic velogenic by intracloacal inoculation of adult chickens. Intracerebral pathogenicity index values for the virulent NDV isolates ranged from 1.54 to 1.90, compared to a possible maximum value of 2.0. These isolates had a dibasic amino acid motif in the fusion protein cleavage site sequence required for host systemic replication. Sequence differences were detected surrounding the fusion protein cleavage site and the matrix protein nuclear localization signal, indicating evolution of highly virulent NDV. Phylogenetically, these isolates were categorized with other highly virulent NDV strains that caused outbreaks in southern California poultry during 1972 and in cormorants in the north central United States and southern Canada during 1990 and 1992. These isolates are related to NDV that may have the APMV1 strain chicken/Australia/AV/32 or a related virus as a possible progenitor. Recent virulent NDV isolates and those recovered during disease outbreaks since the 1970s are phylogenetically distinct from current vaccine viruses and standard challenge strains.

Animals↗
PubMed2002

Generation of velogenic Newcastle disease viruses from a nonpathogenic waterfowl isolate by passaging in chickens.

A benign Newcastle disease virus (NDV) recently became highly virulent during replication in domestic chickens. It is still unclear whether NDVs circulating among wild waterfowl also have the potential to become highly pathogenic (velogenic) in chickens. To demonstrate experimentally the generation of velogenic NDV from a nonpathogenic waterfowl isolate, we passaged an avirulent goose isolate in chickens. After nine consecutive passages by air-sac inoculation, followed by five passages in chick brain, the virus became highly virulent in chickens, producing a 100% mortality rate, and demonstrating typical velogenic properties in pathogenicity tests. Sequence analysis at the fusion protein cleavage site showed that the original isolate contained the typical avirulent type sequence, E-R-Q-E-R/L, which progressed incrementally to a typical virulent type, K-R-Q-K-R/F, during repeated passage in chickens. These results demonstrate that avirulent viruses, maintained in wild waterfowl in nature and bearing the consensus avirulent type sequence, have the potential to become velogenic after transmission to and circulation in chicken populations. The results also suggest that chickens provide a mechanism for the selection of virulent viruses from an avirulent background.

Animals↗
PubMed1981

The correlation of fatty acid content of infected cells and virions with Newcastle disease virus (NDV) virulence.

Chick embryo fibroblasts (CEF) infected with virulent strains of Newcastle disease virus (NDV) showed a dramatic increase in total unsaturated fatty acids (UFA). This increase was not seen in cells infected with the avirulent strains of NDV, Sendai virus or influenza A (PR8). The virions of the virulent strains of NDV harvested from the chorioallantoic cavity also had a higher UFA content compared to the avirulent ones. The kinetics of UFA increase in the virulent strains could be correlated with published data on the kinetics of RNA and protein synthesis inhibition, polykaryon formation and membrane permeability changes.

Animals↗
PubMed1981

Hydrolysis of ribonucleoside 2',3'-cyclic phosphates by influenza and Newcastle disease viruses.

Two enzymatic activities hydrolysing ribonucleoside 2', 3'-cyclic phosphates (2', 3'-cNMP) to 2'- or 3'- nucleoside monophosphate were found associated with influenza and Newcastle disease viruses. The two enzymatic activities differed from each other by temperature optima and thermoresistance. 2', 3'-Cyclic nucleotide 3'-phosphohydrolase was responsible for splitting of the substrate to 2'-NMP. Splitting of the substrate to 3'-NMP was due either to ribonuclease or to 2', 3'-cyclic nucleotide 2'-phosphohydrolase.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1977

An electron microscopic study of MDBK cells persistently infected with Newcastle disease virus.

Ultrastructural examination of a line of MDBK cells persistently infected with Newcastle disease virus (MDBKpi cells) revealed the presence of cytoplasmic aggregates of both smooth and granular nucleocapsids. Only granular nucleocapsids aligned under modified areas of plasma membrane and were incorporated into virus particles. On the grounds of morphogenesis, there was no apparent explanation for the persistent, not-cytocidal nature of the infection. Both nuclear and cytoplasmic aggregates of smooth nucleocapsids were present in MDBKpi cells which had been held without subculture for between 40 and 130 days (aged MDBKpi cells). Modified areas of plasma membrane with associated alignment of nucleocapsids were not present in aged MDBKpi cells, and neither budding nor released virus particles were observed, indicating a block in virus maturation. It is suggested that the granular material coating granular nucleocapsids allows them to interact with modified areas of plasma membrane, thereby inducing virus budding. A deficiency of this material, as apparently occurs in aged MDBKpi cells, would therefore cause a block in virus maturation. The nature of this granular material is discussed, and we suggest that it consists of M protein.

Animals↗
PubMed1979

Isolation and characterization of heat-resistant (HR) mutants of Newcastle disease virus.

Heat-resistant (HR) mutants (MR 70 and HR 74) of Newcastle disease virus (NDV) which exhibited significantly higher thermostability in their infectivity than wild-type virus were isolated and characterized. They differ from each other in their plaque morphology; HR 70 produces small turbid plaques, whereas those of HR 74 are large and clear. Cytopathogenicity of these mutants is much lower than that of the wild-type virus in cultured cells such as CEF, LLCMK2 and HeLa cells. Moreover, these HR mutants exhibited extended mean embryo survival times. Synthesis of cellular RNA's and proteins in cells infected with HR mutants was not significantly reduced under conditions in which synthesis of these macromolecules was strongly reduced in cells infected with wild-type virus. No significant differences were observed between HR mutants and wild-type virus in their other phenotypic characteristics such as the capacity for interferon production, growth characteristics at a low multiplicity of infection, and cleavage of viral glycoproteins in infected cells. From these findings, it was suggested that the inhibitory effect of virus infection on cellular macromolecular synthesis is a possible determinant of cytopathogenicity of NDV.

Animals↗
PubMed1986

Avidity of IgG antibodies against mumps, parainfluenza 2 and Newcastle disease viruses after mumps infection.

Paired serum samples from 39 patients with recent mumps infection were assayed for IgG antibodies against mumps, parainfluenza 2 and Newcastle disease virus (NDV). A modified enzyme immunoassay was used, giving separate estimates of high avidity antibodies (EHAA) and total specific antibodies (ETSA). A marked cross-reaction was seen between mumps and parainfluenza 2 virus, with changes of ETSA between paired samples of about the same magnitude against both these viruses. The mean change of EHAA against mumps was, however, significantly greater than that against parainfluenza 2. There were 16 patients who had a change of ETSA greater against parainfluenza 2 than against mumps. When the EHAA responses were compared, there were only 8 such patients. The responses against NDV were negligible. Estimation of antibody avidity, even by the arbitrary method used, can distinguish between homotypic and cross-reactive heterotypic antibodies after mumps infection. The implications for expressing the results of enzyme immunoassay are discussed.

Adolescent↗
PubMed2000

Newcastle disease virus (NDV): brief history of its oncolytic strains.

BACKGROUND: While genetically engineered viruses are now being tested for the virus therapy of human cancers, some naturally occurring viruses display unmatched oncolytic activity. Newcastle disease virus (NDV) excels as an oncolytic agent. OBJECTIVES: As its virulence versus attenuation can be explained on molecular biological bases, it may be possible to develop or select highly oncolytic strains of NDV without adverse toxicity. STUDY DESIGN: Questions are posed as to the mechanisms of viral oncolysis, the appropriateness of tests to predict oncolytic activity of a given NDV strain and the best modes of administration for oncolytic effects. Answers are provided based on specific data or on considerations drawn from experience (the authors use NDV oncolysates to immunize against melanoma and kidney carcinoma) or from analogous clinical situations (therapeutic use of mumps or measles viruses). RESULTS AND CONCLUSIONS: NDV oncolysates probably suit better for immunotherapy (providing also active tumor-specific immunization) than massive repeated inoculations of NDV strains, especially when the NDV strain used is not proven to be oncolytic by appropriate pre-clinical tests.

Antigens, Viral↗
PubMed1990

Serum protease inhibitor abrogation of Newcastle disease virus enhancement of cytolysis by recombinant tumor necrosis factors alpha and beta.

Newcastle disease virus (NDV) has been used to induce regression of tumors in human cancer patients. We recently demonstrated that human malignant melanoma cells resistant to the lytic effects of tumor necrosis factor-alpha (TNF-alpha) become susceptible after treatment with NDV. We examined the effects of a serine protease inhibitor, N-1-tosylamide-2-phenyl-ethyl-chloromethyl ketone (TPCK), on viral enhancement of TNF cytotoxicity. Virulent NDV (but neither heat- nor UV-inactivated NDV) induced a 100-fold increase in the sensitivity of murine fibroblast L929 cells to recombinant human TNF-alpha (rHuTNF-alpha), rHuTNF-beta, and recombinant murine TNF-alpha (rMuTNF-alpha). TPCK, which is an inhibitor of chymotrypsin-like proteases, blocked between 42% and 93% of the cytolytic activity of rMuTNF-alpha, rHuTNF-alpha, and rHuTNF-beta toward NDV-treated L929 cells. Similarly, TPCK abrogated 62% of the cytotoxicity of rMuTNF-alpha toward dactinomycin-treated L929 cells. In contrast, TPCK had no effect on WEHI 164 clone 13 cells, a murine fibrosarcoma cell line that is much more sensitive to the lytic effects of TNF and does not show enhanced sensitivity to TNF after treatment with either NDV or dactinomycin. These results suggest a role for a cellular protease in the mechanism by which some viruses sensitize tumor cells to the cytolytic activity of TNF.

Amino Acid Chloromethyl Ketones↗
PubMed1979

Local antibody response in chickens: analysis of antibody synthesis to Newcastle disease virus by solid-phase radioimmunoassay and immunofluorescence with class-specific antibody for chicken immunoglobulins.

The antibody response to Newcastle disease virus was monitored in the sera and salivas of adult chickens immunized by two methods: (i) combined intratracheal-intranasal vaccination followed by intratracheal revaccination or (ii) intramuscular vaccination followed by intratracheal revaccination. By solid-phase radioimmunoassay, only immunoglobulin G (IgG) and IgA antibodies to Newcastle disease virus were detected in the salivas, whereas IgA and IgM antibodies were present in egg whites. The first method produced the highest antibody levels in both serum and saliva and, in addition, prevented detectable virus multiplication in the respiratory tracts upon revaccination 4 weeks later. Plasma cells of all three classes were distributed throughout the tissues lining the oral cavities. The highest densities of plasma cells were in the Harderian glands; IgG was the predominant class, whereas IgA and IgM plasma cells were present in almost equal but lower numbers. The Harderian plasma cells were the most likely source of the antibody found in saliva.

Animals↗
PubMed1980

Aerosol vaccination of chickens with the V4 strain of Newcastle disease virus.

Two-week-old chickens, free of detectable maternal antibody to Newcastle disease virus (NDV), or with low levels of maternal antibody, were vaccinated with the V4 strain of NDV. Haemagglutination inhibition (HI) antibodies were determined at intervals after vaccination. Two hundred chickens were vaccinated by exposure to an aerosol, a dose of 10(6) 50% embryo infectious doses (EID50) being allowed per chicken. Forty unvaccinated chickens were placed in direct contact with vaccinated chickens. Most of the vaccinated chickens and the in contact chickens had developed HI antibodies of titre greater than or equal to 8 within 2 weeks of vaccination. The HI antibodies in many chickens persisted for at least 8 weeks. Control chickens in a shed 15 metres from the shed containing the vaccinated chickens did not develop HI antibodies to NDV. NDV could be isolated from some vaccinated chickens for 15 days after vaccination. An aerosol dose of 10(5)EID50 per chicken failed to induce a serological response in 2 groups of 40 chickens each. HI antibodies were produced in 1 of 2 groups, each of 40 chickens, vaccinated with 10(6)EID50 and in both of 2 groups of 40 chickens each vaccinated with 10(7)EID50. Duplicate groups of 40 chickens were vaccinated with 10(6)EID50 of V4 virus per chicken administered either as an aerosol, a coarse spray or a droplet placed in the conjunctival sac. HI antibodies were produced in all the groups of chickens.

Aerosols↗
PubMed1979

Insensitivity of a ricin-resistant mutant of Chinese hamster ovary cells to fusion induced by Newcastle disease virus.

The role of membrane components in the interaction of cells with Newcastle disease virus (NDV) was studied using a ricin-resistant mutant of Chinese hamster ovary cells (CHO-15B), in which there is a deficiency in distal saccharides at the plasma membrane. Compared to the parental wild type, the mutant was shown to be 4- to 10-fold less sensitive to either fusion from without or fusion from within induced by NDV. The mutant and wild type were nearly indistinguishable with respect to other interactions with NDV. Viral attachment was investigated with 125I-labeled NDV and found to be comparable in both lines. Functionally equivalent amounts of hemagglutinin were produced, as measured by the fraction of cells positive for hemadsorption, or by the number of erythrocytes adsorbed per cell. No significant differences in the morphogenesis or yield of progeny virus were seen. The ability of the mutant to produce a fusion factor was measured by transfer of infected cells to uninfected monolayers. Infected CHO-15B cells were capable of inducing fusion normally in the indicator wild-type monolayers, but were incapable of inducing fusion in mutant monolayers. These results suggest that the insensitivity of the CHO-15B mutants to fusion may be due to inhibition of an early virus-cell interaction subsequent to viral attachment, whereas other events in infection appear to be unaffected by the cell surface mutation.

Adsorption↗
PubMed2005

Molecular changes of the fusion protein gene of chicken embryo fibroblast-adapted velogenic Newcastle disease virus: effect on its pathogenicity.

Molecular changes of cell culture-adapted Newcastle disease virus (NDV) were studied by adapting a velogenic NDV isolated from commercial layer chicken-to-chicken embryo fibroblast (CEF) cells. The isolate was passaged 50 times in CEF cells. At every 10th passage the virus was characterized conventionally by mean death time analysis, intracerebral pathogenicity index, and virus titration. As the passage level increased, a gradual reduction in the virulence of the virus was observed. Molecular characterization of the virus included cloning and sequencing of a portion of the fusion gene (1349 bp) encompassing the fusion protein cleavage site (FPCS), which was previously amplified by reverse transcription-polymerase chain reaction. Sequence analysis revealed a total of 134 nucleotide substitutions, which resulted in the change of 41 amino acids between the parent and the 50th passage virus. Pathogenicity studies conducted in 20-wk-old seronegative chickens revealed gross and histopathologic changes in the chickens injected with the parent virus and absence of the lesions in chickens injected with the adapted virus. The 50th passage cell culture virus was back-passaged five times in susceptible chickens and was subjected to virulence attribute analysis and sequence analysis of the FPCS region, with minor differences between them.

Adaptation, Biological↗
PubMed1986

Inhibition of the assembly of Newcastle disease virus by monensin.

Monensin inhibits the intracellular transport of the glycoproteins of Newcastle disease virus between cis and trans Golgi stacks of infected BHK cells, as evidenced by its effect upon their post-translational modifications such as fatty acid acylation, glycosylation and proteolytic cleavage. Thus the drug has markedly altered the subcellular distribution of the glycoproteins so that they accumulate in the internal smooth membranes but are virtually absent in the plasma membrane. These glycoproteins that accumulated in intracellular membranes have a cytoplasmic domain susceptible to protease digestion and thus are transmembranous. Under such conditions, the behavior of M protein, which plays a crucial role in virus assembly (Y. Nagai et al., 1976, Virology 69, 523-538), has been analyzed. It has been found that the M protein can neither associate with the internal membranes nor bind to the plasma membrane. Thus no virus budding has been observed, either at the plasma membranes or at internal membranes. These results substantiate the view that the interaction between M and glycoproteins is of great importance for virus assembly and suggest further that this interaction is possibly only when the glycoproteins have been incorporated into the plasma membrane.

Animals↗
PubMed1986

Modulation of adjuvant-enhanced delayed-type hypersensitivity by the interferon inducers poly I:C and Newcastle disease virus.

The modulation by the interferon (IFN) inducers poly I:C and Newcastle disease virus (NDV) of the effector phase of adjuvant-enhanced delayed-type hypersensitivity (DH) was studied in mice. A strongly enhanced DH was induced in mice to ultraviolet (UV) light inactivated Semliki forest virus (SFV) by the use of the adjuvant dimethyldioctadecylammonium bromide. At day 6 after intracutaneous immunization, DH was elicited with SFV and measured 24 and 48 h later as increase in footpad thickness (footpad swelling test). Systemic, intravenous administration of either poly I:C, UV-inactivated NDV, or NDV-induced IFN prior to elicitation of DH with antigen resulted in a temporarily suppressed DH reaction. Both the poor swelling at 3 h and strong swelling at 24 h were suppressed, while the swelling at 48 h was enhanced. The model described provides a sensitive in vivo method to study modulating effects of drugs and microbial agents on the effector phase of DH.

Animals↗