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At least 865 records · Page 48Linked to original sources
PubMed1984

[Newcastle disease virus carrier state after aerosol vaccination against the disease in chickens of various ages].

Studied was the carrier status with the Newcastle disease virus in experiments with a total of 665 birds at the age of 10 days, one month, and two months following an aerosol vaccination with a La Sota strain vaccine as well as the possibility to isolate the velogenic strain Texas GB after control infection of 10-day-old and one-month-old birds. Established was a short-term carrier status with the La Sota strain in the organs of birds up to the 6th-9th day following the aerosol vaccination. In an experiment with month-old birds originating from parental flocks immunized against Newcastle disease the La Sota virus was isolated also from the brain up to the sixth day. The resistance of birds to the infection was demonstrated at the aerosol immunization of 10-day-old and month-old- birds followed by challenging the birds with high doses of the velogenic virus strain Texas GB.

Aerosols↗
PubMed1991

Analysis of the protective effect of the haemagglutinin-neuraminidase protein in Newcastle disease virus infection.

The role of immune responses to haemagglutinin-neuraminidase (HN) protein in protection against a Newcastle disease virus (NDV) infection was investigated using a recombinant vaccinia virus expressing HN (HN-RVV). Live HN-RVV replicated in chickens and completely protected them from lethal infection with virulent NDV. Inactivated HN-RVV also protected chickens when administered with adjuvant but not when administered without adjuvant. However, large amounts of the inactivated HN-RVV (100-fold excess) without adjuvant provided protection. Specific antibodies against the HN protein of NDV were detected in sera from survivors but not from dying birds. However, the kinetics of antibody responses in chickens inoculated with live HN-RVV and inactivated HN-RVV were considerably different. These results clearly confirm that immune response(s) solely to the HN protein of NDV can provide chickens with protection against NDV challenge, and show that the presence of antibodies to the HN protein correlates significantly with the protection from NDV infection at least in HN-immunized chickens.

Animals↗
PubMedDate not supplied

Genetic variation in resistance of turkeys to experimental infection with Newcastle disease virus.

Seven hundred eighty male and female turkeys representing four genetic lines were challenged in four experiments with the Texas GB strain of Newcastle disease virus (NDV). The lines of turkeys included two randombred control lines (RBC1 and RBC2), a subline (E) of RBC1 selected for increased egg production, and a subline (F) of RBC2 selected for increased 16-week body weight. Mortality in turkeys of subline F (32.5%) was significantly higher than that in turkeys of line RBC2 (15.8%), subline E (17.5%), and line RBC1 (18.4%). At the end of each experiment, surviving birds were tested for antibody to NDV using the enzyme-linked immunosorbent assay (ELISA) and hemagglutination-inhibition (HI) test. Turkeys of subline E and line RBC1 had significantly lower ELISA antibody titers than those of subline F and line RBC2. Subline F had the highest HI antibody titers, followed in decreasing order by lines RBC2 and RBC1 and subline E. No apparent correlation was found between antibody response and mortality after NDV challenge.

Animals↗
PubMed2004

Pathotyping of Newcastle disease virus with a filamentous bacteriophage.

A filamentous phage bearing the peptide sequence TLTTKLY was isolated from a heptapeptide phage display library against a velogenic Newcastle disease virus (NDV). In order to investigate the potential of this specific phage as an immunological reagent in virus pathotyping, an enzyme-linked immunosorbent assay (ELISA)-based method was developed. This method can differentiate the velogenic strains from the mesogenic and lentogenic strains. An equilibrium-binding assay in solution showed that the interactions between the phage and all the NDV strains gave rise to two widely differing dissociation constants (Kdrel). Based upon the first Kdrel values, NDV strains can be classified into two groups; the first comprises the velogenic strains, and the second consists of the mesogenic and lentogenic strains. These results indicate a high degree of correlation between the binding affinities and pathotyping of NDV strains using the TLTTKLY phage.

Enzyme-Linked Immunosorbent Assay↗
PubMedDate not supplied

Pathological changes of tracheal mucosa in chickens infected with lentogenic Newcastle disease virus.

Forty-day-old specific-pathogen-free chickens were exposed by aerosol to lentogenic Newcastle disease virus (NDV) and observed for 24 days for pathological changes in the tracheal mucociliary system. Specific fluorescence of NDV antigen was observed through day 5 postexposure (PE) in the cytoplasm of the tracheal epithelium and desquamated epithelium in the lumen. On day 1 PE, scanning electron microscopy revealed hypertrophy of goblet cells and small patches of the deciliated epithelium scattered mainly around the openings of mucous glands. The deciliated area of tracheal surface increased through day 4 PE. Light microscopy showed small vacuoles containing lymphocytes and heterophils in the epithelial layer. Immature epithelium proliferated in some areas. On days 5 and 6 PE, ciliated areas of the trachea tended to increase as a result of regeneration of the epithelium, still leaving many nonciliated patches of various sizes. On and after day 8 PE, there remained plaques with nonciliated flat epithelium, but most areas were covered with well-ciliated epithelium. Non-ciliated plaques were observed until day 24 PE, but they gradually decreased in size. These plaques were covered by a single layer of flat epithelium and were formed upon lymph follicles in subepithelial tissue.

Animals↗
PubMed1998

Role of carbohydrate processing and calnexin binding in the folding and activity of the HN protein of Newcastle disease virus.

The role of carbohydrate processing and calnexin binding in the folding pathway and activity of the hemagglutinin-neuraminidase (HN) protein of Newcastle disease virus (NDV) was explored in infected cells using the inhibitor castanospermine (CST). Calnexin-HN protein complexes were demonstrated by coimmunoprecipitation using antibody specific for calnexin or HN protein. As in other systems, this complex was not detected in CST treated cells. In cells incubated in CST, the synthesis and stability of the HN protein was unaffected. However, as monitored by the appearance of conformationally sensitive antigenic sites, the folding of the HN protein in CST treated cells was approximately twice as slow than in untreated cells. This folding was ultimately efficient since there was no evidence for significant amounts of irreversibly aggregated forms which never acquired a mature conformation. Most significantly, the folding sequence as measured by the order of appearance of conformationally sensitive antigenic sites (McGinnes and Morrison, Virology 199, 255) was unaffected by CST. Thus while calnexin functions to speed the folding of the HN protein, it is not required for the folding of this protein. In addition, the protein synthesized in the presence of CST had significant levels of neuraminidase and hemagglutination activity suggesting that processing of the carbohydrate has a minimal role in the activity of the protein.

Animals↗
PubMed2002

Phylogenetic analysis of Newcastle disease virus genotypes isolated in Japan.

We genetically analyzed field isolates of the Newcastle disease (ND) virus isolated in Japan from 1930 to 2001. The coding region of the fusion protein was amplified by reverse transcriptase PCR and directly sequenced. Phylogenetic analysis revealed the presence of viruses belonging to six of the eight known genotypes. It can be concluded from this study that ND outbreaks in Japan have been of multiple etiologies. [All sequences used in this study were sent to DDBJ and assigned accession numbers AB 070382 to AB 074042.]

Animals↗
PubMedDate not supplied

Newcastle disease virus pathogenesis in the respiratory tract of local or systemic immunized chickens.

Establishment of selective immunity, local or systemic, made it possible to evaluate the pathogenesis of Newcastle disease virus (NDV) in the respiratory tract of chickens that were previously immunized with beta-propiolactone-inactivated antigen. NDV was inoculated intranasally or intramuscularly to chickens in different states of immunity (local or systemic). Humoral antibodies protected chickens against intranasal as well as intramuscular infection. Local antibodies, on the other hand, conferred immunity only against intranasal challenge. The respiratory tract supported multiplication of the virus, producing a self-limited subclinical infection. Replication of the virus in this system was negligible, playing only a minor role in the pathogenesis of the disease.

Administration, Intranasal↗
PubMed1988

Mapping of three antigenic sites on the haemagglutinin-neuraminidase protein of Newcastle disease virus.

Nine neutralizing monoclonal antibodies (MAbs), each of which react with the haemagglutinin-neuraminidase (HN) glycoprotein of the Beaudette C strain of Newcastle disease virus (NDV), have been used in competitive binding assays to delineate three non-overlapping antigenic sites A, B and C. Epitopes within these sites have been identified on the basis of cross-reactivity of MAb-resistant mutants against the panel of MAbs, determined by plaque assays and Western blotting. Site A contains three non-overlapping epitopes (A1, A2 and A3). A1 is the only linear epitope; all remaining epitopes are conformational. MAbs which react with epitopes A2 and A3 inhibit neuraminidase activity (NA) when assayed with neuraminlactose. Site B contains three partially overlapping epitopes (B1, B2 and B3) and site C is represented by a single epitope (C1). HN gene sequence analysis of MAb-resistant mutants showed that they each had only single amino acid substitutions which range from amino acid residues 347-460 for site A, 284-325 for site B, and at 481 for the C1 epitope. The apparent molecular mass of the HN glycoprotein of one mutant was increased from 72 to 75 kDa. This correlates well with the creation of an additional potential glycosylation site in this mutant from Asn-Ser-Pro(325) to Asn-Ser-Ser(325).

Amino Acid Sequence↗
PubMed1992

Epitope specificity of monoclonal antibodies against Newcastle disease virus: competitive fluorogenic enzyme immunoassay.

A test to determine the epitope specificity of monoclonal antibodies (MCA) was developed for hybridoma clones producing antibodies against Newcastle disease virus (NDV). The virus was first immobilized on nitrocellulose membranes of Millititer HA plates. Dilutions of MCA were then added, singly, or simultaneously in pairs, and bound antibody was quantitated with alkaline phosphatase-labelled detector antibody and a fluorogenic substrate, 4-methylumbelliferyl phosphate (4-MUP). Fluorescence count was measured fluorometrically. Additivity indices were calculated and plotted against dilutions of paired MCA. Antibodies that recognized identical epitopes displayed non-additivity at saturating antibody dilutions, followed by partial additivity and by total additivity at low, non-saturating dilutions. In contrast, MCA that recognized distinct epitopes exhibited total additivity throughout the curve. MCA that exhibited partial additivity were interpreted as competing for overlapping shared epitopes, or, distinct epitopes in close proximity, resulting in steric hinderance.

Antibodies, Monoclonal↗
PubMedDate not supplied

An evaluation of Newcastle disease virus spray vaccination programs of market turkeys.

Commercial market turkeys that were spray-vaccinated at 2 to 3 weeks of age with viable Newcastle disease virus (NDV) vaccine usually did not develop high or persistent levels of serum antibody as detected by the hemagglutination-inhibition test. Vaccinated turkeys exhibited a satisfactory level of resistance to infection and clinical disease when challenged by the oculonasal or aerosol route at 2 weeks post-vaccination, and they resisted clinical disease when challenged at 6 weeks, but the level of protection diminished by 10 weeks post-vaccination. It is suggested that market turkeys produced in an NDV-enzootic area may require two or more NDV vaccinations by spray during their growing period in order to be adequately protected against natural NDV infection.

Aerosols↗
PubMed1988

Newcastle disease virus as an antineoplastic agent: induction of tumor necrosis factor-alpha and augmentation of its cytotoxicity.

The oncolytic strain 73-T of Newcastle disease virus (NDV) has been reported to be beneficial in the treatment of cancer patients, but little is known about its mechanism of action. In this study, NDV strain 73-T and a wild-type isolate of NDV were found to be potent inducers of tumor necrosis factor (TNF) production by both human peripheral blood mononuclear cells (PBMCs) and rat splenocytes. Antibody inhibition experiments identified TNF-alpha as the major species of TNF induced by NDV in PBMCs. The effect of recombinant human TNF-alpha (rHuTNF-alpha) on human cancer cells was then examined. Neither rHuTNF-alpha nor supernatants from NDV-stimulated PBMCs were cytotoxic toward the TNF-resistant human malignant melanoma cell line MEL-14. However, when MEL-14 cells were treated with NDV strain 73-T, both rHuTNF-alpha and supernatants from NDV-stimulated PBMCs killed 48% and 55%, respectively, of these tumor cells. Treatment with NDV also conferred TNF susceptibility to the TNF-resistant human malignant melanoma cell line MEL-21 and the human myelogenous leukemia cell line K562. In contrast to its enhanced cytotoxicity toward NDV-treated cancer cells, rHuTNF-alpha had no effect on NDV-treated normal human PBMCs proliferating in response to concanavalin A. These results suggest two important mechanisms for the antineoplastic activity of NDV: (a) induction of TNF-alpha secretion by human PBMCs and (b) enhancement of the sensitivity of neoplastic cells to the cytolytic effects of TNF-alpha.

Antibodies↗
PubMed1983

Thermostabilities of virion activities of Newcastle disease virus: evidence that the temperature-sensitive mutants in complementation groups B, BC, and C have altered HN proteins.

Four virion activities of Newcastle disease virus (hemagglutinating, neuraminidase, hemolytic, and infectious activities) were examined before and after heat stress in low-salt buffer and physiological salt buffer (phosphate-buffered saline). The hemagglutinating and neuraminidase activities of the Australia-Victoria wild-type (AV-WT) strain were thermostable at both salt concentrations tested, whereas the thermostabilities of the hemolytic and infectious activities were salt dependent (thermostable in phosphate-buffered saline but not in low-salt buffer). Virions of RNA(+) temperature-sensitive (ts) mutants of AV-WT were tested for the stabilities of the four activities. Some mutants in groups B, BC, and C were as stable as AV-WT in all functions, but others were much less stable in all functions. The unstable mutants in groups B, BC, and C affirmed the assignment of the ts lesions of these mutants to the hemagglutinin/neuraminidase (HN) protein gene because HN function(s) are required for all four activities. The instability of these ts mutants was not related to their decreased virion HN protein content and was not due to physical loss of the HN protein from the virions. Three of four ts(+) plaque-forming revertants of the least stable mutant, BC2, coreverted for stability, confirming that the unstable phenotype is indeed the result of the mutation responsible for the ts phenotype. Group D mutants were approximately as stable as AV-WT in hemagglutinating, neuraminidase, and hemolytic activities; this is consistent with this group representing a lesion in a gene other than the HN protein gene. However, the infectivities of two of the three group D mutants were less stable than the infectivity of AV-WT in low-salt buffer.

Genes, Viral↗
PubMed1975

Temperature-sensitive mutants isolated from hamster and canine cell lines persistently infected with Newcastle disease virus.

Evidence is presented which confirms that temperature-sensitive (ts) mutants with an RNA- phenotype are spontaneously selected in persistent infection of cell lines with Newcastle disease virus. Persistently infected BHK-21 cells, maintained since 1973, produce no interferon and are completely susceptible to vesicular stomatitis virus. Persistent infection of a canine kidney cell line (MDCK) terminated with destruction of all cells at about 100 days. Even under these conditions, a high proportion (33%) of RNA- temperature-sensitive mutants was present in the virus population 60 days after the infection was initiated.

Animals↗
PubMed2003

A phylogenetic study of South African Newcastle disease virus strains isolated between 1990 and 2002 suggests epidemiological origins in the Far East.

Genetic comparisons were made of the fusion protein sequences of 155 Newcastle disease virus isolates collected in South Africa between 1990 and 2002. Their evolutionary relationships and origins are described. All of the lentogenic field isolates were shown to be derived from commercial vaccines. No true South African lentogenic wild type strain was identified. Furthermore, it was shown that almost all mesogenic isolates had avirulent F(0) cleavage site sequences. Three major epizootics occurred in South Africa during the period of this study. The first outbreak (1990/1991) was caused by viruses endemic to South Africa since the 1960's (genotype VIII) but were occasionally also isolated in 2000. Genotype VIIb viruses, implicated in the severe outbreaks during 1993/1994, persisted until 1999. Genotype VIId viruses, responsible for the most recent outbreak in 1999/2000, had their origins in the Far East like those of the two previous outbreaks.

Amino Acid Sequence↗
PubMed1976

Viral factors required for interferon induction by Newcastle disease virus in mouse macrophages and chicken embryo cells.

The triggering mechanism for interferon synthesis in mouse peritoneal macrophages and chick embryo (CE) cells by Newcastle disease virus (NDV) exposed to hydroxylamine or homologous antiserum was investigated in relation to the intracellular fate of these agents. Inactivation of NDV at 22 degrees C by I M-hydroxylamine proceeded with first-order kinetics, whereas the interferon-inducing capacity of hydroxylamine-treated virus in macrophages was unimpaired. In contrast to infective NDV, hydroxylamine-inactivated virus produced interferon in CE cells, and such a virus still had partial RNA-dependent RNA polymerase activity. Hydroxylamine-inactivated NDV was adsorbed to and uncoated in both normal and chloroquine diphosphate treated cells, but no viral double-stranded RNA was detected. Hydroxylamine treatment of virion-extracted RNA and neutralization of intact virions by antibody abolished the capacity of the virus to induce interferon. Infective as well as neutralized NDV interacted with macrophages to the same degree, but association between NDV and CE cells was prevented by antibody-coating. In macrophages, the RNA of neutralized NDV became more sensitive to RNase than RNA of infective NDV, but this process was inhibited in chloroquine diphosphate-treated cells. These results suggest that interferon induction by NDV involves components of the virion which are present up to the regular uncoating process.

Animals↗
PubMedDate not supplied

Interactions between viscerotropic velogenic Newcastle disease virus and pet birds of six species. II. Viral evolution through bird passage.

Following in vivo studies in pet birds of 6 species, 279 Newcastle disease virus (NDV) reisolates were selected for characterization by the embryonated-chicken-egg mean-death-time, plaque-assay, hemagglutination-elution, and hemagglutinin-thermostability techniques. Initially, the 279 isolates were screened by the mean-death-time and plaque-assay techniques, and 5 sequential isolates were chosen for each of 3 budgerigars and 2 parrots for characterization by the other 2 in vitro assays to determine whether the Colorado Psittacine Isolate of viscerotropic velogenic (VV) NDV (COPI-VVNDV) had evolved during passage through pet birds. Nineteen isolates were then selected for chicken back-passage studies. Fifteen of the 19 isolates were chosen for potential avirulence for 8-week-old domestic chickens. The 4 remaining isolates produced large red plaques when assayed and were therefore used as virulent virus controls likely to be VVNDV. Subsequent in vitro characterization of selected back-passage chicken NDV isolates demonstrated little change in the 4 parameters originally evaluated for the pet-bird isolates used for the back-passage studies. Although the psittacine isolate slowly evolved to relatively avirulent strains of NDV by passage in pet birds, reversion did not occur during the chicken back-passage studies.

Animals↗