SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Different strains of Newcastle disease virus (NDV) were added to chicken lymphocytes and JMV-1 and MSB-1 Marek's-disease-derived tumor cell lines to determine the virus-cell interaction. NDV caused fusion and lysis of the cells, and cells supported the growth and multiplication of NDV.
The haemagglutinin-neuraminidase gene of Newcastle disease virus was inserted into a non-essential region of the fowlpox virus genome and expressed under control of the vaccinia virus 7.5 kDa polypeptide gene promoter. Immunization with the recombinant fowlpox virus elicited protective immunity in chickens against both virulent Newcastle disease and fowlpox virus infection.
Purified virions of Newcastle disease virus (NDV) were found to contain protein kinase activity which was, like other virion-associated kinases, stimulated by Mg2+, and totally independent of Ca2+ and cAMP. The kinase phosphorylated preferentially the P and NP polypeptides of NDV. Triton-KCl fractionation of the virions has shown that the protein kinase activity may be associated with glycoprotein-free subviral particles, but not with nucleocapsids containing either only NP or some L and P proteins together with NP as protein constituent.
Delayed harvest of Newcastle disease virus (NDV) from eggs was less infective (as expressed by its lower infectious titer and a higher number of virus particles per EID50) and more resistant to a temperature of 50 degrees C than the early harvest. On the other hand, little or no effect of delayed harvesting was found on neuraminidase, erythrocyte-fusing and immunogenic properties. Moreover, haemolytic activity of NDV was moderately enhanced when its harvesting from de-embryonated egg was delayed. Treatment of a fresh NDV preparation with repeated freezing and thawing cycles also caused a marked reduction in virus infectivity and induction of its haemolytic activity.
Five strains of Newcastle disease virus (NDV) were tested for their ability to agglutinate and lyse chicken lymphocytes. All 5 strains agglutinated lymphocytes, and the agglutination was inhibited by anti-NDV sera. All 5 strains also caused a different degree of direct virus-induced lysis of 51Cr-labeled chicken lymphocytes. This direct lymphocyte cytotoxicity was lost after heating at 56 degrees C for 30 min, or after treatment with a high concentration of formalin (1:100 dilution). Neither a low concentration of formalin (1:5000) nor trypsin treatment had any effect on cytotoxicity.
Different strains of Newcastle disease virus vary in their ability to induce cell fusion. When administered to cells at high multiplicities of infection some strains induce cell fusion within three hours. This type of fusion is apparently caused by the virus particles in the inoculum, since it can be induced by noninfectious virus and does not require protein synthesis for induction. It has been designated fusion from without (FFWO). Other strains induce fusion mainly at low multiplicities of infection. This fusion is induced only by infectious virus, and requires protein synthesis for induction. Probably included among these required proteins is a viral antigen which must be available at the cell surface in order for fusion to occur. This type of fusion has been designated fusion from within (FFWI).
The effect of Newcastle disease virus (NDV) on delayed hypersensitivity to oxazolone in CBA mice was studied. There was a significant impairment of the ability of mice to develop cutaneous hypersensitivity shortly after injection of the virus. The effect was evident when NDV was administered up to 2 days before or within 24 h after sensitization, suggesting that NDV interferes with the process of sensitization. The degree of depression was related to the dose of virus inoculated. NDV inactivated by UV irradiation or heat did not depress contact sensitivity to oxazolone. These data are considered to support the hypothesis that the depression is mediated by a direct interaction between lymphocytes and NDV.
Newcastle disease virus (NDV) envelope glycoproteins that are expressed at the surface of fixed NDV (Ploufragan strain)-infected chick fibroblasts induce interferon (IFN) in mouse spleen cells. HN protein appears to be involved, since an anti-HN monoclonal antibody (Mab 3115) reduces the IFN production to 6% at most. However, the precise site of the molecule responsible for IFN induction is probably not exactly superimposed on the Mab 3115-epitope, since the NDV (83309 strain)-HN protein, which exhibits a modified Mab 3115-epitope, is also able to induce IFN. These preliminary results require further investigation in order to characterize the IFN herein demonstrated, to establish whether this induction mechanism exists in chicken lymphoid cells and to more accurately define the part of the HN molecule involved.
The mechanisms of Newcastle disease virus-(NDV) induced inhibition of cell protein and ribonucleic acid (RNA) synthesis were investigated. It was observed that the ability of NDV to inhibit cell RNA synthesis is dependent on the virus strain. The inhibitors, azauridine and cycloheximide, were added to cell cultures at different times after infection to study the roles of protein and RNA synthesis in the viral inhibition process. Viral inhibition of cell RNA synthesis and viral inhibition of cell protein synthesis become resistant to cycloheximide at a different time after infection than that in which they become resistant to azauridine. The results indicate that the inhibition of cell RNA synthesis by the Texas strain involves the synthesis of inhibitory proteins which are coded by the viral genome. The Texas and Beaudette strains of NDV appear to employ different mechanisms for the inhibition of host-cell protein synthesis. Viral inhibition of cell protein synthesis does not appear to cause, or be the result of, viral inhibition of cell RNA synthesis.
Detection of Newcastle disease virus (NDV) and avian pathotyping of NDV isolates are extremely important because the appearance of virulent virus has significant economic consequences in terms of vaccination, eradication, and the ability to export poultry products. By using nucleotide and amino acid (aa) homology analysis, we could demonstrate that a NDV broiler isolate is a velogenic virus. This analysis was done after mean death time and intracerebral pathogenicity index tests gave inconsistent results. By establishing a nucleotide sequence dendrogram, we found that the disputed Ber-Tuvia was clearly in the same group as the known Herev-Laet, a velogenic isolate. The difference between Ber-Tuvia 92 and the Herev-Laet velogenic isolate was 6% as opposed to > 16% of the meso- and lentogenic isolates. The Ber-Tuvia isolate contains the Arg/Arg and Lys/Arg aa at positions 112, 113 and 115, 116, respectively, in the fusion protein cleavage aa sequence, which is typical for virulent NDV isolates.
Velogenic viscerotropic Newcastle disease (vvNCD), which is endemic in Cambodia, can be prevented in theory by a combination of biosecurity and immunization of broiler flocks. The relative contribution of appropriate biosecurity and effective vaccination was quantified at the farm level, applying realistic projections for capital investment, fixed and variable production costs and losses following infection. Non-protected broiler flocks generate a loss when the probability of vvNCD infection exceeds 0.4. Applying both biosecurity and effective vaccination would sustain profitability up to a probability of exposure of 1.0. The benefit to cost ratios for alternative strategies were evaluated for a range of probabilities of exposure to vvNCD extending from 0.1 to 1.0. The benefit-to-cost ratio for biosecurity exceeded unity at a risk of exposure exceeding 0.1, and 0.2 for vaccination and the combination of vaccination and biosecurity respectively. A sensitivity analysis demonstrated that the efficiency of protection, feed cost, and financial consequences of infection markedly affected the projected benefit-to-cost ratios associated with alternative methods of prevention.
Proteins induced in Newcastle disease virus (NDV)-infected chick embryo fibroblasts (CEF) and proteins incorporated into virions grown in ovo were analysed by modified versions of a two-dimensional polyacrylamide gel electrophoresis system. The following previously described NDV-induced proteins were detected and resolved from host proteins: L (mol. wt. approx. 200K), HN (75K), F0 (66K), F1 (56K), NP (55K) and M (39K). Two additional polypeptides, NAP (nucleocapsid-associated protein, mol. wt. 56K) and a 36K mol. wt. protein were induced in NDV-infected cells. NAP but not 36K was found in purified virions. Radioactive labelling studies with 3H-glucosamine and 32P-orthophosphate demonstrated that neither NAP nor 36K is glycosylated, but that both are phosphorylated. Variation in the isoelectric point and apparent mol. wt. of NAP among different strains was seen and exactly reproduced in both CEF and baby hamster kidney (BHK) cells. The synthesis of NDV-induced proteins including NAP and 36K was unaffected by actinomycin D, whereas the synthesis of host cell proteins was drastically reduced. These data are evidence that NAP and 36K are virus coded. Peptide analysis indicated that NAP, NP and F1 are unrelated polypeptides. The demonstration that NAP is virus coded, together with its phosphorylation and association with the nucleocapsid, suggest that NAP may be the NDV analogue of the P protein of Sendai virus.
The effects of Newcastle disease virus (NDV) fusion (F) glycoprotein cleavage mutants on the cleavage and syncytium-forming activity of the wild-type F protein were examined. F protein cleavage mutants were made by altering amino acids in the furin recognition region (amino acids 112 to 116) in the F protein of a virulent strain of NDV. Four mutants were made: Q114P replaced the glutamine residue with proline; K115G replaced lysine with glycine; double mutant K115G, R113G replaced both a lysine and an arginine with glycine residues; and a triple mutant, R112G, K115G, F117L, replaced three amino acids to mimic the sequence found in avirulent strains of NDV. All mutants except Q114P were cleavage negative and fusion negative. However, addition of exogenous trypsin cleaved all mutant F proteins and activated fusion. As expected for an oligomeric protein, the fusion-negative mutants had a dominant negative phenotype: cotransfection of wild-type and mutant F protein cDNAs resulted in an inhibition of syncytium formation. The presence of the mutant F protein did not inhibit cleavage of the wild-type protein. Furthermore, evidence is presented that suggests that the mutant protein and the wild-type protein formed heterooligomers. By measuring the syncytium-forming activity of the wild-type protein at various ratios of expression of mutant and wild-type protein, results were obtained that are most consistent with the notion that the size of the functionally active NDV F protein in these assays is a single oligomer, likely a trimer. That a larger oligomer, containing a mix of both wild-type and mutant F proteins, has partial activity cannot, however, be ruled out.
Studied was the persistance of 3 plaque clones of a velogenic viscerotropic Newcastle disease virus in nonimmune birds. It was found that the first plaque clone (4 mm dia of plaques) possessed higher virulence than that of the parental virus and killed all inoculated birds for 2 to 5 days. Plaque clone II (2.5 mm dia of the plaques) caused up to 30 per cent mortality, and plaque clone III (1.5 mm dia of the plaques) did not bring about death but a transient disease only. Birds inoculated with II and III plaque clones, at identical serologic response, were investigated virologically on the 40th and 60th day post infection. By means of the tracheal organ cultures the Newcastle disease virus was isolated only from birds that were inoculated with plaque clone II. No virus was demonstrated via the same method in birds inoculated with plaque clone III. It is believed that the long-term persistance of the Newcastle disease virus reported on a previous occasion was due to a subpopulation identical with plaque clone II.
Using the rapid glass plate method, the Newcastle disease virus strain MET95 showed much weaker haemagglutination (HA) activity for chicken erythrocytes than 69 other Newcastle disease viruses, including 56 field strains isolated from chickens reared in Japan between 1988 and 2001. Using erythrocytes from other avian species, only the MET95 strain failed to show HA activity for erythrocytes from ducks, geese or pigeons. The haemagglutinin-neuraminidase protein of the MET95 strain was shown to have unique substitutions of isoleucine for thereonine and leucine at amino acide residues 216 and 552. It is suggested that these two substitutions might relate to the unique HA activity of the MET95 strain. This HA activity may be a useful marker for this strain.
The Central Veterinary Laboratory, Weybridge, England, was requested by the WHO Expert Committee on Biological Standardization to obtain suitable material for an international reference preparation of anti-Newcastle-disease serum for standardizing the haemagglutination-inhibition test for Newcastle disease and to arrange a collaborative assay. Ten laboratories in 10 countries assayed a batch of immune chicken serum against 2 test preparations. On the basis of the results obtained, the material has been established as the International Reference Preparation of Anti-Newcastle-Disease Serum and the International Unit of Anti-Newcastle-Disease Serum has been defined as the activity contained in 0.1734 mg of the International Reference Preparation of Anti-Newcastle-Disease Serum.
We have separated the 18-22S putative messenger RNA of Newcastle disease virus into seven species ranging in molecular weight from 0.55 to 1.53 x 10(6) using sodium dodecyl sulfate-acrylamide-gel electrophoresis at relatively high concentrations of acrylamide and for a relatively long time. Studies of the number and molecular weights of the proteins and the 18-22S RNAs of the virus suggests that these RNAs are in the right molecular weight range to code for the known proteins of Newcastle disease virus. In preliminary studies using this separation technique, we have demonstrated that: (a) there is no difference between the 18-22S RNA made during a normal infection and when genome replication is blocked; and (b) there is a strain-specific difference between the RNAs of Newcastle disease virus-AV and Newcastle disease virus-HP.
Two replicate experiments were carried out to verify the efficacy of Aloe species (Aloaceae) as used for the control of Newcastle disease (ND) in rural poultry in free-range systems among several communities in Tanzania. Four months old local chickens free of Newcastle disease antibodies were used. Following inoculation with ND virus, body weights, clinical signs, antibody levels and mortality were monitored. Results showed that there was reduced mortality rate and the severity of clinical signs during the acute phase of the infection in Aloe treated chickens compared with the non-treated ones. However, there was no significant effect of the Aloe on the antibody levels that were attributed to the recovery of the surviving chickens. The findings of this study suggest that Aloe secundiflora could be a potential candidate on the management of Newcastle disease in chickens. Further studies are in progress to identify the active ingredients of A. secundiflora against Newcastle disease virus.