Further studies on in vitro cultivated pneumoencephalitis (Newcastle disease) virus and its use as a vaccine.
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Animals↗
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Effect of butylated hydroxytoluene on Newcastle disease virus.
A study was done to examine the effects of butylated hydroxytoluene (BHT) on purified Newcastle disease virus (NDV). Treatment of the virus with 50 microgram of BHT/ml caused 92% inactivation of the virion infectivity. Virion adsorption to chicken-embryonated cells was inhibited 32% and synthesis of intracellular hemagglutinin was inhibited 29%. Electron microscopy of the BHT-treated virions revealed virion envelope damage. Chicken-embryonated cells treated with 25 microgram of BHT/ml before NDV infection demonstrated 65% inhibition of NDV progeny production.
Butylated Hydroxytoluene↗
EVALUATION OF A TISSUE-CULTURE NEWCASTLE DISEASE VACCINE.
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Animals↗
Identification of phosphoprotein:phosphoprotein and phosphoprotein:nucleocapsid protein interaction domains of the Newcastle disease virus.
The yeast two-hybrid system has been used to identify domains of the Newcastle disease virus (NDV) phosphoprotein (P) involved in self-association and interaction with the nucleocapsid protein (NP). Deletion analysis was used to map the domain(s) of the P protein involved in P:P and P:NP interactions. The C-terminal 45 amino acids (residues 247-291) were shown to play a major role in both of the interactions. Comparison of these findings with other reports suggests that paramyxoviruses are different with respect to interaction domain(s) between these two essential viral proteins involved in genome replication.
Newcastle disease virus↗
Interaction between cytomegalovirus and Newcastle disease virus as mediated by intrinsic interference.
Cytomegalovirus (CMV) was demonstrated to induce intrinsic interference to Newcastle disease virus (NDV) in human fibroblast cells under noncytopathic conditions. This interference is unique in that (i) cytomegalovirus is the first DNA virus demonstrated to have this property and (ii) the state of interference was transient and progressively lost as the condition of the cells changed with the development of cytopathic effect. These observations are consistent with the view that the newly formed protein responsible for interference with NDV has a limited half-life and is no longer made when cytopathic conditions are produced by CMV.
Cell Line↗
Newcastle disease virus-induced functional impairments and biochemical changes in chicken heterophils.
The GB strain of Newcastle disease virus (NDV) is used to infect chicken heterophils in vitro. Heterophils have a decreased ability to phagocytize bacteria 3 h after infection, and those that did engulfed fewer bacteria relative to non-infected heterophils. Infected heterophils have a decreased H2O2 production as shown by flow cytometry, but an increased nitric oxide production, suggesting that NDV can stimulate heterophils to produce and/or utilize nitrogen intermediates but not oxygen intermediates. DNA extracted from the infected heterophils shows a marked fragmentation, suggesting that NDV infection may cause heterophils to undergo apoptosis.
Animals↗
Enhancement of haemolysis by Newcastle disease virus (NDV) after pre-treatment with heterophile antibody and complement.
Pre-treatment of Newcastle disease virus (NDV) with fresh human plasma enhances its haemolytic (HL) capacity by several factors. The effect is due to complement activation by the heterophile anti-chick antibody present in human plasma. All the adult human plasmas tested were effective, also 91/100 human cord blood sera. The antibody was mainly of the IgM class. The enhanced HL was due to integration and transference of the complement 'holed' virus envelope membrane and subsequent leakage of haemoglobin. High concentration of activated complement destroys the integrity of the virus enevelope. Treatment of chick erythrocytes and fibroblasts with human plasma also produced lysis of the cells.
Animals↗
Nucleotide sequence of the haemagglutinin-neuraminidase (HN) gene of a Malaysian heat resistant viscerotropic-velogenic Newcastle disease virus (NDV) strain AF2240.
The nucleotide sequence of the haemagglutinin-neuraminidase (HN) gene of Newcastle disease virus (NDV) viscerotropic-velogenic strain AF2240 was determined by direct RNA sequencing and by sequencing RT-PCR products. It encodes a single open reading frame of 581 amino acids with a calculated Mr of 63.8 kDa. The predicted sequence contains five asparagine glycosylation sites. Comparison of the AF2240 HN protein sequence with 13 other previously published sequences showed 88% homology. This HN protein is unique because it lacked the Arg 403 residue which is present in all of the other strains and cannot be grouped under the proposed three size classes of HN proteins in NDV.
Amino Acid Sequence↗
A temperature-sensitive mutant of Newcastle disease virus defective in intracellular processing of fusion protein.
A temperature-sensitive mutant (ts3) of Newcastle disease virus was physiologically characterized. All major viral structural proteins were synthesized at the permissive (37 degrees C) and nonpermissive (42 degrees C) temperatures, but the fusion (F) glycoprotein was not cleaved at 42 degrees C. In immunocytochemical electron microscopy, the F protein was abundant in the rough endoplasmic reticulum but not in cytoplasmic membrane at 42 degrees C. Noninfectious hemagglutinating virus particles containing all major structural proteins except the F protein were released at 42 degrees C from infected cells. We concluded that the defect in ts3 resides in the intracellular processing of the F protein.
Animals↗
Titration of avirulent Newcastle disease virus by the plaque assay method.
Parameters of a plaque assay for avirulent strains of Newcastle disease virus (NDV) were optimized for reproducibility and optimum titer in LLC-MK2 cells. Plaques were visible after 2 days and maximum virus titers were reached in 3 days. Virus titers were not affected by continued incubation through 6 days, although plaque size increased. An adsorption volume of 0.1 or 0.2 ml per 60 mm Petri dish was optimal, as was an adsorption time of 45 min. Trypsin (2.5 micrograms/ml) and magnesium sulfate (0.03 M) were essential requirements of the overlay medium and the presence of DEAE-dextran (0.02%) resulted in a 30% increase in titer. The use of cell monolayers, 1, 2, or 3 days old facilitated the performance of multiple assays per week and did not affect the virus titer.
Animals↗
Newcastle disease virus-specific RNA: polyacrylamide gel analysis of single-stranded RNA and hybrid duplexes.
Newcastle disease virus-specific [(3)H]uridine-labeled 18S RNA was resolved by polyacrylamide gel electrophoresis into several components with molecular weights from 450,000 to 840,000. The analysis of 35 and 24S virus-specific RNA also revealed several components in each sedimentational class. The conversion of 18S RNA into double-stranded form by hybridization with an excess of unlabeled virion RNA improved the resolution in polyacrylamide gels and revealed at least six distinct components. The same six classes of hybrid duplexes were revealed when (32)P-labeled 50S virion RNA was hybridized with an excess of 18S RNA. The applicability of polyacrylamide gel electrophoresis of hybrid duplexes to the analysis of viral genome structure is discussed.
Animals↗
Inhibition of the multiplication of vesicular stomatitis and Newcastle disease virus by 2-deoxy-d-glucose.
The production of infectious vesicular stomatitis (VSV) and Newcastle disease virus can be completely inhibited by 2-deoxy-d-glucose in pyruvate-containing medium, if virus either grown in pyruvate-containing medium or dialyzed against phosphate-buffered saline is used for infection. Under these conditions, the synthesis of all VSV proteins is reduced. VSV RNA, which is synthesized at reduced rates, seems to be unstable. The effect is completely reversible. If virus grown in glucose-containing medium is used for infection, the production of both viruses is not significantly inhibited by 2-deoxy-d-glucose. Under these conditions the production of the VSV glycoprotein is specifically impaired, but does not lead to a marked reduction of the yield of infectious virus.
Amino Acids↗
Coding assignments of the five smaller mRNAs of Newcastle disease virus.
The polypeptide coding assignments for the five messengers of the 18S size class of Newcastle disease virus (NDV) RNA have been determined by cell-free translation of individual RNAs separated by gel electrophoresis. Listed in order of their decreasing electrophoretic mobilities in acid agarose-urea gels, the coding assignments of the RNAs were as follows: RNA 1, M protein; RNA 2, P protein; RNA 3, NP; RNA 4, F glycoprotein; and RNA 5, HN glycoprotein. RNA 2 also directed the synthesis of 33- and 36-kilodalton proteins, which were tentatively identified as being overlapping segments of the P protein. The 33- and 36-kilodalton polypeptides could be detected in infected cells, but not in purified virions of NDV. Since the other unique NDV RNA, a 35S species, has been shown previously to encode the viral L protein, these results complete the coding assignments of the six known NDV mRNAs.
Animals↗
Early interferon production in human diploid cells induced by Newcastle disease virus in the presence of protein synthesis inhibitors.
When human diploid cells were induced by Newcastle disease virus (NDV) in the presence of cycloheximide or puromycin, an early interferon was produced up to 4 hr after induction, but was not produced without these reagents. Early interferon production in rabbit kidney cells induced by NDV in the presence of cycloheximide was not observed. This early interferon production was also induced in response to hydroxylamine-treated NDV, ultraviolet light-irradiated NDV and Sepharose-coupled NDV, which had no or low induciblity of late interferon, and was inhibited by pretreatment with actinomycin D. Protein and RNA synthesis were enhanced in the cells which were treated with cycloheximide and then washed out as in the induction process. From these findings it has been suggested that the induction of early interferon synthesis in the cells pulse-treated with protein synthesis inhibitors, was triggered by an interaction between viral envelope and cell membrane.
Animals↗
Blood clearance of P32-labeled vesicular stomatitis and Newcastle disease viruses by the reticuloendothelial system in mice.
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Animals↗
The neuraminidase of Newcastle disease virus inhibited in the elution-inhibition reaction.
The neuraminidase (NA) on strain 575 of Newcastle disease virus (NDV) was inhibited with elution-inhibition (EI) antibodies causing permanent agglutination patterns of red blood cells (RBC). Detection of EI antibody was unaffected by passage through sephadex, centrifugation or plaque purification of NDV. The haemagglutination-inhibition (HI) and EI reactions as well as the NA inhibition test all showed an increase in titre as immunization progressed. Fluorescent-stained IgG on RBC from the EI reaction appeared as foci but as a halo if NDV was disrupted with ether suggesting NDV aggregation. The haemagglutinin (HA) on "sensitized' RBC from the EI reaction was not neutralized and agglutinated newly added RBC. The NA cleaved fetuin at 49 to 88% of the maximum values while bound to RBC by EI antibody. Added NA substrates failed to block the EI reaction. The order of inactivation at 53 or 56 degrees C but not 50 degrees C was: the putative EI antibody determinant > NA > HA. The term elution inhibition is suggested for the antibody responsible for the EI reaction.
Animals↗
Sequence variation in the Newcastle disease virus genome.
Full-length genome sequences of five virulent and five avirulent strains of Newcastle disease virus isolated between 1998 and 2002 in Victoria and New South Wales, Australia were determined. Comparisons between these strains revealed that coding sequence variability in the haemagglutinin-neuraminidase (HN), matrix (M) and phosphoprotein (P) gene sequences appeared to be more variable than in the fusion (F), nucleocapsid (N) and RNA dependent-RNA replicase (L) genes. Sequence analysis of a number of other isolates made during the recent virulent NDV outbreaks, also identified the presence of a number of variants with altered F gene cleavage sites, which resulted in altered biological properties of those viruses. Quasispecies analysis of a number of field isolates indicated the presence of virulent virus in one particular isolate. Gene sequence analysis of the progenitor virus isolated in 1998 showed very little sequence variation when compared to that of a progenitor-like virus isolated in 2001, demonstrating that in the field, viral genome sequence variation appears to be biologically restricted to that of a consensus sequence.
Amino Acid Sequence↗
Nucleocapsid protein subunits of simian virus 5, Newcastle disease virus, and Sendai virus.
Helical nucleocapsids of each of the paramyxoviruses simian virus 5 (SV5), Newcastle disease virus (NDV), and Sendai virus have been isolated in two different forms. One form contains larger protein subunits and is obtained from mature virions or infected cells dispersed by ethylenediaminetetraacetic acid. The other form possesses smaller subunits and is obtained from infected cells dispersed by trypsin. The estimated molecular weights of the larger subunits in the three viruses are similar: SV5, 61,000; Sendai virus, 60,000; NDV, 56,000. The smaller nucleocapsid subunits are also very similar: SV5, 43,000; Sendai virus, 46,000; NDV, 47,000. The helical nucleocapsid composed of the smaller subunit appears to be less flexible and more stable than that formed by the larger subunit. There is suggestive evidence that conversion of the larger subunit to the smaller by proteolytic cleavage may occur intracellularly. The possibility that such a mechanism could be involved in the accumulation of nucleocapsid in cells persistently infected with paramyxoviruses is discussed.
Acrylates↗