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PubMed2006

Integrity of membrane lipid rafts is necessary for the ordered assembly and release of infectious Newcastle disease virus particles.

Membrane lipid raft domains are thought to be sites of assembly for many enveloped viruses. The roles of both classical lipid rafts and lipid rafts associated with the membrane cytoskeleton in the assembly of Newcastle disease virus (NDV) were investigated. The lipid raft-associated proteins caveolin-1, flotillin-2, and actin were incorporated into virions, while the non-lipid raft-associated transferrin receptor was excluded. Kinetic analyses of the distribution of viral proteins in lipid rafts, as defined by detergent-resistant membranes (DRMs), in non-lipid raft membranes, and in virions showed an accumulation of HN, F, and NP viral proteins in lipid rafts early after synthesis. Subsequently, these proteins exited the DRMs and were recovered quantitatively in purified virions, while levels of these proteins in detergent-soluble cell fractions remained relatively constant. Cholesterol depletion of infected cells drastically altered the association of viral proteins with DRMs and resulted in an enhanced release of virus particles with reduced infectivity. Decreased infectivity was not due to effects on subsequent virus entry, since the extraction of cholesterol from intact virus did not significantly reduce infectivity. Particles released from cholesterol-depleted cells had very heterogeneous densities and altered ratios of NP and glycoproteins, demonstrating structural abnormalities which potentially contributed to their lowered infectivity. Taken together, these results indicate that lipid rafts, including cytoskeleton-associated lipid rafts, are sites of NDV assembly and that these domains are important for ordered assembly and release of infectious Newcastle disease virus particles.

Animals↗
PubMed1996

Effect of mixed infection of Mycoplasma gallinarum and Newcastle disease virus (F strain) on the tracheal epithelium of village chickens.

The effects of a mixed infection of Mycoplasma gallinarum and Newcastle disease virus (F strain) on the tracheal epithelium of village chickens were investigated and observed by scanning electron microscopy. Day-old village chicks were vaccinated intranasally with F strain Newcastle disease virus and inoculated intratracheally on the same day with 10(8) colony forming units of M gallinarum. In another study the chicks were vaccinated and then infected with M gallinarum seven days later. The first group of chicks was euthanased three, seven, 10, 14 and 21 days after vaccination and infection and the vaccinated chicks were euthanased three, seven, 10 and 14 days after infection. In the chicks vaccinated and infected on the same day, major alterations to the tracheal epithelium were visible three days later. There were fewer ciliated cells and the borders of the non-ciliated cells were prominent. Several depressions had formed in the epithelial surface. At higher magnification, clumps of microvilli were visible on some of the non-ciliated cells. Seven days after vaccination and infection, the tracheal epithelium appeared normal, with an increase in the numbers of ciliated cells, although raised borders were observed on the non-ciliated cells in some areas. No clumping of microvilli or depressions in the epithelial surface were observed. In the chicks infected seven days after vaccination, the tracheal epithelium appeared normal with no visible changes on its surface.

Animals↗
PubMed1973

Thermal inactivation of Newcastle disease virus. I. Coupled inactivation rates of hemagglutinating and neuraminidase activities.

The thermal stability of Newcastle disease virus has been characterized in terms of the rate constants for inactivation of hemagglutinating activity (HA), neuraminidase activity (NA), and infectivity. Inactivation of HA results in the concomitant loss of NA. Infectivity, however, is much more thermolabile. Disintegration of the virus particle is not responsible for the identical rate constants for inactivation of HA and NA, nor is their parallel inactivation uncoupled in envelope fragments produced by pretreating the virus with phospholipase-C. The data indicate that a common envelope factor(s) can influence the thermal stability of both activities.

Animals↗
PubMed1988

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↗
PubMed1975

Radioiodination of the envelope proteins of Newcastle disease virus.

Lactoperoxidase-catalyzed iodination selectively labels the two glycoproteins (VP1 and VP2) of Newcastle disease virus. The low-molecular-weight, nonglycosylated major viral protein, VP6, was not iodinated in the intact virus but was iodinated in disrupted virions, suggesting a localization on the inner, rather than the outer, envelope surface. Studies on the distribution of virion proteins labeled with 125-I and 3-H-isoleucine between detergent-soluble and detergent-insoluble fractions show that the virion proteins VP4, VP5, and VP6 are solubilized to a much lesser extent than are VP1 and VP2.

Animals↗
PubMed1989

Effect of Newcastle disease virus infection on vitamin A metabolism in chickens.

The effect of Newcastle disease virus (NDV, La Sota strain) infection on vitamin A metabolism was investigated in chickens maintained on normal or marginal vitamin A intake. NDV, a virus of the Paramyxoviridae family that primarily affects epithelial tissue, was administered at 4 wk of age. Plasma levels of retinol, retinol-binding protein and, to a lesser extent, transthyretin were found to be significantly lower during both the acute and postacute phases of infection in chickens fed a diet marginally deficient in vitamin A compared to noninfected birds fed the same diet, while vitamin A content in liver was unaffected. However, in chickens fed adequate vitamin A, NDV infection did not influence the parameters measured. Levels of retinol-binding protein in liver were significantly increased by inadequate vitamin A nutriture, but infection partly reduced this increase. The results suggest that the reduced vitamin A status in marginally vitamin A-deficient chickens infected with NDV can be attributed to a combination of a direct effect of the virus on retinol-binding protein metabolism in liver and an increased rate of utilization and catabolism of retinol and retinol-binding protein by extrahepatic tissues.

Age Factors↗
PubMedDate not supplied

Characterization of isolates of Newcastle disease virus from migratory birds and turkeys.

The susceptibility of wild birds to infection with Newcastle disease virus (NDV) has resulted in speculation about the role of these free-flying birds in the origin and transmission of the virus infection. Since several NDV isolates from free-flying waterfowl and turkey flocks in the Midwest were avirulent for chickens and had thermostable hemagglutinins, isolates were collected from both waterfowl and turkeys over a seven-year period, 1974-1980, for comparison. Strains from both waterfowl and turkeys were avirulent, based on mean death times in chicken embryos, and could be differentiated from licensed vaccine strains with similar mean death times by in vitro markers. Waterfowl strains were generally thermostable, were slow to elute from chicken red blood cells, and produced plaques in chicken embryo fibroblasts. Some of the turkey isolates were similar to the waterfowl strains in thermostability, elution, and production of plaques in chick embryo fibroblasts. However, in the latter years of the study, there was a tendency toward isolation from turkey flocks of vaccine-like strains that did not produce plaques without additives and whose hemagglutinin was thermolabile. The appearance of these strains reflects either a selection for this virus type by the host or replacement of field strains by vaccine strains as the result of an increased usage of vaccines by producers.

Animals↗
PubMed1966

Role of interferon-like viral inhibitor in endotoxin-induced corneal resistance to Newcastle disease virus.

Oh, J. O. (University of British Columbia, Vancouver, B.C., Canada), and E. J. Gill. Role of interferon-like viral inhibitor in endotoxin-induced corneal resistance to Newcastle disease virus. J. Bacteriol. 91:251-256. 1966.-A state of marked resistance to the toxic corneal effects of Newcastle disease virus (NDV) was observed in rabbit eyes after intravenous injection of 10 or 100 mug of typhoid endotoxin. By use of tissue cultures of rabbit corneal endothelial cells for assay, high titers of an interferon-like viral inhibitor were detected in serum and in ocular aqueous humor of these animals. The pretreatment of eyes with aqueous humor or serum containing the inhibitor markedly suppressed the production of corneal toxicity by NDV. The intravenous injection of 1 mug of the endotoxin had a negligible effect on the corneal reaction, and little or no inhibitor was found in either serum or aqueous humor. Normal aqueous humor or serum contained no inhibitor and had no suppressive effect on the NDV-induced reactions. The results indicated that the inhibitor played an important role in the induction of corneal resistance to NDV in vivo. The inhibitor in aqueous humor of endotoxin-injected rabbits was found to be derived from blood after an increase in the permeability of "blood-aqueous barrier" of iris due to the endotoxin. Therefore, intravenously administered typhoid endotoxin induced corneal resistance to NDV in rabbits through its dual action on host: (i) release of an interferon-like viral inhibitor into the blood stream and (ii) disruption of the blood-aqueous barrier of the iris, thus allowing the passage of the viral inhibitor from blood into the anterior chamber, where it modified the corneal endothelial cells to render them resistant to NDV.

Animals↗
PubMed1973

Temperature-sensitive defect of mutants isolated from L cells persistently infected with Newcastle disease virus.

The temperature-sensitive defects of virus mutants isolated from L cells persistently infected with Newcastle disease virus (NDV) were analyzed. Genetic grouping of the mutants by complementation tests was attempted by using several different methods, including yield analysis, RNA synthesis, and heterozygote formation at 42 to 43 C, the nonpermissive temperature. In each case, specific interference prevented detection of complementation. This interference was shown to occur prior to or at the level of virus RNA synthesis. Temperature-shift experiments with five different NDV(pi) clones showed that virus replication begun at 37 C could not be completed at the nonpermissive temperature. The activity of the NDV-specific RNA-dependent RNA polymerase in the cytoplasm of infected chicken embryo cells was not stable and could not be demonstrated directly. However, indirect measurement of RNA polymerase activity at the nonpermissive temperature was accomplished by studying the kinetics of virus-specific RNA synthesis in infected cells after temperature shift. Two types of response were obtained: with three NDV(pi) clones, virus-specific RNA synthesis ceased immediately upon transfer of infected cells to 42 to 43 C, whereas in cells infected with two other NDV(pi) clones, RNA synthesis continued for several hours at this temperature. These results suggested that there may be two types of ts defects in NDV(pi), both associated with virus-specific RNA polymerase activity.

Animals↗
PubMedDate not supplied

[Sedimentation properties of virion RNA of Newcastle disease virus after annealing under different conditions].

After annealing at high temperatures 50S RNA of Newcastle disease virus was partially degraded. The resulting fragments had the sedimentation coefficient of 23--32S. Solution of dimethylsulfoxide and formamide were used to decrease the temperature of annealing. However, annealing with denaturating agents caused agglomeration of 50S RNA molecules. This phenomenon is discussed.

Centrifugation, Density Gradient↗
PubMed2003

Role of the cytoplasmic domain of the Newcastle disease virus fusion protein in association with lipid rafts.

To explore the association of the Newcastle disease virus (NDV) fusion (F) protein with cholesterol-rich membrane domains, its localization in detergent-resistant membranes (DRMs) in transfected cells was characterized. After solubilization of cells expressing the F protein with 1% Triton X-100 at 4 degrees C, ca. 40% of total, cell-associated F protein fractionated with classical DRMs with densities of 1.07 to l.14 as defined by flotation into sucrose density gradients. Association of the F protein with this cell fraction was unaffected by the cleavage of F(0) to F(1) and F(2) or by coexpression of the NDV attachment protein, the hemagglutinin-neuraminidase protein (HN). Furthermore, elimination by mutation, of potential palmitate addition sites in and near the F-protein transmembrane domain had no effect on F-protein association with DRMs. Rather, specific deletions of the cytoplasmic domain of the F protein eliminated association with classical DRMs. Comparisons of deletions that affected fusion activity of the protein and deletions that affected DRM association suggested that there is no direct link between the cell-cell fusion activity of the F protein and DRM association. Furthermore, depletion of cholesterol from cells expressing F and HN protein, while eliminating DRM association, had no effect on the ability of these cells to fuse with avian red blood cells. These results suggest that specific localization of the F protein in cholesterol-rich membrane domains is not required for cell-to-cell fusion. Paramyxovirus F-protein cytoplasmic domains have been implicated in virus assembly. The results presented here raise the possibility that the cytoplasmic domain is important in virus assembly at least in part because it directs the protein to cholesterol-rich membrane domains.

Amino Acid Sequence↗
PubMed2006

Adaptation of a velogenic Newcastle disease virus to vero cells: assessing the molecular changes before and after adaptation.

A velogenic Newcastle disease virus isolate was passaged 50 times in Vero cell culture and the virus was assessed for the molecular changes associated with the passaging. At every 10th passage, the virus was characterized conventionally by mean death time (MDT) analysis, intracerebral pathogenicity index (ICPI) and virus titration. At increasing passage levels, 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 135 nucleotide substitutions which resulted in the change of 42 amino acids between the velogenic virus and the 50th passage virus. The predicted amino acid motif present at the cleavage site of the virulent virus was (109)SRRRRQRRFVG(119) and the corresponding region of the adapted adapted virus was (109)SGGRRQKRFIG(119). Pathogenicity studies conducted in 20-week-old seronegative birds revealed gross lesions such as petechial haemorrhages in the trachea, proventricular junction and intestines, and histopathological changes such as depletion and necrosis of the lymphocytes in thymus, spleen, bursa and caecal tonsils in the birds injected with the velogenic virus and absence of the lesions in birds injected with the adapted virus. The 50th-passage cell culture virus was back-passaged five times in susceptible chickens and subjected to virulence attribute analysis and sequence analysis of the FPCS region, with minor difference found between them.

Amino Acid Sequence↗