Mechanism of the teratogenic action of Newcastle disease virus in the chick embryo.
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Animals↗
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Mouse hydrocephalus and encephalitis following intracerebral infection with Newcastle disease vaccine viruses.
Hydrocephalus and encephalitis in 14-day-old mice was induced by an intracerebral inoculation of a high dose of live Newcastle disease vaccine viruses. The distended lateral ventricles occurred as a result of aqueduct stenosis superimposed on ciliary degeneration and destruction of ependymal cells. The brain virus titres were high on Days 3, 5 and 7 but never exceeded the titre of the original dose given. Positive serum haemagglutination-inhibition titres persisted throughout the experiment.
Animals↗
Studies on the chemotherapy of influenza virus. I. Effect of thiosemicarbazones on influenza and Newcastle disease virus multiplication.
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Animals↗
Repair replication of HeLa cell deoxyribonucleic acid in cells infected with Newcastle disease virus or mengovirus or treated with puromycin.
We examined repair replication of HeLa cell deoxyribonucleic acid (DNA) in cells infected with mengovirus or Newcastle disease virus or treated with puromycin. Cellular DNA was damaged by ultraviolet light and then pulse-labeled with (3)H-thymidine. Autoradiographic analysis of non-S-phase DNA synthesis (repair replication) showed that there was no inhibition of this process at a time when overall cellular DNA synthesis was severely inhibited by either virus infection or puromycin treatment.
Autoradiography↗
[Differences in the polypeptide composition of virulent and avirulent strains of Newcastle disease virus in reproduction in chick embryo fibroblast culture].
The loss of the capacity for secondary infection of the cells in reproduction of avirulent Newcastle disease virus strains in chick embryo fibroblast cultures was found. This loss was shown to be associated with changes in the polypeptide composition of the virions. In virions of the avirulent Queensland strain incapable of infection CEF cultures an additional polypeptide was found with molecular mass of 67,000 daltons which was lacking in virions of the virulent Beaudette strain and corresponded to F0 protein of paramyxoviruses.
Animals↗
An alternative method of oligonucleotide fingerprinting for resolving Newcastle disease virus-specific RNA fragments.
The technique of "RNA oligonucleotide fingerprinting" was adapted for the purpose of identifying genetic differences among strains of Newcastle disease virus (NDV). The specific method used for visualizing patterns of viral RNA fragments in two-dimensional polyacrylamide gels has several advantages over previously published procedures: It has low input radiation, high resolution, and low biohazard considerations. For demonstration purposes, the La Sota strain of NDV was fingerprinted. These initial results suggest that oligonucleotide mapping may provide an approach for correlating changes in the pathogenicity of NDV with the presence or absence of specific viral RNA sequences.
Animals↗
Selective inhibition of Newcastle disease virus-induced glycoprotein synthesis by D-glucosamine hydrochloride.
d-Glucosamine selectively affected the synthesis of virus-induced glycoproteins in Newcastle disease virus-infected chick fibroblasts, but had no effect upon post-translational cleavage of the glycoprotein precursor for one of the two major glycoproteins of the mature virion. In response to glucosamine, at least one of the two virus-induced glycoproteins is formed in reduced quantity and the second is either not formed or has an electrophoretic mobility identical to that of another virus-induced protein.
Animals↗
Enhanced production of virus-inhibiting factor (interferon) in human diploid cells by ultraviolet irradiation and temperature shift-down after stimulation with Newcastle disease virus.
The production of the virus-inhibiting factor or interferon (IF) was highest in cells incubated at 37 C after inoculation with Newcastle disease (ND) virus and decreased as the incubation temperature was lowered. Shift-down of incubation temperature to 32 C or 34 C after incubation at 37 C for 4--7 hr enhanced IF production in cell cultures stimulated with ND virus, as compared with cultures incubated continuously at 37 C. Shift-down to 32 C after incubation at 37 C for 6 hr was optimal for this enhancement of IF yield. Enhanced IF production was also observed in cell cultures irradiated by ultraviolet light 4--7 hr after stimulation with ND virus.
Cell Line↗
Effect of route of Newcastle disease vaccination on the incidence of airsacculitis in chickens infected with Mycoplasma synoviae.
In two separate experiments, broiler-type chickens were vaccinated at 11 days old with either the B-1 or LaSota strain of Newcastle disease virus (NDV) by aerosol, drinking water, or eyedrop and simultaneously infected with Mycoplasma synoviae (MS). The MS-infected and aerosol-vaccinated chickens had the highest mean lesion scores for airsacculitis. The aerosol-vaccinated groups had the highest hemagglutination-inhibition titers against NDV. Infection with MS had no effect on antibody titers against NDV, and there were no consistent effects on weight gains.
Administration, Oral↗
Plaque formation of Newcastle disease virus in primary chicken kidney cells.
Using primary chicken kidney (PCK) cells, a plaque assay was carried out with an avirulent strain of Newcastle disease virus (NDV) without adding trypsin to the agar overlay medium. The plaque assay was done in less than 4 days in PCK cells, by 3 days earlier than in primary chicken embryo (CE) cells maintained in the presence of trypsin. The curves of the progeny virus production began to rise 6 h after the infection and reached a plateau at 12 h. Equal amounts of virus were produced in PCK cells both in the presence and absence of trypsin in the culture medium. Viral peptide analysis revealed that a large portion of the HN and F precursor envelope glycoproteins of the NDV-Ulster strain remained uncleaved in PCK-grown virions. This suggests that a marginal proteolytic cleavage of these glycoprotein suffices for the full growth of the progeny virus in PCK cells. A higher shut-off in the host protein synthesis occurred in the virus-infected PCK cells than in the infected CE cells.
Animals↗
Vaccination of chickens with a recombinant fowlpox virus containing the hemagglutinin-neuraminidase gene of Newcastle disease virus under the control of the fowlpox virus thymidine kinase promoter.
When chickens were vaccinated with a recombinant fowlpox virus (FPV) containing the Newcastle disease virus (NDV) hemagglutinin-neuraminidase (HN) cDNA under the control of the thymidine kinase (TK) promoter and inserted into the FPV TK gene, the FPV antibody response to the recombinant virus was similar to the response to vaccination with standard FPV, and the recombinant virus protected chickens against challenge with virulent FPV. While the presence of the NDV HN cDNA was demonstrated in the recombinant virus, which was stable on serial passage, expression of HN was not detected by hemagglutination, Western blot analysis or immunoprecipitation of infected cell lysate. Chickens vaccinated with the recombinant virus failed to mount an NDV hemagglutination-inhibition antibody response, and they did not resist challenge with velogenic NDV. It was concluded that the TK promoter was too weak to drive the HN gene, but that the insertion into the FPV TK gene did not reduce the immunogenicity of the virus.
Animals↗
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↗
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↗
Succinic dehydrogenase activity in HeLa cells infected with Newcastle disease virus.
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Animals↗
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↗
Inclusion bodies from Newcastle disease virus in HeLa cells.
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Animals↗
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↗
Vitamin A deficiency impairs cytotoxic T lymphocyte activity in Newcastle disease virus-infected chickens.
The effect of vitamin A deficiency on cytotoxic T lymphocyte (CTL) activity was investigated during the acute phase of disease 7 days after primary inoculation and 1 day after secondary inoculation in chickens with or without Newcastle disease virus (NDV, La Sota strain) infection. Day-old chickens with limited vitamin A reserves were fed purified diets containing either marginal (ad libitum) or adequate (pair-fed) levels of vitamin A, and at 3 weeks of age half of the chickens in each group were infected with NDV. Cytotoxic activity was investigated during the acute phase of disease (7 days after primary inoculation) and 1 day after secondary inoculation, in an assay system with either peripheral blood lymphocytes (PBL) or nonadherent splenocytes as effector cells and adherent splenocytes from the same animal as target cells. After primary inoculation, cytotoxic activity could only be demonstrated in nonadherent splenocytes. Vitamin A deficiency resulted in significantly reduced CTL activity at all effector/target cell ratios tested. After reinfection CTL activity could also be demonstrated in PBL, but only from chickens fed the control diet, suggesting a diminished pool of CTL in vitamin A deficiency. The results of this study indicate that vitamin A deficiency impairs CTL activity - a part of the cell-mediated defense system - and this may have important implications for recovery from viral infection.
Animals↗