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PubMed1999

Differences in receptor specificity between Newcastle disease viruses originating from chickens and waterfowl.

We compared the receptor specificity of Newcastle disease viruses from a variety of avian species, including chickens and wild waterfowl, using hemagglutination tests with erythrocytes from different animal species. All isolates from wild waterfowl agglutinated horse erythrocytes, while the chicken isolates did not. The results showed that the receptor specificity of Newcastle disease viruses is different, depending on the avian species from which the viruses are isolated.

Animals↗
PubMedDate not supplied

interactions between escherichia coli and Newcastle disease virus in chickens.

We investigated the interaction between Newcastle disease virus (NDV) and Escherichia coli in cell cultures, embryonated eggs, and 8-wk-old chickens. We measured the interactions on the basis of bacterial adherence and NDV hemagglutination titer in chickens, chicken embryos, and chicken embryo cell culture. Depending on the inoculation order of E. coli, a significant alteration of the growth of NDV was observed in both chickens and chicken embryos. When certain strains of E. coli were given before NDV exposure, the virus titers were lowered. In chickens, the mean virus titer was significantly (P < 0.05) lowered in the crop, the proventriculus, the gizzard, and the jejunum. However, there were no significant differences (P < 0.05) between the two groups for NDV titers in the duodenum, ileum, and cecum. In chicken embryos, when E. coli serotypes O78 and O119:B14 were inoculated before NDV exposure, the mean NDV titers were significantly (P < 0.5) lowered. However, there were no significant differences (P < 0.05) in NDV titer between the two groups when E. coli serotypes O78:K80:NM and O1ab:K NM were inoculated 24 hr before NDV exposure. When NDV was given prior to E. coli exposure, NDV titer was higher in both chickens and chicken embryos. In chickens, when NDV was given 48 hr before E. coli inoculation, NDV was detected in the proventriculus, gizzard, jejunum, ileum, and cecum, whereas no virus was detected in the control groups (NDV only). In the crop, NDV was detected at a significantly (P < 0.05) higher titer in the E. coli-inoculated group when compared with the control group that received NDV alone. In chicken embryos, virus titer was significantly (P < 0.05) higher when NDV was given 24 hr before E. coli inoculation for all three NDV strains used (Ulster and V4 strains). Adherence of E. coli to chicken embryo kidney (CEK) cells was significantly higher (P < 0.05) when the CEK cells were infected first with NDV and then by E. coli. The mean bacterial count per microscopic field in NDV-uninfected monolayers was eight compared with 112 for the NDV-infected monolayers. In approximately 10% of the fields in NDV-infected monolayers, the bacteria were too numerous to count.

Animals↗
PubMed2006

Differentially regulated interferon response determines the outcome of Newcastle disease virus infection in normal and tumor cell lines.

Newcastle disease virus (NDV) is a negative-strand RNA virus with oncolytic activity against human tumors. Its effectiveness against tumors and safety in normal tissue have been demonstrated in several clinical studies. Here we show that the spread of NDV infection is drastically different in normal cell lines than in tumor cell lines and that the two cell types respond differently to beta interferon (IFN-beta) treatment. NDV rapidly replicated and killed HT-1080 human fibrosarcoma cells but spread poorly in CCD-1122Sk human skin fibroblast cells. Pretreatment with endogenous or exogenous IFN-beta completely inhibited NDV replication in normal cells but had little or no effect in tumor cells. Thus, the outcome of NDV infection appeared to depend on the response of uninfected cells to IFN-beta. To investigate their differences in IFN responsiveness, we analyzed and compared the expression and activation of components of the IFN signal transduction pathway in these two types of cells. The levels of phosphorylated STAT1 and STAT2 and that of the ISGF3 complex were markedly reduced in IFN-beta-treated tumor cells. Moreover, cDNA microarray analysis revealed significantly fewer IFN-regulated genes in the HT-1080 cells than in the CDD-1122Sk cells. This finding suggests that tumor cells demonstrate a less-than-optimum antiviral response because of a lesion in their IFN signal transduction pathway. The rapid spread of NDV in HT-1080 cells appears to be caused by their deficient expression of anti-NDV proteins upon exposure to IFN-beta.

Animals↗
PubMed1984

Structure of the major oligosaccharides in the fusion glycoprotein of Newcastle disease virus.

The fusion glycoprotein (F0) was isolated from Newcastle disease virus (NDV) particles metabolically labelled with [2-3H]mannose; it was successively digested with protease and with endo-beta-N-acetylglucosaminidase from Streptomyces griseus. In this manner, the majority of the oligosaccharides in NDV F0 could be liberated. After reduction with NaBH4, they were separated by high-performance liquid chromatography, and were subjected to structural analysis. Using micromethylation/capillary gas chromatography/mass fragmentography, alpha-mannosidase digestion, and acetolysis, it was found that the enzymatically released NDV F0 oligosaccharides are common oligomannosidic glycoprotein glycans of size classes (Man)8GlcNAc, Man)7GlcNAc, (Man)6GlcNAc, (Man)9GlcNAc, and (Man)5GlcNAc (in order of prevalence). The major structural isomers present in the NDV F0 (Man)8GlcNAc to (Man)5GlcNAc fractions were shown to lack mannose residues D2, D1D2 or D2D3, D1D2D3, and CD1D2D3, respectively, of (Man)9GlcNAc.

Acetone↗
PubMed2000

Newcastle disease virus activates macrophages for anti-tumor activity.

Newcastle Disease Virus (NDV), an agent with interesting immune stimulatory and anti-tumor activity, was investigated for its capacity to activate anti-tumor activity in murine macrophages in vitro and in vivo. Direct macrophage activation was seen under a variety of experimental conditions using two different strains of NDV, different sources of macrophages (spleen and peritoneum) and different strains of mice (DBA/2, C57BL/6, 615). Various macrophage enzymes (ADA, iNOS, lysozyme, acid phosphatase) became upregulated and anti-tumor effector molecules such as nitric oxide (NO) and TNF-alpha were found in the supernatant. NDV activated macrophages performed anti-tumor activity in vitro such as anti-tumor cytostasis and anti-tumor cytotoxicity. The cytotoxic anti-tumor activity was broad and active against all tumor lines tested including mammary carcinoma, lung carcinoma, mastocytoma and immune escape variants (lymphoma). Macrophage activation via BCG/LPS also caused a broad range anti-tumor cytotoxic activity while activation via mixed lymphocyte culture conditioned medium had restricted anti-tumor activity. Anti-tumor activity of NDV activated macrophages could be transfered in vivo. Transfer of macrophages which had not been appropriately activated exerted either no effect or a tumor growth augmenting effect. Repeated intravenous transfer of NDV activated macrophages exerted a significant suppressive effect on pulmonary metastases in a mammary carcinoma tumor model as well as in a lung carcinoma model. Taken together these results demonstrate that NDV can strongly activate macrophages to perform anti-tumor activities in vitro and in vivo.

Animals↗
PubMed2004

[Antitumor research on mouse melanoma with combined application of Newcastle disease virus and its HN gene].

BACKGROUND & OBJECTIVE: Although Newcastle disease virus (NDV) shows antitumor effect on many tumors, its mechanism is unclear. Hemagglutinin-neuraminidase (HN) gene was found to play an important role in NDV antitumor effect and HN protein located on tumor cell surface. This research was to evaluate the possibility of HN protein as a foreign antigen of tumor cell and the antitumor effect of the combined application of HN gene and NDV. METHODS: C57BL/6 mice were subcutaneously inoculated with 2 x 10(5) B16 tumor cells in the right hindlimb. Combination group: on 2nd day post-inoculation, the recombinant plasmid containing HN gene was injected intramuscularly in the left hindlimb; on 7th day post-inoculation, 2 x 10(9) pfu NDV was administrated intratumorally. The alone HN gene group, NDV group, and PBS control group were treated as above. The antitumor effect was observed through tumor suppression rate, the antitumor mechanisms were researched with specific cytotoxic T lymphocyte (CTL) assay, and the expression determination of HN protein, ICAM-I, and CD48 on the B16 tumor cells. RESULTS: The antitumor efficacy of the combined application of NDV and its HN gene increased compared with NDV,and its HN gene alone, the tumor suppression rates were 82.8%, 41.0%, and 56.6%; the specific CTL activity were 18.4%, 10.1%, and 4.4%, respectively. Furthermore, the expression of HN gene had been detected, and the expression of ICAM-I and CD48 were up-regulated on the tumor cells after NDV injection. CONCLUSION: HN protein located on the surface of tumor cells and mediated the specific repulsion to tumor cells; the antitumor efficacy increased after the combined application of NDV and its HN gene.

Animals↗
PubMed1990

Aberrant membrane insertion of a cytoplasmic tail deletion mutant of the hemagglutinin-neuraminidase glycoprotein of Newcastle disease virus.

The hemagglutinin-neuraminidase (HN) protein of Newcastle disease virus (NDV) is a type II glycoprotein oriented in the plasma membrane with its amino terminus in the cytoplasm and its carboxy terminus external to the cell. We have previously shown that the membrane insertion of HN protein requires signal recognition particle SRP, occurs cotranslationally, and utilizes the same GTP-dependent step that has been described for secretory proteins, type I proteins, and multispanning proteins (C. Wilson, R. Gilmore, and T. Morrison, Mol. Cell. Biol. 7:1386-1392, 1987; C. Wilson, T. Connolly, T. Morrison, and R. Gilmore, J. Cell Biol. 107:69-77, 1988). The role of the amino-terminal cytoplasmic domain in the faithful membrane insertion of this type II protein was explored by characterizing the membrane integration of a mutant lacking 23 of the 26 amino acids of the cytoplasmic domain. The mutant protein was able to interact with SRP, resulting in translation inhibition, membrane targeting, and membrane translocation, but the efficiency of translocation was considerably lower than for the wild-type HN protein. In addition, a significant proportion of the mutant protein synthesized in the presence of SRP and microsomal membranes was associated with the membrane in an EDTA- and alkali-insensitive manner yet integrated into membranes with its carboxy-terminal domain on the cytoplasmic side of membrane vesicles. Membrane-integrated molecules with this reverse orientation were not detected when the mutant protein was synthesized in the absence of SRP or a functional SRP receptor. Truncated mRNAs encoding amino-terminal segments of the wild-type and mutant proteins were translated to prepare ribosomes bearing arrested nascent chains. The arrested mutant nascent chain, in contrast to the wild-type nascent chain, was also able to insert into membranes in a GTP- and SRP-independent manner. Results suggest that the cytoplasmic domain plays a role in the proper membrane insertion of this type II glycoprotein.

Amino Acid Sequence↗
PubMed1957

An electron microscopic study of incomplete virus formation; infection of Ehrlich ascites tumor cells with chick embryo-adapted Newcastle disease virus (NDV).

The morphologic changes occurring in Ehrlich ascites tumor cells infected with chick embryo-adapted Newcastle disease virus were studied with phase microscope, conventional light microscope, and electron microscope. Intracytoplasmic inclusions appeared 2 to 4 hours following infection and progressively increased in size and numbers until cytolysis occurred. No significant alterations in mitochondria or other cell organelles were detected during the initial period of inclusion development. The inclusions were composed of a multilaminated shell, probably derived from the agranular reticulum of the EAT cell, surrounding an inner core packed with dense particles, measuring 3 to 14 mmicro in diameter. These particles were tentatively identified as the newly synthesized "incomplete virus" which had been previously demonstrated by fluorescent antibody techniques. The possible role of the inclusions is discussed.

Animals↗
PubMed1977

Effect of infectious bursal disease on the response of chickens to Mycoplasma synoviae, Newcastle disease virus, and infectious bronchitis virus.

At 35 days of age, chickens which as 1-day-old chicks were inoculated with the infectious bursal disease virus (IBDV) had significantly lower antibody titers against Mycoplasma synoviae, Newcastle disease virus, and infectious bronchitis virus than did those never inoculated with IBDV. The IBDV also had a marked effect on the development of air-sac lesions. Birds infected with IBDV that were later inoculated with M synoviae (day 14), Newcastle disease virus (days 14 and 28) experienced an increased incidence and greater seversity of airsacculitis than did chicks which were not exposed to IBDV.

Air Sacs↗
PubMedDate not supplied

Virus characterization and sequence of the fusion protein gene cleavage site of recent Newcastle disease virus field isolates from the southeastern United States and Puerto Rico.

Nine Newcastle disease virus (NDV) isolates obtained from Puerto Rico, Georgia, Alabama, Mississippi, and Texas were analyzed for in vivo pathogenicity, biological properties (hemagglutination of mammalian erythrocytes), and for sequence variation at the amino acid and sense RNA level of the fusion protein cleavage site. Intracerebral pathogenicity index values ranged from 0 to 0.3 and the intravenous pathogenicity index obtained for all isolates was 0. Four isolates hemagglutinated bovine erythrocytes, whereas no hemagglutination was observed using equine erythrocytes. By direct sequencing of reverse transcription polymerase chain reaction products, all the isolates had a predicted fusion cleavage sequence comparable to lentogenic NDV strains. Based on nucleotide sequence, the viruses could be grouped phylogenetically with the B1 vaccine-type virus. However, nucleotide sequences were not 100% similar to the B1 or La Sota NDV strains, indicating that minor genetic heterogeneity occurs among lentogenic field isolates of NDV.

Amino Acid Sequence↗
PubMed1975

Micro-radioimmunoassay for antibodies to Newcastle disease virus in the chicken.

An indirect micro-radioimmunoassay is described in which chicken anti-Newcastle disease virus antibody was detected, with radioactively labeled rabbit anti-chicken Fab, on virus-infected microcultures of chick embryo fibroblasts. Newcastle disease virus-infected microcultures were formalin fixed and stored at 4 degrees C for up to 4 months without affecting the sensitivity of the test. The micro-technique was found to be highly sensitive and specific assay of anti-viral antibody and may allow detection of immunoglobulin class of anti-Newcastle disease virus antibody.

Agammaglobulinemia↗
PubMed1999

Dot-enzyme linked immunosorbent assay for demonstration of Newcastle disease virus infection.

Dot-enzyme linked immunosorbent assay (ELISA) was standardised to detect Newcastle disease virus (NDV) specific antigen in chicken tissues, embryos and allantoic fluid samples. Samples positive by virus isolation were also found positive by haemagglutination (HA) and haemagglutination inhibition (HI) tests and by dot-ELISA but negative samples were found negative by all the serological tests used. Dot-ELISA was able to detect 0.25-0.50 HA units of virus. The emerging utility of dot-ELISA for diagnosis of Newcastle disease virus infection has been discussed.

Animals↗
PubMed1976

Comparative electrophoresis of the 18-22S RNAs of Newcastle disease virus.

Between 80 and 90% of the 18-22S Newcastle disease virus intracellular RNA molecules contain poly(A) sequences. Electrophoresis of the 18S RNA in formamide-polyacrylamide gels resolves five species resolved by electrophoresis in aqueous gels. Thus, these five RNA species are probably unique size classes of RNA and not different conformations of the same RNAs. They are of sufficient size to code for the five smaller Newcastle disease virus proteins, and their combined molecular weights represent 60% of the viral genome-a value identical to that obtained by annealing 18-22S RNA with genome RNA. Formamide or heat treatment of the 22S RNA converts most of it into species with migration rates similar to those of the 18S species. Thus, the 22S RNA may not contain unique RNA species.

Chromatography, Gel↗
PubMed2005

Environmental air sampling to detect exotic Newcastle disease virus in two California commercial poultry flocks.

The 2002--2003 Exotic Newcastle Disease (END) outbreak in Southern California poultry provided an opportunity to evaluate environmental air sampling as an efficient and cost-effective means of sampling flocks for detection of a circulating virus. Exotic Newcastle Disease virus was detected by real-time reverse transcriptase PCR from air samples collected using a wetted-wall cyclone-style air sampler placed within 2 m of birds in 2 commercial flocks suspected of being naturally exposed to END virus during the outbreak. Exotic Newcastle Disease virus was detected after 2 hours of air sampling the poultry-house environments of the 2 naturally infected flocks.

Animals↗
PubMed2004

Gangliosides and N-glycoproteins function as Newcastle disease virus receptors.

The interaction of enveloped viruses with cell surface receptors is the first step in the viral cycle and an important determinant of viral host range. Although it is established that the paramyxovirus Newcastle Disease Virus binds to sialic acid-containing glycoconjugates the exact nature of the receptors has not yet been determined. Accordingly, here we attempted to characterize the cellular receptors for Newcastle disease virus. Treatment of cells with tunicamycin, an inhibitor of protein N-glycosylation, blocked fusion and infectivity, while the inhibitor of O-glycosylation benzyl-N-acetyl-alpha-D-galactosamide had no effect. Additionally, the inhibitor of glycolipid biosynthesis 1-phenyl-2-hexadecanoylamino-3-morpholino-1-propanol blocked viral fusion and infectivity. These results suggest that N-linked glycoproteins and glycolipids would be involved in viral entry but not O-linked glycoproteins. The ganglioside content of COS-7 cells was analyzed showing that GD1a was the major ganglioside component; the presence of GM1, GM2 and GM3 was also established. In a thin-layer chromatographic binding assay, we analyzed the binding of the virus to different gangliosides, detecting the interaction with monosialogangliosides such as GM3, GM2 and GM1; disialogangliosides such as GD1a and GD1b, and trisialogangliosides such as GT1b. Unlike with other viruses, our results seem to point to the absence of a specific pattern of gangliosides that interact with Newcastle disease virus. In conclusion, our results suggest that Newcastle disease virus requires different sialic acid-containing compounds, gangliosides and glycoproteins for entry into the target cell. We propose that gangliosides would act as primary receptors while N-linked glycoproteins would function as the second receptor critical for viral entry.

Animals↗
PubMed1992

Induction of C3 expression in astrocytes is regulated by cytokines and Newcastle disease virus.

Synthesis of complement proteins and their regulation in resident cells of the central nervous system are important pathophysiologic factors that can affect the outcome of inflammatory central nervous system diseases. Primary cultures of rat astrocytes constitutively express C3 mRNA and produce C3 protein; both of them were enhanced by LPS or by a live as well as inactivated Newcastle disease virus, a neurotropic paramixovirus. TNF, IL-1 beta, and IL-8 also increased the levels of C3 mRNA and protein whereas IL-1 alpha and IL-6 had no effect, although all of these cytokines are inducible by LPS. LPS stimulation in the presence of cycloheximide decreased the LPS-mediated C3 mRNA induction by 60%. These data suggest that LPS effect on C3 regulation is mediated directly by LPS as well as by LPS-induced cytokines. Interestingly, C3 mRNA induced by Newcastle disease virus or inactivated Newcastle disease virus was inhibited by protein kinase inhibitors, H-7 and staurosporine, whereas these inhibitors had no effect on C3 induction mediated by LPS or cytokines, indicating the existence of different signal transduction pathways.

Alkaloids↗