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At least 19 recordsLinked to original sources
PubMed1978

Isolation and characterization of defective interfering particle of Newcastle disease virus.

Newcastle disease virus grown in embryonated eggs was separated and purified by sucrose density gradient centrifugation into two distinct type of particles, B and T, the former being normal virus particles with high activities of hemagglutination, hemolysis, neuraminidase and infectivity, the latter being non-infectious virus particles with low activities of hemolysis and neuraminidase but high hemagglutination activity. B and T particles were shown to share a common antigen by immunodiffusion test. T particles were deficient in viral RNA, since they contained only 13s RNA in a small amount, whereas B particles possessed a large amount of 57s RNA and a small amount of 13s RNA. T particles interfered with the multiplication of normal Newcastle disease virus in primary cultures of chick embryo cells.

Animals↗
PubMed1970

Effect of temperature on radiosensitivity of Newcastle disease virus.

Newcastle disease virus was irradiated at temperatures ranging from 2.2 to 60 C. An interaction between the thermal and ionizing energy was observed in the temperature region of 49 to 60 C. At 2.2 C, the hemagglutinin was considerably more radioresistant than the infectivity property. It is believed that radiation inactivation of Newcastle disease virus infectivity at low temperatures was due to nucleic acid degradation and at higher temperatures was due to protein denaturation.

Antibodies↗
PubMed1988

Quantitative basic residue requirements in the cleavage-activation site of the fusion glycoprotein as a determinant of virulence for Newcastle disease virus.

Newcastle disease virus exhibits a wide range of pathogenicity and virulence which, as with all paramyxoviruses, is directly related to the cleavability of a precursor (F0) of the fusion glycoprotein by cellular proteases. Sequence analyses of the cleavage site of several virulent and avirulent isolates of the Newcastle disease virus serotype reveal a correlation between virulence or pathogenicity and a high content of basic amino acid residues at the cleavage site. A similar correlation has been seen for other paramyxoviruses.

Amino Acid Sequence↗
PubMed1957

Immunohistochemical studies on the interaction between Ehrlich ascites tumor cells and Newcastle disease virus.

Newcastle disease virus infection of Ehrlich ascites tumor cells resulted, after a period of time, in the appearance of intracellular viral antigen which could be demonstrated by the fluorescent antibody technique. This antigen appeared in the cytoplasm of infected cells only after inoculation of cell-virus mixtures into the peritoneal cavities of mice. The latent period prior to the appearance of antigen depended inversely on the number of viral particles adsorbed onto the cells prior to inoculation. The final intensity of staining appeared not to be proportionate to the number of viral particles adsorbed to each cell. The appearance of this antigen was not correlated with a rise of titer of infectious, hemagglutinating, or complement-fixing virus. Viral antigen was demonstrated on the surface of tumor cells after adsorption of NDV onto these cells at 0 degrees C. At appropriate virus:cell ratios, antigen was noted to disappear from the surface at 37 degrees C. in vitro, and in vivo, in the absence of demonstrable elution of virus. The appearance of intracellular viral antigen could not be detected in vitro when tumor cell-NDV mixtures were incubated at 37 degrees C., even when an average of 1550 "infectious particles" had adsorbed to each cell.

Animals↗
PubMedDate not supplied

The avian response to Newcastle disease virus.

Newcastle disease virus (NDV) is classified as a member of the superfamily Mononegavirales in the family Paramyxoviridae. This virus family is divided into two subfamilies, the Paramyxovirinae and the Pneumovirinae. In 1993 the International Committee on the Taxonomy of Viruses rearranged the order of the Paramyxovirus genus and placed NDV within the Rubulavirus genus among the Paramyxovirinae. The enveloped virus has a negative sense single-stranded RNA genome of 15,186 kb which codes for an RNA directed RNA polymerase, hemagglutinin-neuraminidase protein, fusion protein, matrix protein, phosphoprotein and nucleoprotein in the 5' to 3' direction. The virus has a wide host range with most orders of birds reported to have been infected by NDV. Isolates are characterized by virulence in chickens and are categorized into three main pathotypes depending on severity of disease. Lentogenic isolates are of low virulence while viruses of intermediate virulence are termed mesogenic. Highly virulent viruses that cause high mortality in birds are termed neurotropic or viscerotropic velogenic. Velogenic NDV are List A pathogens that require reporting to the Office of International Epizootics and outbreaks result in strict trade embargoes. The primary molecular determinant for NDV pathogenicity is the fusion protein cleavage site amino acid sequence. Vaccination for NDV is primarily by mass application of live-virus vaccines among commercial poultry. Although protection is measured by presence of antibodies to NDV, vaccinated B-cell depleted chickens are resistant to disease. Consequently, immune protection involves responses that are presently incompletely defined.

Animals↗
PubMedDate not supplied

Characterization of Nigerian strains of Newcastle disease virus.

Newcastle disease virus was isolated from outbreaks of the disease in vaccinated and unvaccinated poultry flocks representing commercial and backyard farms in different parts of Nigeria. On characterization, all 12 isolates were found to be velogenic.

Animals↗
PubMed1976

The mediator of cellular immunity. XII. Inhibition of activated T cells by Newcastle disease virus.

Newcastle disease virus (NDV) can interact in at least two ways with rat T cells. By adsorbing to circulating lymphocytes, the virus can transiently deflect the cells from lymph nodes and inflammatory exudates induced in the peritoneal cavity. T cells are affected regardless of age, state of activation, or position in the mitotic cycle. The effect is reversible and is mediated not only by infectious (I)-NDV, but also by UV-NDV which cannot achieve a complete replication cycle in eggs. But I-NDV has another lasting effect on activated T cells. It is revealed in the failure of virus-treated thoracic duct lymphocytes to transfer cellular resistance to Listeria monocytogenes, delayed-type hypersensitivity to soluble antigens of the parasite, and the permanent exclusion of labeled S-phase lymphocytes from inflammatory foci. Activated T cells are inhibited by virus multiplicites which have little if any effect upon the proliferative potential of antigen-sensitive T cells or localization of labeled small lymphocytes in lymph nodes. The underlying mechanism has not been determined; however, there are reasons for thinking that NDV has a lethal effect upon activated T cells, because the latter are permissive for virus replication.

Animals↗
PubMed1975

The role of interferon in interference and auto-interference elicited by Newcastle disease virus.

Newcastle disease virus (NDV) strains interfere in different degree with the growth of the velogenic NDV strain Texas GB (homologous interference) and Sindbis virus (heterologous interference) in chick embryo fibroblast cells. Homologous interference was elicited by interferon-producing live or UV-inactivated strains and non-interferon-producing live or beta-propiolactone-inactivated strains and it was not influenced by actinomycin D. Thus, interferon had apparently no role in homologous interference of NDV. The growth of Sindbis virus was, however, much more inhibited by interferon-producing live or UV-inactivated NDV strains than with non-inducing ones and the interference was reversible by actinomycin D. Thus heterologous interference is apparently mediated by interferon. In chicken cells infected with the mesogenic NDV strain H, virus yields were 50 to 100 times lower at multiplicities of infection above 0.1 p.f.u./cell than below it. The interferon formed during infection played no role in auto-interference, but may well be held responsible for the mild cytopathic effect observed.

Animals↗
PubMed1993

Retinoic acid enhances killing of neuroblastoma cells by Newcastle disease virus.

Newcastle disease virus (NDV), an avian pathogen, selectively replicates in and kills neuroblastoma (NB) cells, but not normal fibroblasts in vitro and in vivo in nude mice. NDV cytotoxicity towards NB cells is enhanced by N-myc oncogene amplification. To further define the antineoplastic effects of NDV, we examined NDV's interaction with NB cells following short-term exposure to the differentiating agent, all-trans retinoic acid (RA), and to neuraminidase. The human NB cell line IMR-32, after treatment with 50 mumol/L RA, became eight times more sensitive to NDV in a cytotoxicity assay. A time course study to determine the optimal incubation period of IMR-32 cells with RA indicated that a fourfold increase in sensitivity towards NDV killing occurred after only 8 hours of RA incubation prior to addition of virus. Maximal sensitivity was achieved at 24 hours of RA incubation and remained constant for longer incubation periods (up to 72 hours). The sensitization of IMR-32 NB cells to NDV was constant for RA doses between 3 mumol/L and 50 mumol/L. Plaque formation, which indicates replication, virus spread and cytotoxicity by a single infectious virus particle, was also enhanced by RA. This effect does not appear to require N-myc amplification in the target NB cells since RA had similar effects upon the high N-myc (IMR-32) and the low N-myc expressing cells (SK-N-SH). Enhanced sialylation has been shown by others to mediate the growth inhibitory effects of RA on a variety of tumor lines. Removal of sialic acid from the IMR-32 NB cell surface using Clostridium neuraminidase (2.7 mg/mL) inhibited 75% of NDV plaque formation. These results demonstrate that NDV killing of two NB cell lines is enhanced using clinically achievable levels of RA and that sialylation of the NB cell surface is important for virus binding and cytotoxicity.

Cytopathogenic Effect, Viral↗
PubMed2004

Role of fusion protein cleavage site in the virulence of Newcastle disease virus.

Newcastle disease virus (NDV) causes a highly contagious and economically important disease in poultry. Viral determinants of NDV virulence are not completely understood. The amino acid sequence at the protease cleavage site of the fusion (F) protein has been postulated as a major determinant of NDV virulence. In this study, we have examined the role of F protein cleavage site sequence in NDV virulence using reverse genetics technology. The sequence G-R-Q-G-R present at the cleavage site of the F protein of avirulent strain LaSota was mutated to R-R-Q-K-R, which is present in the F cleavage site of neurovirulent strain Beaudette C (BC). The resultant mutated LaSota V.F. virus did not require exogenous protease for infectivity in cell culture, indicating that the F protein was cleaved by intracellular proteases. The virulence of the mutant and parental viruses was evaluated in vivo by intracerebral pathogenicity index (ICPI) and intravenous pathogenicity index (IVPI) tests in chickens. Our results showed that the modification of the F protein cleavage site resulted in a dramatic increase in virulence from an ICPI value of 0.00 for LaSota to a value of 1.12 for LaSota V.F. However, the ICPI value of LaSota V.F. was lower than that of BC, which had a value of 1.58. Interestingly, the IVPI tests showed values of 0.00 for both LaSota and LaSota V.F. viruses, compared to the IVPI value of 1.45 of BC. In vitro characteristics of the viruses were also studied. Our results demonstrate that the efficiency of cleavage of the F protein plays an important role if the NDV is delivered directly into the brains of chicks, but there could be other viral factors that probably affect peripheral replication, viremia, or entry into the central nervous system.

Amino Acid Sequence↗
PubMedDate not supplied

Isolation and biological properties of some Moroccan strains of Newcastle disease virus.

Newcastle disease virus was isolated from six field cases in Morocco. On the basis of the mean death time of chicken embryos, the intracerebral pathogenicity index, and plaque formation on chicken embryo fibroblast monolayers, five isolates were determined to be of the velogenic pathotype. One of these differed from the others in that it agglutinated equine erythrocytes. The sixth isolate was found to be of low virulence but differed from the vaccinal strain tested.

Animals↗
PubMed2004

Importance of serine 200 for functional activities of the hemagglutinin-neuraminidase protein of Newcastle Disease Virus.

Newcastle disease virus (NDV) is an avian paramyxovirus with replication competence in human tumor cells and interesting anti-neoplastic and immune stimulatory properties. In order to increase tumor selectivity of replication, we prepared mutants from the avirulent strain Ulster with monocyclic replication cycle and adapted them for multicyclic replication in human melanoma cells. Two mutants (M1 and M2) showed interesting functional differences: while M2 showed T cell co-stimulatory effects in a tumor-specific cytotoxic T lymphocyte (CTL) assay, M1 did not. A distinct difference of these 2 virus mutants appeared also when testing their capacity to induce interferon-alpha and -beta as well as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) molecules in human monocytes. Sequence analysis of the hemagglutinin-neuraminidase (HN) molecules of the 2 virus mutants showed 7 non-silent mutational differences. Upon cloning of the HN mutant genes into an expression vector and transfection of cells, only HN derived from M2 (HN-M2) was detected at the cell surface by immunostaining with specific antibodies and showed hemadsorption and neuraminidase activity. In order to define which amino acid was responsible for the loss of functional activity of HN derived from M1 (HN-M1), distinct HN mutants were generated via site-directed mutagenesis and tested. Substitution of serine 200 by a proline abrogated HN expression and its hemadsorption and neuraminidase activities. Molecular modeling revealed that proline 200 in HN influences flexibility of a loop near the entrance to the neuraminidase active site, a function that may be crucial for the functions of this viral protein.

Animals↗
PubMedDate not supplied

Serological profiles of commercial broiler breeders and their progeny. 2. Newcastle disease virus.

Newcastle disease virus (NDV) hemagglutination-inhibition (HI) titers were determined for serum samples from eight commercial broiler breeder flocks and their progeny. The chickens sampled had been vaccinated and reared by different producers in different regions of the United States. Breeder flocks had the highest number of NDV-positive HI titers (greater than or equal to 1:10). Eighty percent or more of the samples from six of eight breeder flocks were positive; the geometric mean titers (GMTs) for those six breeder flocks ranged from 19 to 92. Only 3 of 8 broiler flocks had an increased frequency of positive titers and higher GMTs after vaccination. The frequency of positive titers was greater than 80% in only 2 of 8 of the oldest broiler flocks. The number of NDV-negative titers (less than 1:10) increased with age in most broiler flocks, even though all had been vaccinated once or more with live NDV vaccines.

Animals↗
PubMed1987

Fusion of erythrocytes by Newcastle disease virus.

Newcastle disease virus-induced fusion of chick embryo (CE) and chicken erythrocytes has been studied at the ph range between 5.5 and 8.0. The highest degree of fusion of CE erythrocytes was observed at pH 5.5, whereas the chicken erythrocytes fused at pH 5.5-6.0 only. Freezing and thawing of low-haemolytic virus preparation increased its erythrocyte fusion activity. Ammonium chloride did not cause a statistically significant effect on the multiplication of virus preparations expressing different haemolysis and erythrocyte fusion activity.

Animals↗
PubMed1982

Vaccination with CDF-66 strain of newcastle disease virus.

Newcastle disease vaccine CDF-66 has been proved effective by the drinking water route. A chicken dose of 10(6.2) EID50 in 12 ml of water containing 2.5% skimmed milk was found to be effective. This produced sufficient GMHI antibody response (105) and 86.6% of birds withstood challenge with the Mukteswar strain of virulent virus. The in-contact birds did not show either immune or antibody response. The vaccinated birds excreted vaccine virus only from the respiratory tract not from cloaca. The vaccine given in drinking water protected only 50% of chickens when it was given 168 h prior to challenge virus. With lesser intervals the protection was negligible. Diluted vaccine when held for 2 h at 37 degrees C and room temperature did not show a drop in potency.

Animals↗
PubMed1978

Interaction between infectious bursal disease virus and Newcastle disease virus in chickens.

The Australian strain of infectious bursal disease virus (IBDV), 002/73, affected the response of chickens to Newcastle disease virus (NDV). The titre of serum antibodies to NDV in chickens infected with IBDV was significantly lower than that of birds infected with NDV alone. It also appeared that IBDV affected NDV excretion from chickens as NDV was more frequently isolated from chickens infected with IBDV, IBDV infection did not alter the pathogenicity of NDV in chickens. This Australian strain of IBDV therefore appeared to be immunodepressive in one-day-old chickens.

Animals↗
PubMed1996

Differential sensitivity of two related viruses, Newcastle disease virus and Sendai virus, to interferon in mouse Had-2 cells: selective inhibition of translation of NDV mRNA.

Had-2, a mouse mutant cell line derived from FM3A, constitutively releases interferon-alpha and beta and acquires resistance to Newcastle disease virus (NDV) and other viruses. However, Had-2 was found as susceptible to Sendai virus (HVJ) as FM3A. Even when Had-2 cells were infected simultaneously with NDV and HVJ, only the replication of NDV was inhibited, while that of HVJ was not. Northern blot hybridization analysis indicated that accumulation of NDV-specific primary transcripts was somewhat reduced in Had-2, but the reduction was insufficient to critically suppress the viral replication. Moreover, this decrease was not observed in the presence of cycloheximide, and a closely comparable amount of the primary transcripts was detected in both Had-2 and FM3A cells. The mRNA accumulated in the presence of cycloheximide was translated efficiently on removal of the inhibitor in FM3A cells, but not at all in Had-2 cells. Thus the translation of NDV mRNA was the major target of interferon in Had-2 cells. The fact that the synthesis of HVJ proteins was unaffected in Had-2 cells may imply that a host-cell component that distinguishes between NDV and HVJ mRNAs is involved in their translation.

Animals↗
PubMedDate not supplied

The in vivo and in vitro effects of chicken interferon alpha on infectious bursal disease virus and Newcastle disease virus infection.

The in vitro and in vivo effects of chicken interferon alpha on infectious bursal disease virus (IBDV) infection were investigated in this study. A cDNA of interferon alpha was first cloned from a Chinese strain chicken Shiqi by reverse transcription-polymerase chain reaction. The deduced amino acid sequence has one amino acid substitution with chicken interferon alpha 1 at residue 65 (N to S) and two amino acid substitutions with chicken interferon alpha 2 at residues 50 (N to S) and 58 (P to L), respectively. A prokaryotic expression system was employed to produce a large quantity of recombinant protein. Recombinant interferon was purified in a one-step process, and an optimal refolding process was devised. About 51% recombinant protein from inclusion bodies was refolded, and the final yield of the recombinant interferon reached 24.66 mg/liter culture. The recombinant interferon suppressed IBDV plaque formation in a dose-dependent manner and ameliorated IBDV and Newcastle disease virus infection in both specific-pathogen-free (SPF) and commercial chickens. The antiviral effect of interferon alpha is more significant in commercial chickens than in SPF chickens, and the route of administration affects the efficacy of interferon therapy. This is the first reported study of the effects of interferon alpha on IBDV infection.

Amino Acid Sequence↗