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PubMedDate not supplied

Induction of apoptosis by a Newcastle disease virus vaccine (MTH-68/H) in PC12 rat phaeochromocytoma cells.

The attenuated Newcastle Disease Virus (NDV) vaccine MTH-68/H has been found to cause regression of various tumors including certain types of human neoplasms (See Table 1 and References 86-88). The mechanism of its oncolytic action is poorly understood, but it appears to affect specific signaling pathways in the target cell. We studied the cellular effects of NDV employing PC12 rat phaeochromocytoma cells, a widely used model system to analyze differentiation, proliferation and apoptosis. The MTH-68/H vaccine was found to be cytotoxic on PC12 cells. It caused internucleosomal DNA fragmentation, the most characteristic feature of programmed cell death (PCD). A brief exposure (30 min) of P12 cells to the virus was sufficient to produce a full-blown apoptotic response. Major mitogen-activated protein kinase pathways (including the stress inducible c-Jun N-terminal kinase pathway and p38 pathway) or mechanisms regulated by reactive oxygen species appear to have no role in virus-induced cell death. The PCD-inducing effect of MTH-68/H could not be prevented by simultaneous treatment of the P12 cells with growth factors or second messenger analogs stimulating protein kinase C or Ca(++)-mediated pathways. In contrast, treatment with a cyclic AMP analog partially protected the them from virus-induced apoptosis. These experimental results suggests that MTH-68/H might disrupt a growth factor-stimulated survival pathway and that direct stimulation of protein kinase A-catalyzed phosphorylation events bypass this NDV-induced block.

Adolescent↗
PubMed1998

Introduction of adhesive and costimulatory immune functions into tumor cells by infection with Newcastle Disease Virus.

We demonstrate in this study that infection of tumor cells by Newcastle Disease Virus (NDV) leads to changes in tumor cell surface adhesiveness and tumor immune costimulatory function. While adsorbtion of virions to the cell surface occurs after short-term (10 min) incubation and leads to cells expressing viral antigens at low antigen density (LAD), viral replication in the cytoplasm occurs within 5-24 h leading to tumor cells expressing viral antigens at high antigen density (HAD) as shown by quantitative FACS flow cytometry. Virus infected tumor cells showed an increased adhesiveness for erythrocytes and lymphocytes. When IL-2 preactivated human lymphocytes with cytotoxic potential were coincubated with 51Cr-labeled NDV-infected or non-infected human colon carcinoma cells increased lysis of the virus infected targets was observed. The virus mediated cell adhesion could be inhibited by monoclonal antibody (mAb) against the hemagglutinin-neuraminidase (HN) molecule but not by antibody against the fusion protein. HN cDNA transfectants also mediated increased lymphocyte adhesion in comparison to wild-type or neo-vector transfected control cells. Further experiments demonstrated that not only the adhesion domain of HN but also the neuraminidase plays a role in cell-cell interactions. A comparison of an NDV neuraminidase mutant of the strain Australian Victoria (AV-L1) with the parental AV strain revealed pronounced differences in their capacity to mediate lymphocyte binding and costimulatory activity. The mutant with highly decreased neuraminidase activity was very similar to NDV Ulster in adhesive and costimulatory activity while the parental line with high neuraminidase activity was negative for both functions. Costimulatory effects of NDV Ulster and AV-L1 were revealed when virions and suboptimal concentrations of anti-CD3 mAbs were coated to microtiter plates for induction of murine CD4 T cell proliferation. In human autologous mixed lymphocyte-tumor cell cultures up-regulation of T cell activation markers CD69 and CD25 was seen with NDV modified but not with non-modified tumor cells.

Animals↗
PubMed1990

Insertion of the fusion gene from Newcastle disease virus into a non-essential region in the terminal repeats of fowlpox virus and demonstration of protective immunity induced by the recombinant.

In this paper we report on the identification of non-essential genes in the terminal repeats of the avipox-virus fowlpox virus and the use of these as insertion sites in a vector system. Foreign genes inserted into these sites are shown to be present in two copies in the resultant recombinant virus. To test the potential use of this vector as a live vaccine the fusion gene of Newcastle disease virus has been inserted into a vaccine strain of fowlpox virus and inoculated into chickens. The experiments demonstrate the ability of the recombinant to protect chickens against challenge by a virulent strain of Newcastle disease virus and to elicit the formation of an anti-fusion protein antibody.

Animals↗
PubMed1992

Effects of vitamin A deficiency and Newcastle disease virus infection on lymphocyte subpopulations in chicken blood.

The effect of vitamin A deficiency and Newcastle disease virus (NDV)-infection on peripheral blood lymphocytes (PBL) was studied by differential cell counting and flow cytometry. Day-old chickens were fed purified diets containing either marginal or adequate levels of vitamin A and at 26 days of age half of the chickens in each group were infected with NDV. The absolute numbers of PBL and their subpopulations were studied until 10 days after infection. Vitamin A deficiency resulted in significantly lower numbers of PBL throughout the experiment. NDV-infection produced lymphopenia during the first 3 days, followed by a strong increase in PBL numbers after 6 days. Both changes in PBL were less pronounced in vitamin A-deficient birds. For flow cytometric analysis monoclonal antibodies reacting specifically with B-cells or a subpopulation of T-cells were used. Vitamin A-induced lymphopenia could be attributed to a decreased number of PBL, negative for both antibodies, and to the absence of an increase in B-cells which normally occurs at this age. The negative cells are suggested to represent, at least partially, cytotoxic T-cells, which may explain the impaired cytotoxic T-cell-activity found in earlier studies. NDV-induced lymphopenia and subsequent increase of PBL could be attributed to all cell types investigated. However, in vitamin A-deficient birds negative cells did not show these reactions. Therefore, it can be concluded that vitamin A deficiency has a detrimental effect on PBL, negative for both antibodies used, and on the normal growth of the number of B-cells at this age.

Animals↗
PubMedDate not supplied

Methods of spread of velogenic viscerotropic Newcastle disease virus in the southern Californian epidemic of 1971-1973.

Data collected during the velogenic viscerotropic Newcastle disease (VVND) epidemic that occurred in southern California from 1971 to 1973 were analyzed to determine the methods of spread of the disease. Spread between chicken flocks was extensive and due mainly to the movement of live birds and mechanical transport of virus by man, especially by vaccination and poultry service crews. Spread to exotic birds was from contact with infected imported stock. Spread to other species was most probably through contact with infected chickens. Infection persisted in commercial chicken flocks because of intensive vaccination programs, heavy traffic and contact between layer operations, and the maintenance of multi-age flocks. These foci of infection probably led to spread of the disease to areas from which VVND had been eradicated several months before. There was no evidence of significant wind-borne spread of virus between flocks.

Air Microbiology↗
PubMed2003

Recombinant Newcastle disease virus as a vaccine vector.

Veterinary vaccines remained conventional for more than fifty years. Recent advances in the recombinant genetic engineering techniques brought forward a leap in designing vaccines for veterinary use. A novel approach of delivering protective immunogens of many different pathogens in a single virus vector was made possible with the introduction of a "reverse genetics" system for nonsegmented negative-sense RNA viruses. Newcastle disease virus (NDV), a nonsegmented negative-sense virus, is one of the major viruses of economic importance in the poultry industry throughout the world. Despite the availability of live virus vaccines of good potency, the intrinsic ability of attenuated strains to revert in virulence makes control of this disease by vaccination difficult. Armed with the knowledge of virulence factors of this virus, it is now possible to produce genetically stable vaccines and to engineer mutations that enhance immunogenicity. The modular nature of the genome of this virus facilitates engineering additional genes from several different pathogens or tumor-specific antigens to design contemporary vaccines for animals and humans. This review will summarize the developments in using NDV as a vaccine vector and the potential of this approach in designing next generation vaccines for veterinary use.

Animals↗
PubMed1985

Conformational changes in Newcastle disease virus fusion glycoprotein during intracellular transport.

The migration on polyacrylamide gels of nascent (pulse-labeled) and more processed (pulse-labeled and then chased) forms of nonreduced Newcastle disease virus fusion glycoprotein were compared. Results are presented which demonstrate that pulse-labeled fusion protein, which has an apparent molecular weight of 66,000 under reducing conditions (Collins et al., J. Virol. 28: 324-336), migrated with an apparent molecular weight of 57,000 under nonreducing conditions. This form of the Newcastle disease virus fusion protein has not been previously detected. This result suggests that the nascent fusion protein has extensive intramolecular disulfide bonds which, if intact, significantly alter the migration of the protein on gels. Furthermore, upon a nonradioactive chase, the migration of the fusion protein in polyacrylamide gels changed from the 57,000-molecular-weight species to the previously characterized nonreduced form of the fusion protein (molecular weight, 64,000). Evidence is presented that this change in migration on polyacrylamide gels is due to a conformational change in the molecule which is likely due to the disruption of some intramolecular disulfide bonds: Cleveland peptide analysis of the pulse-labeled nonreduced fusion protein (molecular weight, 57,000) yielded a pattern of polypeptides quite different from that obtained from the more processed form of the fusion protein (molecular weight, 64,000). However, the pattern of polypeptides obtained from the nonreduced 64,000-molecular-weight species was quite similar to that obtained from the fully reduced nascent protein (molecular weight, 66,000). This conformational change occurred before cleavage of the molecule. To determine the cell compartment in which the conformational change occurs, use was made of inhibitors which block glycoprotein migration at specific points. Monensin allowed the appearance of the 64,000-molecular-weight form of the fusion protein, whereas carboxyl cyanide m-chlorophenylhydrazine blocked the appearance of the 64,000-molecular-weight form of the fusion protein. Thus, the fusion protein undergoes a conformational change as it moves between the rough endoplasmic reticulum and the medial Golgi membranes.

Animals↗
PubMed1975

The effect of maternal immunity, age at vaccination and doses or live vaccines on immune response to Newcastle disease.

The short life span of domestic fowls necessitates the use of early vaccination, but the response is affected by the immaturity of the immune mechanism and by the presence ofmaternal immunity: this results in an uneven immunity of the large and continually changing poultry population. This paper compares the response of groups of chicks from vaccinated and non-vaccinated hens after vaccination at various ages with Newcastle Disease vaccines of different pathogenicity (lentogenic and mesogenic strains). The results show that: 1. maternal immunity has a great effect on the pathogenicity of the vaccine viruses and the subsequent immune response; 2. the older the chicks are at the time of vaccination, the better is their immune response; 3. for vaccines of low pathogenicity the immune response can be enhanced by increasing the dose of the virus irrespective of the presence of maternal immunity.

Age Factors↗
PubMed1992

Investigation of an outbreak of velogenic viscerotropic Newcastle disease in pet birds in Michigan, Indiana, Illinois, and Texas.

An outbreak of velogenic viscerotropic Newcastle disease in exotic pet birds in the United States from April through July 1991 was investigated. More than 2,000 pet birds in 5 states (Michigan, Indiana, Illinois, Texas, and Maryland) were tested. Infected birds were found in Michigan, Illinois, Indiana, and Texas. This disease was eradicated without spread to domestic poultry. Epidemiologic investigations revealed the source of infection to be double yellow-headed Amazon parrots suspected to be illegally imported into Texas.

Animals↗
PubMed1990

A fowlpox virus vaccine vector with insertion sites in the terminal repeats: demonstration of its efficacy using the fusion gene of Newcastle disease virus.

In this paper we report the development and testing of a fowlpox virus vector system. Insertion sites in non-essential regions within the terminal inverted repeats of the virus have been characterised. Foreign genes inserted into these sites are shown to be present in two copies in the resultant recombinant virus. To test the potential use of this vector as a live vaccine the fusion gene of Newcastle disease virus (NDV) has been inserted into a vaccine strain of fowlpox virus, and inoculated into chickens. The experiments demonstrate the ability of the recombinant to protect chickens against challenge by a virulent strain of NDV and to elicit the formation of anti-fusion protein antibody.

Animals↗
PubMed2005

Primary survey of avian influenza virus and Newcastle disease virus infection in wild birds in some areas of Heilongjiang Province, China.

Two hundred thirty specimens of wild birds were collected from some areas in Heilongjiang Province during the period of 2003-2004, including two batches of specimens collected randomly from a same flock of mallards in Zhalong Natural Reserve in August and December, 2004, respectively. Primary virus isolation and identification for avian influenza virus (AIV) and Newcastle disease virus (NDV) were performed. The results showed that only two specimens of young mallards collected from Zhalong Natural Reserve in August, 2004 were positive to AIV (isolation rate 0.9%), and one strain (D57) of these two virus isolates was identified to be H9 subtype by hemagglutination inhibition test. Meanwhile, the two batches of blood serum samples of mallards from Zhalong were also examined for antibodies against AIV and NDV. Among 38 blood serum samples collected in August, antibodies against the hemagglutinin of H1, H3, H5, H6 and H9 subtypes of AIV were found in 1, 0, 2, 0 and 8 samples, respectively; and 11 samples were found with antibody against NDV. Whereas the NDV isolation in both two batches of specimens of mallard was negative, all of the 32 blood serum samples collected in December were negative for antibodies against AIV and NDV.

Animals↗
PubMedDate not supplied

Aerosol vaccination against Newcastle disease. I. Studies on particle size.

Studies revealed that the majority of particles emitted by three different aerosol generators were in the size ranges of 0.5-1 and 1-3 mum. In general, the smaller the aperture setting, the larger the total number of particles. The difference between the generators in number of particles emitted were not significant enough to produce appreciable difference in antibody titers obtained from vaccinated chickens. Antibody titers were higher in birds vaccinated with the LaSota strain of Newcastle disease virus than in birds vaccinated with the B-1 strain, although protection against challenge was approximately similar. Aerosol challenge was found as effective as intramuscular challenge.

Aerosols↗
PubMed1984

Effect of N-acetyl-muramyl-L-alanyl-D-isoglutamine on interferon production in mice by Newcastle disease virus.

The activity (carbon clearance) of the reticuloendothelial system (RES) of mice inoculated intraperitoneally with N-acetyl-muramyl-L-alanyl-D-isoglutamine (muramyl dipeptide, MDP) was greatly stimulated 1 day, but not 7 days after MDP treatment. No enhancement of resistance to ectromelia virus infection and influenza virus infection in mice treated with MDP was observed. In mice splenectomized 1 week after MDP pretreatment, normal levels of circulating interferon were produced in response to Newcastle disease virus (NDV), whereas in the mice treated with MDP after splenectomy, circulating interferon levels were reduced to the same level as produced in the MDP-untreated and splenectomized mice. Interferon production in response to NDV was augmented in non-adherent peritoneal and spleen cell cultures derived from MDP-pretreated mice, whereas it was reduced in peritoneal and splenic macrophage cultures. These results suggest that the non-adherent spleen cells activated with MDP were disseminated from the spleen to other organs, that the lack of enhancement of interferon production in mice pretreated with MDP might be due to reduced interferon production in macrophages, and that the activation of the RES of the whole body by MDP did not correlate with the enhancement of interferon production in spleen cells or with the reduction of interferon production in macrophages.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMedDate not supplied

Effect of social stress on Newcastle disease virus (LaSota) infection.

Individual immature chickens were socially stressed when placed into an established group of chickens. The stress response was determined by periodic measurement of plasma cortisol and by determination of the relative regression of the bursa of Fabricius. Stressed chickens had elevated cortisol levels during the first 24 hours following the initiation of social stress. The bursa-to-body-weight ratios of stressed birds at 96 hours following stress were significantly lower than the ratios in control birds, and their tuberculin reaction was significantly depressed. Newcastle disease virus was more invasive and attained higher titers in stressed birds. The hemagglutination-inhibition (HI) response of the stressed birds was higher in one trial and lower in another.

Animals↗