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PubMed1986

Identification of the sequence content of four polycistronic transcripts synthesized in Newcastle disease virus infected cells.

During infection, the Newcastle disease virus (NDV) genome is transcribed to produce 5 to 7 species of polycistronic messenger RNA (Wilde and Morrison, J. Virol. 51, 71-76) in addition to the well characterized monocistronic messenger RNA. To identify the specific sequences present in each of the polycistronic RNA species, cDNA clones generated by reverse transcription of NDV mRNAs were characterized and used as probes on Northern blots of total NDV cytoplasmic RNA. By this method, it was shown that four of these large RNA species are polycistronic transcripts containing sequences from two genes: one species contains nucleocapsid protein (NP) and phosphoprotein (P) gene sequences; another, P and membrane protein (M) gene sequences; another, M and fusion protein (F0) gene sequences; and another, F0 and hemagglutinin-neuraminidase protein (HN) gene sequences. The existence of these transcripts yields a transcription map order of NP, P, M, F0, HN. The remaining RNA bands may be composed of at least three different polycistronic transcripts, each of which represents transcription through three adjacent genes.

Animals↗

PubMed1984

Analysis of the T suppressor cell circuit which regulates contact sensitivity in mice infected with the virus of Newcastle disease.

The interaction between the virus of Newcastle disease (NDV) and the different cellular elements involved in the T suppressor cell circuit which regulates the expression phase of contact sensitivity has been investigated. NDV does not interfere with the production of the antigen-specific T suppressor factor (TsF) but inhibits its binding to T acceptor cells (Tacc). This cell when armed with TsF and exposed to the antigen corresponding to TsF releases a non-specific inhibitor of the transfer of contact sensitivity. More detailed analysis of the effect of NDV on the Tacc system showed that not only Tacc activity is impaired by NDV, but also the ability of antigen presenting cells (APC) to trigger Tacc armed with TsF is inhibited. The impairment of APC activity by NDV has been also investigated using another system, such as the induction of contact sensitivity by footpad cell transfer. The possibility that a virus-induced membrane modification might be responsible for the effect of NDV on the regulation of contact sensitivity is discussed.

Animals↗

PubMed1981

Relation of interferon production to the limited replication of Newcastle disease virus in L cells.

Growth of Newcastle disease virus (NDV) in L cells, where the virus undergoes limited replication, has been compared to that in fully permissive BHK-21 host cells. The synthesis of viral proteins and the production of infectious progeny were found to occur normally at early times of infection in L cells. However, the subsequent amplification of viral protein synthesis did not take place and instead of infectious virions, non-infectious haemagglutinin was the predominant product. This shift of replication pattern from complete to incomplete virus production seemed to be temporally related to the appearance and accumulation of interferon (IFN) in the system. The addition of specific antiserum against mouse IFN to the infected L cell cultures was able to circumvent such restriction of virus growth. In the presence of the antiserum, synthesis of viral proteins was found to progress normally, with the production of a high amount of infectious progeny comparable to that of the permissive system. These results suggest that the limited replication of NDV in L cells may be due to interference by the endogenously produced IFN during the course of infection.

Animals↗

PubMed1983

Elemental analysis in murine central nervous system: elevation of rubidium subsequent to Newcastle disease virus encephalopathy.

The Cg strain of Newcastle disease virus (NDV) produces neurologic signs and death in mice. This illness is unusual because of the lack of typical features of a viral encephalitis. Specifically, there is a paucity of infectious virus, detectable cellular inflammatory reaction, cytopathic effect, and viral antigen by immunofluorescence. We previously showed an elevation of alpha-aminoisobutyric acid in the CNS of moribund NDV-infected mice, indicating cellular membrane dysfunction. In an attempt to further our understanding of the pathogenesis of the illness, we evaluated CNS concentrations of sodium, potassium, iron, copper, zinc, magnesium, selenium, and rubidium. Elemental analysis revealed no difference between infected and control mice for all elements except for rubidium, which was significantly elevated in infected mice. Elevation in rubidium was detected in infected mice by X-ray fluorescence and atomic absorption spectrophotometry, whereas rubidium concentrations for control mice were similar by both methods. Neurologic symptoms correlated directly with rising rubidium concentrations. Our data suggest that abnormal trace element levels during viral infection may be one mechanism responsible for the clinical symptoms.

Animals↗

PubMed1997

Functional chimeric HN glycoproteins derived from Newcastle disease virus and human parainfluenza virus-3.

Newcastle disease virus (NDV) is primarily a respiratory tract pathogen of birds, particularly chickens, but it occasionally produces infection in man. Human parainfluenza virus type 3 (hPIV3) is a common respiratory pathogen, particularly in young children. These two viruses gain entry to host cells via direct fusion between the viral envelope and the cell membrane, mediated by the two surface glycoproteins: the hemagglutinin-neuraminidase (HN) and fusion (F) proteins. Promotion of fusion by HN and F requires that they are derived from homologous viruses. We have constructed chimeric proteins composed of domains from heterologous HN proteins. Their ability to bind cellular receptors and to complement the F protein of each virus in the promotion of fusion were evaluated in a transient expression system. The fusion specificity was found to segregate with a segment extending from the middle of the transmembrane anchor to the top of the putative stalk region of the ectodomain. All of the chimeras, in which the globular domain is derived from the NDV HN and various lengths of the stalk region are derived from the hPIV3 HN maintain receptor binding activity, but some have markedly reduced neuraminidase (NA) activity. Decrease in the NA activity of the chimeras correlates with alteration in the antigenic structure of the globular domain. This suggests that the stalk region of the HN spike is important for maintenance of the structure and function of the globular domain of the HN protein spike.

Amino Acid Sequence↗

PubMed1996

Serum immunoglobulin responses among broiler chickens fed Ugandan commercial poultry feeds and vaccinated against Newcastle disease.

Responses to the La Sota strain Newcastle disease (ND) vaccine virus were monitored in 240 Ross breed broilers fed 4 Ugandan commercial feeds, Fs, F1, F2 and F3. The production of IgM, IgG and haemagglutination-inhibition (HI) antibodies, were monitored from day 28 of age for 4 weeks using the ELISA assay and HI-test. All broilers were sero-negative before vaccination. The Fs, F1, F2 and F3 feeds had metabolisable energy/crude protein ratios of 599, 870, 823 and 685 respectively, and had significant (P < 0.05) differences in the development of IgM, IgG and HI titres. Commercial feed FI reduced IgM (31.9%); IgG (30.9%) and HI (54.5%) titres. Commercial feed F2 reduced IgG (30.2%) and HI (36.4%) titres but did not affect IgM. Commercial feed F3 reduced IgG (16.3%) but affected neither IgM nor HI titres. Peak HI titres of F1 (2(2.5)) and F2 (2(3.5)) were below the HI titre (2(5.2)) that prevents 100% mortality due to virulent ND virus infection. Per cent loss of IgM titres in broilers that had sero-converted was 100% (F1), 25% (F2), 25% (F3) and 20% (Fs) by week 4. Per cent loss of IgG titre was 12.5% (F1), 16.7% (F2), 7.2% (F3) and 4% (Fs) by week 5. However, none of the feeds affected the time of attaining maximum sero-conversion at week 2 (IgM), week 3 (HI titres) and week 4 (IgG) in the flocks. The lack of standardisation of poultry feed quality in Uganda may be a shortcoming in successful protection of poultry by vaccination against ND.

Animal Feed↗

PubMed1992

Newcastle disease virus selectively kills human tumor cells.

Newcastle disease virus (NDV), strain 73-T, has previously been shown to be cytolytic to mouse tumor cells. In this study, we have evaluated the ability of NDV to replicate in and kill human tumor cells in culture and in athymic mice. Plaque assays were used to determine the cytolytic activity of NDV on six human tumor cell lines, fibrosarcoma (HT1080), osteosarcoma (KHOS), cervical carcinoma (KB8-5-11), bladder carcinoma (HCV29T), neuroblastoma (IMR32), and Wilm's tumor (G104), and on nine different normal human fibroblast lines. NDV formed plaques on all tumor cells tested as well as on chick embryo cells (CEC), the native host for NDV. Plaques did not form on any of the normal fibroblast lines. To detect NDV replication, virus yield assays were performed which measured virus particles in infected cell culture supernatants. Virus yield increased 10,000-fold within 24 hr in tumor and CEC supernatants. Titers remained near zero in normal fibroblast supernatants. In vivo tumoricidal activity was evaluated in athymic nude Balb-c mice by subcutaneous injection of 9 x 10(6) tumor cells followed by intralesional injection of either live or heat-killed NDV (1.0 x 10(6) plaque forming units [PFU]), or medium. After live NDV treatment, tumor regression occurred in 10 out of 11 mice bearing KB8-5-11 tumors, 8 out of 8 with HT-1080 tumors, and 6 out of 7 with IMR-32 tumors. After treatment with heat-killed NDV no regression occurred (P less than 0.01, Fisher's exact test). Nontumor-bearing mice injected with 1.0 x 10(8) PFU of NDV remained healthy. These results indicate that NDV efficiently and selectively replicates in and kills tumor cells, but not normal cells, and that intralesional NDV causes complete tumor regression in athymic mice with a high therapeutic index.

Animals↗

PubMedDate not supplied

Comparative efficacy of the B-1 and VG/GA vaccine strains against velogenic viscerotropic Newcastle disease virus in chickens.

Groups of eight 1-day-old white rock chickens were vaccinated with either B-1 or VG/GA strain of Newcastle disease virus (NDV) by eyedrop instillation. Some of the chickens were vaccinated a second time at 17 days of age. Eight groups of chickens vaccinated either once or twice were challenged with the California 1083 strain of velogenic viscerotropic Newcastle disease virus (VVNDV) at 30 days of age by either intramuscular injection or eyedrop instillation. One group of unvaccinated control chickens was challenged by eyedrop instillation. All eight unvaccinated controls, two of the 16 B-1 vaccinates, and none of the 16 VG/GA vaccinates died following challenge. There were no obvious differences in pre-challenge serum antibody levels among the vaccinates. Only the twice-vaccinated chickens that were challenged by eyedrop and the unchallenged vaccinates failed to show a marked rise in serum antibody titers. The VG/GA strain of NDV provided protection against the mortality associated with VVNDV challenge similar to that provided by the B-1 strain within the conditions of this experiment.

Animals↗

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↗

PubMed1996

Newcastle disease virus-induced apoptosis in the peripheral blood mononuclear cells of chickens.

Specific pathogen-free chickens were inoculated with the GB strain of Newcastle disease virus by the ocular route, and were killed at daily intervals after infection. Peripheral blood mononuclear cells (PBMCs) were harvested for DNA extraction, electron microscopy, and flow cytometry studies to detect the presence of cellular apoptosis and necrosis. Extracted DNA showed fragmentation at 4 and 6 days after infection. Electron microscopy showed that the chromatin of the lymphocytes became condensed and occasionally crescent-shaped; apoptotic bodies could also be seen. Some heterophils became darkly stained and their nuclei degenerated; others seemed to have lost their cytoplasmic membrane, but had intact granules and condensed chromatin. Flow cytometry studies showed that the number of normal PBMCs gradually decreased from 99.04% at the beginning of the infection to 45.24% on the sixth day of infection, with a concomitant increase of apoptotic cells. The results show that PBMCs of chickens exhibit typical signs of apoptosis after infection by the Newcastle disease virus.

Animals↗

PubMed1999

Antigenic and genetic characterisation of Newcastle disease viruses isolated from outbreaks in domestic fowl and turkeys in Great Britain during 1997.

Antigenic and genetic analyses of viruses from the 11 outbreaks of Newcastle disease in Great Britain, 12 of the outbreaks in Northern Ireland and the single outbreak in the Republic of Ireland which occurred in 1997, indicated that they were all essentially similar. In addition, the viruses from the British Isles were very similar to viruses isolated from three outbreaks in pheasants in Denmark between August and November 1996, from a goosander in Finland in September 1996, from an outbreak in chickens in Norway in February 1997, and from an outbreak in chickens in Sweden in November 1997. Viruses from outbreaks in other countries during 1995 to 1997 could be distinguished antigenically and/or genetically from the 1996 to 1997 Scandinavian/British Isles isolates, as could viruses responsible for two separate outbreaks in caged birds in quarantine premises in Great Britain in March 1997. Minor nucleotide differences in the 413-base region of the fusion gene and the 187-base region of the haemagglutinin-neuraminidase gene sequenced in this study allowed the 1996 to 1997 Scandinavian/British Isles isolates to be divided into groups. These groups broadly corresponded to the clusters of disease outbreaks, but suggested that the discrete outbreak in Scotland was probably the result of virus spread from Northern Ireland. Overall, the antigenic and genetic analyses of these viruses were consistent with the theory that the virus was introduced into the British Isles by migratory birds moving from north-east Europe. However, it was not possible to rule out other sources, such as the movement of pheasants from Denmark.

Animals↗

PubMed1976

[Effect of iosan and bradofen on the viruses of Newcastle disease, laryngotracheitis and fowl pox].

Tested was the effect of the iodoform preparation iosan and the quaternary ammonium preparation bradofen against the viruses of the Newcastle disease (strain La Sota), laryngotracheitis (strain TsNIIP) and fowl pox (strain FK) in birds. The following results were obtained: 1. To a concentration of 3% (262 ppm of active iodine) and exposure of 45 min. to iosan the virus of laryngotracheitis was sensitive; that of Newcastle disease perished at a conc. of 5% (525 ppm of active iodine for 15 min); and that of fowl pox was not inactivated at a 30 min. exposure to a conc. of 7% (875 ppm of active iodine.) 2. Bradofen inactivated the Newcastle disease virus in a conc. of 0.5 per cent for 30 min., while the pox virus withstood a conc. of 1.5% up to the 30 th min. The virus of laryngotracheitis was inactivated by a conc. of 2 per cent for 45 min. The disinfection effect of the tested preparations was assessed as satisfactory.

Disinfectants↗

PubMed1999

Two novel genetic groups (VIIb and VIII) responsible for recent Newcastle disease outbreaks in Southern Africa, one (VIIb) of which reached Southern Europe.

34 strains of Newcastle disease virus (NDV) isolated during epizootics in the Republic of South Africa and in Mozambique between 1990 and 1995, and in Bulgaria and Turkey in 1995-1997 were identified by restriction enzyme and partial sequence analysis of the fusion (F) protein gene. The majority of isolates in southern Africa and those from Bulgaria and Turkey were placed into a novel group which has been termed VIIb. Group VIIb is part of a larger genetic cluster (VII) that also includes NDV strains from the Far East and some western European countries (VIIa). The genetic distance of 7-8, 5% between genotype VIIa and VIIb viruses excludes the existence of a direct epidemiological link between recent southern African epizootics and outbreaks in either western Europe in the 1990's or those of the Far East. Another hitherto unrecorded genotype (VIII) was also found in South Africa with descendants of putative ancestral members isolated in the 1960's. The genetic distance of recent group VIII strains from the major epizootic genotype (VIIb) is over 11%, therefore outbreaks caused by them were epidemiologically unrelated. Genotype VIII viruses must have been maintained in South Africa by endemic infections during the past decades while group VIIb appears to be introduced more recently.

Animals↗

PubMedDate not supplied

Viscerotropic velogenic Newcastle disease in Turkeys: virus shedding and persistence of infection in susceptible and vaccinated poults.

Susceptible turkeys and turkeys vaccinated with live lentogenic B1 strain Newcastle disease virus (NDV) were inoculated intracularly with viscerotropic velogenic (VV) Fontana strain NDV and studied for virus shedding and persistence of infection. Susceptible poults that survived infection (15%) continued to shed NDV from the intestinal tract up to 46 days postinoculation. Turkeys that were vaccinated with B1 strain NDV did not develop clinical signs when their immunity was challenged with VV Fontana strain virus. Virus was covered up to 53 days postchallenge (PC) from the cloaca of poults that were vaccinated once at 4 days of age and challenged at 1 month of age. Older turkeys that had been vaccinated one to three times did not generally shed virus after 4 days PC. Newcastle disease virus was recovered later in convalescence by the organ-culture method when swabs of trachea and cloaca were negative for virus. Persistent infection was detected as long as 88 days PC in organ cultures of cecal tonsil. Five of seven NDV isolants from organ cultures or from swabs caused fatal disease in chickens.

Administration, Oral↗

PubMed1990

Retroviral expressed hemagglutinin-neuraminidase protein protects chickens from Newcastle disease virus induced disease.

The hemagglutinin-neuraminidase (HN) gene and the phosphoprotein (P) gene of Newcastle disease virus (NDV) were inserted into a replication competent avian leukosis virus vector. The expression of the HN gene from this vector in chick embryo cells has been previously reported. The P gene is also expressed from this vector in chick embryo cells. The retroviruses were used to immunize 4-week-old chickens. Birds receiving the virus containing the HN gene developed low levels of serum HI titers and NDV neutralization titers. Upon challenge, all birds vaccinated with the HN gene containing virus were protected from disease but not viral infection and replication. In contrast, birds immunized with the P gene containing retrovirus developed more severe clinical signs of disease earlier than birds receiving no immunization or retrovirus alone. The results obtained with the HN gene may have potential application to reducing disease due to NDV genetically engineered vaccines.

Animals↗

PubMed1976

Thymidine metabolism and DNA synthesis in Newcastle disease virus-infected cells.

The inhibition of thymidine incorporation into DNA in Newcastle disease virus-infected cells has been studied. At 6 h after infection of L-929 cells at high multiplicity, transport of exogenous thymidine across the cell membrane was inhibited. The kinetics of this inhibition, decreased Vmax with no change in Km, suggest that there are fewer sites available for transport in infected cells. The conversion of thymidine to dTTP was not inhibited. Equilibrium of exogenous thymidine with the acid-soluble pool occurred more slowly and at a lower level of radioactivity than in uninfected cells, and there was a reduction in the rate of incorporation of exogenous thymidine into DNA. The reduction of incorporation into the pool and into DNA was proportionate. The size of total cellular dTTP pools was changed very little in infected cells. DNA synthesized in infected cells in the presence of [3H]BrdUrd had reduced incorporation of tritium but similar buoyant density to that from uninfected cells. The results show that Newcastle disease virus inhibits DNA synthesis directly and, in addition, decreases thymidine transport. Together these account for the overall decrease in thymidine incorporation into DNA of infected cells.

Biological Transport, Active↗

PubMed2002

Phylogenetic analysis of Newcastle disease virus genotypes isolated in Japan.

We genetically analyzed field isolates of the Newcastle disease (ND) virus isolated in Japan from 1930 to 2001. The coding region of the fusion protein was amplified by reverse transcriptase PCR and directly sequenced. Phylogenetic analysis revealed the presence of viruses belonging to six of the eight known genotypes. It can be concluded from this study that ND outbreaks in Japan have been of multiple etiologies. [All sequences used in this study were sent to DDBJ and assigned accession numbers AB 070382 to AB 074042.]

Animals↗

PubMed1991

[Aerosol immunization against Newcastle disease].

The NDV-6-strain was selected by Lomniczi from naturally occurring Newcastle-disease-virus-strains. This strain was administered to chicken of different ages without detrimental effects. The strain was thermoresistant and adapted by serial passages in gut epithelial cells (NDV-6/10 variant). By using an aerosol of this strain (10(7),(3) EID50/m3) more than 1,3 millions chicken were immunised either in the incubator and up to an age of 10 days. Vaccine reactions were not observed. Vaccination against Marek's disease did not interfere with NDV-vaccination efficacy when day-old chicken were vaccinated with the NDV-6/10 aerosol. Obviously, the vaccine elicits a distinct cell-associated immunity. This explains, why chicken exhibiting low hemagglutination inhibition serum-antibody titers were found resistant to challenge infection with velogenic NDV. Immunity of chicken which have been vaccinated within 1 to 8 days post hatch by the NDV-6/10 aerosol vaccine, persisted 6 to 8 weeks and can be extended by revaccination up to onset of laying. The vaccine is now commercially available and designated VITAPEST.

Aerosols↗