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PubMed1988

Antibody response to Newcastle disease virus and Pasteurella multocida of two strains of turkeys.

The primary and secondary response to Newcastle disease virus (NCDV) and Pasteurella multocida (PM) of two turkey lines were studied following vaccinations with either NCDV or PM alone, or in combination. The two turkey strains were 1) a randombred control line (RBC1) and 2) a subline (E) of Line RBC1 selected 27 generations for increased egg production. This study consisted of five trials. Each trial represented a separate hatch. In Trial 1, poults of each line were subcutaneously vaccinated with a 1-mL dilution of B1 type LaSota strain NCDV vaccine. In Trial 2, poults of each line were wing-web vaccinated with the M-9 strain of PM Heddleston Type 3 x 4 cross at 6 and 10 wk of age. In Trial 3, poults of each line were subcutaneously vaccinated on the back of the neck with 1 mL of inactivated NCDV at 6 and 10 wk of age. In Trial 4, .5 mL of a PM bacterin containing Types 1, 3, and 4 in an oil emulsion was used to subcutaneously vaccinate poults of each line at 6 and 10 wk of age. In Trial 5, poults of each line were simultaneously vaccinated with inactivated NCDV (subcutaneously) and a PM bacterin (intramuscularly) at 6 and 10 wk of age. Line RBC1 had significantly (P less than .01) higher maternal antibodies to Newcastle disease at 3 wk of age than those of Line E. The RBC1 line generally had significantly higher levels of antibodies than Line E in response to vaccination for both NCDV and PM when administered singularly or in combination.

Animals↗
PubMed1982

Coding assignments of the five smaller mRNAs of Newcastle disease virus.

The polypeptide coding assignments for the five messengers of the 18S size class of Newcastle disease virus (NDV) RNA have been determined by cell-free translation of individual RNAs separated by gel electrophoresis. Listed in order of their decreasing electrophoretic mobilities in acid agarose-urea gels, the coding assignments of the RNAs were as follows: RNA 1, M protein; RNA 2, P protein; RNA 3, NP; RNA 4, F glycoprotein; and RNA 5, HN glycoprotein. RNA 2 also directed the synthesis of 33- and 36-kilodalton proteins, which were tentatively identified as being overlapping segments of the P protein. The 33- and 36-kilodalton polypeptides could be detected in infected cells, but not in purified virions of NDV. Since the other unique NDV RNA, a 35S species, has been shown previously to encode the viral L protein, these results complete the coding assignments of the six known NDV mRNAs.

Animals↗
PubMed1985

Early interferon production in human diploid cells induced by Newcastle disease virus in the presence of protein synthesis inhibitors.

When human diploid cells were induced by Newcastle disease virus (NDV) in the presence of cycloheximide or puromycin, an early interferon was produced up to 4 hr after induction, but was not produced without these reagents. Early interferon production in rabbit kidney cells induced by NDV in the presence of cycloheximide was not observed. This early interferon production was also induced in response to hydroxylamine-treated NDV, ultraviolet light-irradiated NDV and Sepharose-coupled NDV, which had no or low induciblity of late interferon, and was inhibited by pretreatment with actinomycin D. Protein and RNA synthesis were enhanced in the cells which were treated with cycloheximide and then washed out as in the induction process. From these findings it has been suggested that the induction of early interferon synthesis in the cells pulse-treated with protein synthesis inhibitors, was triggered by an interaction between viral envelope and cell membrane.

Animals↗
PubMed1975

Host resistance mechanisms to Newcastle disease virus in immunodeficient chickens (38540).

In order to assess the mechanisms of host resistance to Newcastle disease virus (NDV), the susceptibility of young adult normal, T cell deficient and agammaglobulinemic chickens to an avirulent live vaccine (Bl) and a mesogenic strain of NDV was studied. All animals, regardless of immunological status resisted the vaccine strain. Most normal birds resisted mesogenic NDV, HOWEVER T cell deficient birds were much more susceptible and agammaglobulinemic chickens were extremely susceptible. There was no difference in the kinetics and levels of hemmagglutination-inhibition activity of plasma between normal, control-irradiated and T cell deficient birds nor between dying and surviving birds. Agammaglobulinemic chickens could be partially protected against an otherwise lethal challenge following immunization with avirulent NDV, low doses of mesogenic NDV inoculated intranasally or im injection of beta-propriolactone inactivated NDV mixed in complete Freund's adjuvant. The possible mechanisms for this protection together with the relative roles of humoral, cell mediated and non-specific immunity are discussed.

Agammaglobulinemia↗
PubMed1996

The neuraminidase of Newcastle disease virus inhibited in the elution-inhibition reaction.

The neuraminidase (NA) on strain 575 of Newcastle disease virus (NDV) was inhibited with elution-inhibition (EI) antibodies causing permanent agglutination patterns of red blood cells (RBC). Detection of EI antibody was unaffected by passage through sephadex, centrifugation or plaque purification of NDV. The haemagglutination-inhibition (HI) and EI reactions as well as the NA inhibition test all showed an increase in titre as immunization progressed. Fluorescent-stained IgG on RBC from the EI reaction appeared as foci but as a halo if NDV was disrupted with ether suggesting NDV aggregation. The haemagglutinin (HA) on "sensitized' RBC from the EI reaction was not neutralized and agglutinated newly added RBC. The NA cleaved fetuin at 49 to 88% of the maximum values while bound to RBC by EI antibody. Added NA substrates failed to block the EI reaction. The order of inactivation at 53 or 56 degrees C but not 50 degrees C was: the putative EI antibody determinant > NA > HA. The term elution inhibition is suggested for the antibody responsible for the EI reaction.

Animals↗
PubMed1986

Monoclonal antibodies to hemagglutinin-neuraminidase and fusion glycoproteins of Newcastle disease virus: relationship between glycosylation and reactivity.

Eighteen hybridoma lines obtained by immunization of mice with Newcastle disease virus (NDV) lentogenic strain La Sota or velogenic strain Italien produced hemagglutinating monoclonal antibodies. The 18 monoclones were divided into four groups according to their reactivity toward native hemagglutinin neuraminidase protein (HN), nonglycosylated HN precursor, and heat-denatured HN blotted on nitrocellulose membranes. Only group II reagents were reactive toward their targets in all conditions tested. They were considered sequence-specific antibodies. Group I antibodies did not require glycosylation but lacked reactivity towards the denatured glycosylated antigen. Monoclonal antibodies from group III recognized only the native HN. Group IV was made up of a single monoclone that lacked reactivity with NDV Italien but recognized the La Sota strain in hemagglutination inhibition and enzyme-linked immunosorbent assays. Five hybridoma lines produced monoclonal antibodies which neutralized viral infectivity but failed to inhibit hemagglutination. One monoclonal antibody obtained after immunization of mice with NDV La Sota showed a low neutralization index versus NDV Italien. Four monoclonal antibodies derived from mice immunized with NDV Italien showed higher neutralization indices towards this strain. Neither the denatured F protein nor its nonglycosylated precursor was reacted against by the five monoclonal antibodies.

Animals↗
PubMed1983

Biological consequences of neuraminidase deficiency in Newcastle disease virus.

A second-step revertant (L1) of a temperature-sensitive mutant (C1) of Newcastle disease virus agglutinated erythrocytes normally but had less than 3% of the wild-type (strain AV) levels of neuraminidase activity. Revertant L1 had seven times more virion-associated N-acetylneuraminic acid (NANA) than strain AV. NANA residues on purified virions were specifically labeled with periodate and tritiated borohydride. Analyses of radiolabeled L1 virions on sodium dodecyl sulfate-polyacrylamide gels showed that most of the virion-associated NANA was in a high-molecular-weight component with an electrophoretic mobility different from that of any known viral protein. NANA was also detected in molecules with the electrophoretic mobility of the viral glycoproteins HN and F1. Revertant L1 had a twofold lower rate constant of attachment to HeLa cells than that of the wild-type. Treatment of L1 virions with Vibrio cholerae neuraminidase removed the excess NANA and returned L1 attachment kinetics to normal. Revertant N1, which has 10-fold more neuraminidase activity than L1, penetrated host cells at the same rate as L1. L1 was impaired in elution from erythrocytes. Removal of virion-associated NANA exacerbated this defect. Despite a small disadvantage in attachment and a major defect in elution relative to strain AV, revertant L1 enjoyed a slight advantage over the wild-type during a single reproductive cycle in cultured chicken embryo cells.

Animals↗
PubMed1972

Hemolytic interaction of Newcastle disease virus and chicken erythrocytes. I. Quantitative comparison procedure.

The extent to which erythrocytes are hemolyzed by Newcastle disease virus is a function of the relative concentrations of both virus and erythrocytes. Under proper conditions, the interaction of a single virus particle with an erythrocyte is sufficient to cause lysis. The extent of hemolysis is directly proportional to virus concentration only when the virus-erythrocyte ratio is very low. At the higher virus-erythrocyte ratios usually employed in hemolysis experiments, the extent of hemolysis is proportional to the logarithm of the virus concentration. Thus, quantitative comparisons of hemolytic activities of different virus preparations cannot be made by directly comparing the extent of hemolysis. Relative hemolytic activities must be determined by comparing virus concentrations which yield equivalent amounts of hemolysis (the quantitative comparison procedure).

Animals↗
PubMed2006

Newcastle disease virus exerts oncolysis by both intrinsic and extrinsic caspase-dependent pathways of cell death.

Newcastle disease virus (NDV), an avian paramyxovirus, is tumor selective and intrinsically oncolytic. Here, we present evidence that genetically modified, recombinant NDV strains are cytotoxic to human tumor cell lines of ecto-, endo-, and mesodermal origin. We show that cytotoxicity against tumor cells is due to multiple caspase-dependent pathways of apoptosis independent of interferon signaling competence. The signaling pathways of NDV-induced, cancer cell-selective apoptosis are not well understood. We demonstrate that NDV triggers apoptosis by activating the mitochondrial/intrinsic pathway and that it acts independently of the death receptor/extrinsic pathway. Caspase-8-methylated SH-SY5Y neuroblastoma cells are as sensitive to NDV as other caspase-8-competent cells. This demonstrates that NDV is likely to act primarily through the mitochondrial death pathway. NDV infection results in the loss of mitochondrial membrane potential and the subsequent release of the mitochondrial protein cytochrome c, but the second mitochondrion-derived activator of caspase (Smac/DIABLO) is not released. In addition, we describe early activation of caspase-9 and caspase-3. In contrast, cleavage of caspase-8, which is predominantly activated by the death receptor pathway, is a TNF-related, apoptosis-inducing ligand (TRAIL)-induced late event in NDV-mediated apoptosis of tumor cells. Our data, therefore, indicate that the death signal(s) generated by NDV in tumor cells ultimately converges at the mitochondria and that it acts independently of the death receptor pathway. Our cytotoxicity studies demonstrate that recombinant NDV could be developed as a cancer virotherapy agent, either alone or in combination with therapeutic transgenes. We have also shown that trackable oncolytic NDV could be developed without any reduction in oncolytic efficacy.

Animals↗
PubMed1994

Complete regression of human fibrosarcoma xenografts after local Newcastle disease virus therapy.

We have recently demonstrated that a single local injection of the avian pathogen Newcastle disease virus (NDV; strain 73-T) causes complete regression of human neuroblastoma xenografts in athymic mice (R. M. Lorence, K. W. Reichard, B. B. Katubig, H. M. Reyes, A. Phuangsab, B. R. Mitchell, C. J. Cascino, R. J. Walter, and M. E. Peeples. J. Natl. Cancer Inst., 86: 1228-1233, 1994). In this report, we tried to determine if this in vivo antineoplastic effect of NDV extends to human sarcomas. Athymic mice with s.c. HT1080 fibrosarcoma xenografts (7-14 mm) were randomly divided into two groups and treated i.t. with a single injection of either 10(7) plaque-forming units of NDV or phosphate-buffered saline. Complete tumor regression occurred in 8 of 10 mice treated with NDV while unabated tumor growth occurred in all 9 mice treated with phosphate-buffered saline (P < 0.001). To determine if complete tumor regression was long lasting, the 8 mice were monitored for 1 year, during which time no tumor recurred. To test the antitumor effects of NDV on tumors derived from a fresh human sarcoma, a similar experiment was performed in athymic mice using TH15145 synovial sarcoma xenografts at their first and second passages. Of 9 mice with TH15145 xenografts, a single i.t. injection of NDV (10(7) plaque-forming units) caused complete regression of 3 tumors and > 80% regression in 3 more tumors. In contrast, tumors in all 5 mice treated with phosphate-buffered saline exhibited unabated growth (P < 0.03 for > 80% tumor regression). Since HT1080 fibrosarcoma cells express the N-ras oncogene, we explored the effects that transfection of this oncogene has on the sensitivity to NDV. Cultured human fibroblasts that were made tumorigenic following N-ras-transfection were found to be 1000-fold more sensitive to NDV than normal fibroblasts in a cytotoxicity assay. Oncogene expression by the HT1080 fibrosarcoma may therefore contribute to the long-lasting complete regression of this sarcoma following a single local injection of NDV.

Animals↗
PubMedDate not supplied

The production of colibacillosis in turkeys following sequential exposure to Newcastle disease virus or Bordetella avium, avirulent hemorrhagic enteritis virus, and Escherichia coli.

Female large white turkeys were intranasally inoculated with either Newcastle disease virus (ND) or Bordetella avium (BA) at 4 weeks of age. This was followed by oral inoculation with an avirulent (vaccine) strain of hemorrhagic enteritis virus (HE) at 5 weeks and intravenous inoculation with Escherichia coli (EC) at 6 weeks. Control birds received ND, BA, or HE followed by EC; EC alone; or nothing at all. Turkeys receiving one agent prior to EC challenge did not experience a significant increase in mortality or pericarditis. Those exposed to ND or BA followed by HE and EC experienced a significant elevation in mortality and pericarditis. A highly significant positive correlation between the number of infectious agents encountered during primary exposure and the incidence of colibacillosis after EC challenge was demonstrated.

Administration, Intranasal↗
PubMed1994

Measurement of antibody titer to fowl pox virus by enzyme-linked immunosorbent assay.

The usefulness of the measurement of antibody titer to fowl pox virus (FPV) by enzyme-linked immunosorbent assay (ELISA) was evaluated in SPF chickens with or without inoculation with FPV. The optimum concentration of purified antigen was 10 micrograms/ml of protein. The absorbance at 492 nm was less than 0.10 in the chickens negative to FPV from 1 to 63 days old. By contrast, a higher titer was detected in SPF chickens with various FPVs inoculated into the wing web than in non-inoculated chickens. Moreover, there was no cross response to chicken sera immunized with Haemophilus paragallinarum, Marek's disease virus, Newcastle disease virus or infectious bronchitis virus. The titers increased after vaccination were not increased after subsequent challenge with virulent FPV. These findings suggested the usefulness of the measurement of the antibody response to FPV vaccine by ELISA.

Animals↗