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Identification of a phosphorylated non-structural form of the P protein of Newcastle disease virus and analysis of P multimers.

Two phosphorylated and two non-phosphorylated variants of P protein isolated from Newcastle disease virions are known. Here, a fifth form of P was identified using two-dimensional polyacrylamide gel electrophoresis and peptide mapping. P form 5 was phosphorylated; however, unlike the four known variants of P, the new form was not a major protein in virions, which suggested an intracellular function. The subunit composition of four electrophoretically distinct, disulphide-linked multimers of P from virions was determined. Each homomultimer was composed of at least three molecules of a different one of the four virion-associated P variants.

Animals↗

Suppression of the humoral immune response to inactivated Newcastle disease virus by Mycoplasma meleagridis in the Turkey.

Groups of Mycoplasma meleagridis-free and -infected turkeys were vaccinated against Newcastle disease virus (NDV) at 5 and 8 weeks of age. The two groups did not differ significantly in antibody response to NDV as measured by the hemagglutination-inhibition test when a live vaccine (TCND) was used, but the two groups differed significantly when an inactivated vaccine was used; titers were higher in the mycoplasma-free group in both primary and secondary responses. The difference between responses of the mycoplasma-free and -infected groups to inactivated and live NDV was explained by a current hypothesis about the ontogeny of B-cell differentiation in the bursa of Fabricius and by its interference by M. meleagridis.

Animals↗

Immune response to Newcastle disease virus vaccine, fowl-pox vaccine, and Escherichia coli vaccine in Bedouin and White Leghorn chickens.

Immune response to Newcastle disease virus (NDV) vaccine, fowl pox, and E. coli vaccine was compared in the native Bedouin fowl of the Sinai desert, in a commercial Leghorn layer strain, and in the reciprocal crosses between them. Differences were not found in antibody titer levels to attenuated or inactivated NDV vaccines, in the proportion of birds showing post-vaccination immunity to fowl pox, or in the kinetics of postvaccination NDV titer levels. Rate of development of titer to Escherichia coli from day 1 to day 4, however, was significantly more rapid in Bedouin chicks than in the purebred Leghorn or the reciprocal crosses.

Animals↗

Epizootiologic aspects of viscerotropic velogenic Newcastle disease in six pet bird species.

Pet birds of 6 species were exposed to a psittacine isolate to viscerotropic velogenic Newcastle disease (VVND) virus to evaluate the impact of VVND in those species. Species examined were the budgerigar, yellow-headed Amazon parrot, canary, halfmoon conure, lesser hill mynah, and blackheaded nun. Five of the 6 species were highly susceptible to infection with VVND virus. Canaries were relatively refractory to infection with the virus. Contact birds of the same species developed infections almost as rapidly as did the birds directly exposed to nebulized VVND virus. Mortality was most marked for the conures. Less than half of the parrots exposed to nebulized virus died of VVND. Of the directly exposed budgerigars, mynahs, and nuns, 16% to 22% died during an observation period of postexposure days 0 through 28.

Animals↗

Effects of Newcastle disease virus (NDV) on infection of adult mice with the Thogoto-like Ar-126 arbovirus.

Inoculation of mice with Newcastle disease virus (NDV) alters the course of infection with the Thogoto-like arbovirus Tho-Ar-126. The Tho-Ar-126 content of liver, spleen, and lymph nodes was approximately 10 times greater in mice treated with NDV 24 h before infection; the mortality was somewhat increased, but liver damage (as indicated by serum transaminase levels) did not seem to be potentiated. Lymphocytopenia was observed in NDV-inoculated mice, and in the spleen and lymph nodes the proportion of lymphocytes susceptible to lysis by anti-theta (a marker for thymus-derived lymphocytes) was markedly decreased in these animals. This suggests that NDV potentiates infection by Tho-Ar-126 through its action on thymus-derived lymphocytes.

Alanine Transaminase↗

Characterization of a battery of monoclonal antibodies for differentiation of Newcastle disease virus and pigeon paramyxovirus-1 strains.

Twenty monoclonal antibodies (MCAs) prepared against the velogenic GB-Texas strain of Newcastle disease virus (NDV) and the type 1 pigeon paramyxovirus (PPMV-1) were characterized and examined as potential immunodiagnostic reagents. All MCAs generated were found to bind specifically, but with varying reactivity, to various NDV strains in direct binding assays. In addition, MCA 15C4 neutralized and inhibited hemagglutination (HA) of all lentogenic, mesogenic, and velogenic NDV strains tested but not the PPMV-1 strain. Antibody 10D11 also inhibited HA activity, but inhibition was more selective and limited to the mesogenic and domestic or indigenous velogenic strains of NDV. MCA 79 reacted in all serologic assays with an antigenic site common to all serotype 1 avian paramyxoviruses. Passive immunization studies involving three different neutralizing MCAs (35, 79, and 15C4) showed that enhanced, but not complete, protection against virulent NDV challenge was provided when the three MCAs were administered in combination.

Animals↗

Polyadenylate sequences on Newcastle disease virus mRNA synthesized in vivo and in vitro.

Polyadenylate [poly(A)] sequences are associated with the 35 and 50S Newcastle disease virus (NDV)-specific RNAs as well as all six to seven of the 18-22S NDV-specific messenger RNAs extracted from infected chicken embryo cells. The poly(A) associated with the 18-22S RNA has an average size of 120 to 130 nucleotides. The 18-22S RNA synthesized in vitro by NDV's virion-bound polymerase contains six to seven species of the same size and relative proportions as its intracellular counterpart. This in vitro synthesized 18-22S RNA also contains covalently linked poly(A) sequences which, although variable in size, are usually larger and more heterogeneous than those from the infected cell. In vitro RNA synthesis is supported not only by magnesium (at an optimal concentration of mM) but by manganese (at an optimal concentration of 0.5 to 1.0 mM) as well. However, the major product made in the presence of manganese, although sedimenting at 18 to 22S, differs somewhat from the product made in the presence of magnesium.

Adenosine↗

Characterization of Newcastle disease virus vaccines by biological properties and sequence analysis of the hemagglutinin-neuraminidase protein gene.

Six commercially available monovalent Newcastle disease virus (NDV) live-vaccines were examined for their biological and genomic stability in comparison to their stated parent virus. Thermostability of the hemagglutinin at 56 degrees C for 5 min was consistently observed among the majority of the vaccine viruses. One exception was a recently developed NDV vaccine isolated from turkeys that had a thermostability of 15 min. Neuraminidase activity, as measured by elution rate of agglutinated red blood cells, varied among vaccine viruses and correlated with that of the parent isolate. Virulence as measured by intracerebral pathogenicity index ranged from 0 to 0.39 among NDV vaccine-type viruses, well within the range of avirulent lentogens. Sequence of the fusion protein cleavage site from all the NDV vaccine isolates examined was consistent with that for lentogens. The entire hemagglutinin-neuraminidase gene sequence was 98% similar among all the NDV vaccine viruses examined and phylogenetic classification of commercial vaccine types correlated with their respective parent virus. Consequently, the commercially produced NDV vaccines reported here appear relatively stable when mass produced in avian embryonated eggs.

Amino Acid Sequence↗

An in vitro and in vivo evaluation of the virulence of Newcastle disease virus and vaccines for the chicken reproductive tract.

The virulence of two vaccine strains and two field strains of Newcastle disease virus (NDV) for the female reproductive tract of chickens was assessed using oviduct organ cultures (OOC) prepared from precociously-induced oviducts in young chicks by oestrogen treatment. Ciliostasis, haemagglutination and virus isolation from infected OOC supernatants, histopathology and immunoperoxidase test results indicated the pathogenic nature of both vaccine and virulent NDVs for the precocious oviducts. The virulent viruses, mesogenic and lentogenic vaccines caused damage in that order of magnitude and the uterus had a higher susceptibility than oviducts. One virulent and the mesogenic strain of NDV were used for in vivo trials. The pathogenicity was assessed in oestrogen-treated infected chickens using histopathology and immunoperoxidase test. The vaccine virus produced transient damage up to 6 days post-infection, while the damage with the virulent isolate persisted for at least 9 days post-infection. This technique could be a pointer to possible variations in virulence of NDV vaccine and field strains, and warrants further investigation. The potential value of OOC from young chickens for testing the possibility of NDV vaccines causing damage by themselves and offering protection against damage of the reproductive tract caused by virulent isolates is emphasized.

Animals↗

Disulfide bond formation is a determinant of glycosylation site usage in the hemagglutinin-neuraminidase glycoprotein of Newcastle disease virus.

Determinants of glycosylation site usage were explored by using the hemagglutinin-neuraminidase (HN) glycoprotein of the paramyxovirus Newcastle disease virus. The amino acid sequence of the HN protein, a type II glycoprotein, has six N-linked glycosylation addition sites, G1 to G6, two of which, G5 and G6, are not used for the addition of carbohydrate (L. McGinnes and T. Morrison, Virology 212:398-410, 1995). The sequence of this protein also has 13 cysteine residues in the ectodomain (C2 to C14). Mutation of either cysteine 13 or cysteine 14 resulted in the addition of another oligosaccharide chain to the protein. These cysteine residues flank the normally unused G6 glycosylation addition site, and mutation of the G6 site eliminated the extra glycosylation found in the cysteine mutants. These results suggested that failure to form an intramolecular disulfide bond resulted in the usage of a normally unused glycosylation site. This conclusion was confirmed by preventing cotranslational disulfide bond formation in cells by using dithiothreitol. Under these conditions, the wild-type protein acquired extra glycosylation, which was eliminated by mutation of the G6 site. These results suggest that localized folding events on the nascent chain, such as disulfide bond formation, which block access to the oligosaccharyl transferase are a determinant of glycosylation site usage.

Amino Acid Sequence↗

Newcastle disease virus V protein is a determinant of host range restriction.

It has been demonstrated that the V protein of Newcastle disease virus (NDV) functions as an alpha/beta interferon (IFN-alpha/beta) antagonist (M. S. Park, M. L. Shaw, J. Muñoz-Jordan, J. F. Cros, T. Nakaya, N. Bouvier, P. Palese, A. García-Sastre, and C. F. Basler, J. Virol. 77:1501-1511, 2003). We now show that the NDV V protein plays an important role in host range restriction. In order to study V functions in vivo, recombinant NDV (rNDV) mutants, defective in the expression of the V protein, were generated. These rNDV mutants grow poorly in both embryonated chicken eggs and chicken embryo fibroblasts (CEFs) compared to the wild-type (wt) rNDV. However, insertion of the NS1 gene of influenza virus A/PR8/34 into the NDV V(-) genome [rNDV V(-)/NS1] restores impaired growth to wt levels in embryonated chicken eggs and CEFs. These data indicate that for viruses infecting avian cells, the NDV V protein and the influenza NS1 protein are functionally interchangeable, even though there are no sequence similarities between the two proteins. Interestingly, in human cells, the titer of wt rNDV is 10 times lower than that of rNDV V(-)/NS1. Correspondingly, the level of IFN secreted by human cells infected with wt rNDV is much higher than that secreted by cells infected with the NS1-expressing rNDV. This suggests that the IFN antagonist activity of the NDV V protein is species specific. Finally, the NDV V protein plays an important role in preventing apoptosis in a species-specific manner. The rNDV defective in V induces apoptotic cell death more rapidly in CEFs than does wt rNDV. Taken together, these data suggest that the host range of NDV is limited by the ability of its V protein to efficiently prevent innate host defenses, such as the IFN response and apoptosis.

Amino Acid Sequence↗

Studies on persistent infections of tissue culture. VI. Reversible changes in Newcastle disease virus populations as a result of passage in L cells or chick embryos.

Populations of the Victoria strain of Newcastle disease virus (NDV), reisolated from persistently infected L-cell cultures and passed twice in the embryonated hen's egg (NDV(L-E-2)), were found to differ strikingly from the original, chick embryo-adapted virus (NDV(o)). After exposure of L cells to NDV(o) at high multiplicities of infection, all cells became abortively infected; they produced only small aggregates of viral antigen and few, if any, infectious virus particles, but they yielded large amounts of interferon. No cytopathic effects (CPE) were noted, and the cultures survived readily as viral carriers. In contrast, NDV(L-E-2) yielded under similar conditions large quantities of viral antigen and infectious virus particles, but no detectable interferon, and the cultures were rapidly destroyed. This change in "virulence" was at least partially reversible by further serial passages of NDV(L-E-2) in chick embryos, as was evident from a consecutive decrease in CPE with a concomitant increasingly rapid recovery of the L-cell cultures, gradually diminishing yields of infectious viral progeny, and the returning of a capacity to induce interferon synthesis. Thus, NDV(L-E-16) resembled NDV(o) in many aspects, except for a less striking reduction in its ability to replicate in L cells. Although a selection of viral variants under the given sets of conditions has not been entirely excluded, the establishment of "avirulence" appears to be largely explained by a gradual accumulation of noninfectious, interferon-inducing components in the course of serial passages in the embryonated hen's egg, and the acquisition of "virulence" by a loss of these components. The evidence is as follows. (i) By a step-wise decrease in the dose of virus and restriction of the analyses to the first infectious cycle, a multiplicity of infection was ultimately reached for all "avirulent" populations at which infected cells produced normal yields of infectious viral progeny; i.e., the interferon-inducing components were diluted to noneffective levels. The lowest multiplicity which resulted in a measurable reduction in infectious virus replication was also the last one to induce detectable interferon synthesis. (ii) All viral clones derived from "avirulent" populations behaved like NDV(L-E-2) rather than like the parent viral suspensions, except that some of them elicited small amounts of interferon in L cells. The interferon-inducing components were reduced or lost in the cloning procedures. The nature of the interferon-inducing components has not been established. These components, which were neutralized by rabbit sera against "virulent" NDV(L-E-2) populations, may represent largely inactive or incomplete virus particles; however, the infectious virus-hemagglutinin ratios of "avirulent" populations were mostly of an order similar to those of "virulent" populations. The interferon-inducing components aborted the infectious process in cells simultaneously invaded by infectious virus particles. The implications of these findings are discussed.

Animals↗

Cleavage of mouse ribosomal RNAs by the endonuclease associated with Newcastle disease virus.

Mouse ribosomal ribonucleic acids (rRNAs) are specifically cleaved to polynucleotides of lower molecular mass by the endonuclease associated with Newcastle disease virus (NDV). The 28 S RNA yielded a fragment of about Mr = 1.7 X 10(5) which is resistant to the endonuclease. We assume that one molecule of 28 S RNA contains one such resistant region. 18 S RNA does not possess resistant regions of this character and it is cleaved by the endonuclease to smaller molecules.

Animals↗