The hemagglutinin-neuraminidase protein of Newcastle disease virus determines tropism and virulence.
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The hemagglutinin-neuraminidase (HN) protein of Newcastle disease virus (NDV) plays a crucial role in the process of infection. However, the exact contribution of the HN gene to NDV pathogenesis is not known. In this study, the role of the HN gene in NDV virulence was examined. By use of reverse genetics procedures, the HN genes of a virulent recombinant NDV strain, rBeaudette C (rBC), and an avirulent recombinant NDV strain, rLaSota, were exchanged. The hemadsorption and neuraminidase activities of the chimeric viruses showed significant differences from those of their parental strains, but heterotypic F and HN pairs were equally effective in fusion promotion. The tissue tropism of the viruses was shown to be dependent on the origin of the HN protein. The chimeric virus with the HN protein derived from the virulent virus exhibited a tissue predilection similar to that of the virulent virus, and vice versa. The chimeric viruses with reciprocal HN proteins either gained or lost virulence, as determined by a standard intracerebral pathogenicity index test of chickens and by the mean death time in chicken embryos (a measure devised to classify these viruses), indicating that virulence is a function of the amino acid differences in the HN protein. These results are consistent with the hypothesis that the virulence of NDV is multigenic and that the cleavability of F protein alone does not determine the virulence of a strain. (+info)
Phylogenetic relationships among virulent Newcastle disease virus isolates from the 2002-2003 outbreak in California and other recent outbreaks in North America.
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Isolates from the 2002-2003 virulent Newcastle disease virus (v-NDV) outbreak in southern California, Nevada, Arizona, and Texas in the United States were compared to each other along with recent v-NDV isolates from Mexico and Central America and reference avian paramyxovirus type 1 strains. Nucleotide sequencing and phylogenetic analyses were conducted on a 1,195-base genomic segment composing the 3' region of the matrix (M) protein gene and a 5' portion of the fusion (F) protein gene including the M-F intergenic region. This encompasses coding sequences for the nuclear localization signal of the M protein and the F protein cleavage activation site. A dibasic amino acid motif was present at the predicted F protein cleavage activation site in all v-NDVs, including the California 2002-2003, Arizona, Nevada, Texas, Mexico, and Central America isolates. Phylogenetic analyses demonstrated that the California 2002-2003, Arizona, Nevada, and Texas viruses were most closely related to isolates from Mexico and Central America. An isolate from Texas obtained during 2003 appeared to represent a separate introduction of v-NDV into the United States, as this virus was even more closely related to the Mexico 2000 isolates than the California, Arizona, and Nevada viruses. The close phylogenetic relationship between the recent 2002-2003 U.S. v-NDV isolates and those viruses from countries geographically close to the United States warrants continued surveillance of commercial and noncommercial poultry for early detection of highly virulent NDV. (+info)
Molecular characterization and phylogenetic study of newcastle disease virus isolates from recent outbreaks in eastern Uganda.
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Newcastle disease virus isolates from chickens in eastern Uganda in 2001 were found to be velogenic by fusion protein cleavage site sequence analysis and biological characterization; the intracerebral pathogenicity index was 1.8. Analysis of their hemagglutinin-neuraminidase protein gene sequences revealed a novel genotype unrelated to those that caused previous outbreaks. (+info)
A recombinant Newcastle disease virus (NDV) expressing VP2 protein of infectious bursal disease virus (IBDV) protects against NDV and IBDV.
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Infectious bursal disease virus (IBDV) causes a highly immunosuppressive disease in chickens. Currently available, live IBDV vaccines can lead to generation of variant viruses. We have developed an alternative vaccine that will not create variant IBDV. By using the reverse genetics approach, we devised a recombinant Newcastle disease virus (NDV) vector from a commonly used vaccine strain LaSota to express the host-protective immunogen VP2 of a variant IBDV strain GLS-5. The gene encoding the VP2 protein of the IBDV was inserted into the most 3'-proximal locus of a full-length NDV cDNA for high-level expression. We successfully recovered the recombinant virus, rLaSota/VP2. The rLaSota/VP2 was genetically stable, at least up to 12 serial passages in chicken embryos, and was shown to express the VP2 protein. The VP2 protein was not incorporated into the virions of recombinant virus. Recombinant rLaSota/VP2 replicated to a titer similar to that of parental NDV strain LaSota in chicken embryos and cell cultures. To assess protective efficacy of the rLaSota/VP2, 2-day-old specific-pathogen-free chickens were vaccinated with the recombinant virus and challenged with a highly virulent NDV strain Texas GB or IBDV variant strain GLS-5 at 3 weeks postvaccination. Vaccination with rLaSota/VP2 generated antibody responses against both NDV and IBDV and provided 90% protection against NDV and IBDV. Booster immunization induced higher levels of antibody responses against both NDV and IBDV and conferred complete protection against both viruses. These results indicate that the recombinant NDV can be used as a vaccine vector for other avian pathogens. (+info)
Receptor destruction by viruses of the mumps-NDV-influenza group.
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A strain each of mumps and Newcastle disease virus and five strains of influenza virus were found to be capable of removing all the receptors for this group of viruses from fowl red cells. Five virus strains were tested for their capacity to inactivate the virus hemagglutinin of human plasma and of egg white. In the case of egg white all strains including mumps and Newcastle disease virus inactivated the inhibitor completely, or nearly so. With plasma the influenza strains inactivated the inhibitor completely but mumps and NDV destroyed only that portion of the complex which effected mumps inhibition. The inhibitor for some strains was destroyed more rapidly than that for others and the sequence in which they were destroyed (inhibitor gradient) was similar, regardless of the strain employed. The inhibitor gradient for egg white was very different from that for plasma and these in turn differed significantly from the receptor gradient for fowl red cells. (+info)
The relationship of the receptors of a new strain of virus to those of the mumps-NDV-influenza group.
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The interrelationships of the cellular receptors and the hemagglutinin inhibitors of a new strain of virus (1233) to members of the mumps-Newcastle disease-influenza group have been investigated. It was found that strain. 1233 does not destroy the receptors or inhibitors of the other group, nor does the latter destroy 1233 receptors or inhibitor. The sole exception to this statement was a moderate destruction of 1233 inhibitor in egg white by Newcastle disease virus. The classification of strain 1233 was discussed in the light of this evidence, evidence which tends to place strain 1233 in a different category from that of any other strain of the MNI group. (+info)
Impairment of contrasuppressor activity in mice infected with the paramyxovirus of Newcastle disease.
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Spleen cells from mice infected with the virus of Newcastle disease (NVD) fail to mediate the passive transfer of contact sensitivity to simple chemical haptens such as picryl chloride (Pcl) and oxazolone (Ox). The inhibitory effect of NDV can be bypassed by treating recipient mice with low doses of cyclophosphamide (Cy), suggesting that the T-effector cell which mediates the passive transfer of contact sensitivity is not affected by NDV infection. Vicia Villosa-adherent cells from immune mice display contrasuppressor activity and restore the ability of cells from NDV-infected mice to transfer contact sensitivity to naive recipients. In contrast, Vicia Villosa-adherent cells from NDV-infected mice fail to exert any contrasuppressor activity. Furthermore, contrasuppressor activity can also be detected in the culture supernatants of Vicia Villosa-adherent cells from uninfected, sensitized mice, but not in culture supernatants of Vicia Villosa-adherent cells from NDV-infected mice. The present results suggest that a Vicia Villosa-adherent contrasuppressor cell population is impaired by NDV infection. (+info)
Loop-mediated isothermal amplification for rapid detection of Newcastle disease virus.
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We have evaluated a diagnostic system based on the loop-mediated isothermal amplification (LAMP) assay for the rapid, simple, and sensitive detection of Newcastle disease virus (NDV) directly from culture isolates as well as clinical samples. By using one set of specific primers targeting the fusion protein gene, the LAMP assay rapidly amplified the target gene within 2 h, requiring only a regular laboratory water bath or heat block for reaction. The results obtained from testing the genomes of 38 NDV strains, other different viruses, and clinical samples of experimentally infected chickens showed that LAMP was as sensitive and specific as nested PCR. All LAMP-positive samples were positive by nested PCR. The LAMP assay is faster than nested PCR, cost-effective, and easy to perform. Our results clearly demonstrate that the LAMP-based assay is a useful tool for the rapid and sensitive diagnosis of NDV infection. (+info)