Submitted to: Virus Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 14, 2007
Publication Date: October 19, 2007
Citation: Estevez, C., King, D.J., Seal, B.S., Yu, Q. 2007. Evaluation of Newcastle disease virus chimeras expressing the hemagglutinin-neuraminidase protein of velogenic strains in the context of a mesogenic recombinant virus backbone. Virus Research. 129:182-190. Interpretive Summary: Newcastle disease virus (NDV) is an important poultry pathogen that can produce severe economic losses in the poultry industry. The more virulent forms of the disease are not prevalent in the United Sates and are a major concern to the national industry due to the severe losses that would occur in the event of a major outbreak of virulent disease in the country, both through increased mortality of infected flocks and impediments of exporting processed poultry meat and products to other countries. Determining what causes the increase of pathogenicity in the most virulent strains of the virus is an important first step for preventing the occurrence of disease outbreaks. In this study, the contribution of the hemagglutinin-neuraminidase (HN) protein to the virulence of the virus was assessed by using recombinant viruses carrying the HN protein of known virulent strains of NDV, and observing the effects of the protein in pathogenesis by inoculation of susceptible chickens and embryonated eggs. Our results suggest that a variety of genetic factors are required for highly virulent virus and that the HN proteins tested in the context of our recombinant virus system were not enough to increase the virus pathogenicity.
Technical Abstract: A major factor in the pathogenicity of Newcastle disease virus (NDV) is the amino acid sequence of the fusion protein cleavage site, but the role of other viral genes that contribute to virulence and different clinical forms of the disease remain undefined. To assess the role of other NDV genes in virus pathogenicity, a reverse genetics system was developed using the mesogenic NDV Anhinga strain to provide a backbone for generating gene mutations or gene exchanges in attempts to enhance or attenuate the virulence of that virus. Chimeras created by exchange of the Anhinga hemagglutinin-neuraminidase (HN) gene with HN genes of neurotropic and viscerotropic velogenic viruses produced no significant change of virus pathogenicity as assessed by conducting the mean death time and intracerebral pathogenicity index assays and by inoculation of susceptible day-old SPF birds. An HN gene exchange alone within the context of the NDV Anhinga backbone failed to increase virus virulence from mesogenic to velogenic pathotype and suggests a multigenic role for NDV pathogenicity.