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Title: THE PATHOGENESIS OF NEWCASTLE DISEASE: A COMPARISON OF SELECTED NEWCASTLE DISEASE VIRUS WILD-TYPE STRAINS AND THEIR INFECTIOUS CLONES

Author
item WAKAMATSU, NOBUKO - UNIV OF GEORGIA-ATHENS,GA
item King, Daniel
item Seal, Bruce
item SAMAL, SIBA - UNIV OF MD-COLLEGE PK,MK
item BROWN, CORIE - UNIV OF GEORGIA-ATHENS,GA

Submitted to: Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/9/2006
Publication Date: 9/30/2006
Citation: Wakamatsu, N., King, D.J., Seal, B.S., Samal, S.K., Brown, C.C. 2006. The pathogenesis of Newcastle disease: A comparison of selected Newcastle disease virus wild-type strains and their infectious clones. Virology. 353:333-343.

Interpretive Summary: Newcastle disease virus (NDV) strains are all members of the same serotype but they cause infections of poultry that vary from those that may be clinically inapparent to those with severe disease and high mortality. The viral genetic basis for the different clinical disease forms resulting from infections with different strains remains undefined. Infectious copies of NDV LaSota, a low virulence virus used as a Newcastle disease vaccine strain, and NDV Beaudette C, a virulent strain provided the framework to produce gene mutations in both viruses and gene exchanges between those two viruses. Changes in the fusion gene of LaSota to make that locus identical to known virulent viruses like Beaudette C had the greatest impact on virulence. Gene exchanges or mutations in genes other than the fusion gene of the virulent virus reduced the pathogenicity of those viruses and consequently the severity of the resultant clinical disease. The results add to the accumulating evidence defining the role that different NDV genes play in the virulence of NDV, but a complete understanding of the genetic factors in disease remains undefined.

Technical Abstract: The effect of mutations of Newcastle disease virus (NDV) fusion (F) gene, hemagglutinin-neuraminidase (HN) gene, and phosphoprotein (P) gene and HN chimeras between the virulent Beaudette C and low virulence LaSota strains on pathogenesis and pathogenicity in fully susceptible chickens was examined. A virulent F cleavage site motif within a LaSota backbone increased pathogenicity and severity of clinical disease. A LaSota HN within a Beaudette C backbone decreased pathogenicity indices and disease severity. A Beaudette C HN within a LaSota backbone did not change either pathogenicity indices or severity of disease in chickens. Loss of glycosylation at site 4 of the HN or modified P gene of Beaudette C decreased pathogenicity indices and caused no overt clinicopathologic disease in chickens. Both pathogenicity indices and clinicopathologic examination demonstrated that the F, HN, and P genes of NDV collectively or individually can contribute to viral virulence.