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United States Department of Agriculture

Agricultural Research Service

Title: The Glycoprotein of Vesicular Stomatitis Virus (Vsv) Is Associated with Virulence in a Natural Host.

Authors
item Martinez, Isidoro - UNIVERSITY OF ALABAMA
item Rodriguez, Luis
item Wertz, G - UNIVERSITY OF ALABAMA

Submitted to: International Congress of Virology
Publication Type: Proceedings
Publication Acceptance Date: July 27, 2002
Publication Date: N/A

Interpretive Summary: Vesicular stomatitis virus (VSV) causes a costly disease in livestock that is clinically undistinguishable from foot-and-mouth disease (FMD). Two virus types have been recognized by serology; New Jersey (VSV-NJ) causes 85-90% of the clinical outbreaks from northern South America to North America and Indiana (VSV-IN) causes the remaining cases. Recent reports suggest that VSV-NJ causes more severe clinical disease and is more readil transmitted among experimentally inoculated swine than VSV-IN. The basis for this difference in pathogenesis remains unknown. In this work we wanted to determine if the glycoprotein of VSV was associated to its pathogenicity. By using reverse genetics we generated recombinant viruses based on the Indiana (IN) serotype that contained either: 1) one copy of the IN glycoprotein gene (G), 2) one copy from each IN and New Jersey (NJ), or 3) a single copy of the NJ-G. All recombinant viruses grew to similar titers in vitro, expressed the expected glycoproteins, and incorporated them in the virions. The virus expressing the two glycoproteins was neutralized by antibodies to either the IN or NJ serotypes. The pathogenesis of the viruses was examined in mice and pigs. Recombinant NJ-G and IN-G plus NJ-G viruses were attenuated in mice, as compared to the parental IN-G virus. In pigs, viruses containing NJ-G caused more severe lesions and grew to higher titers than the parental IN-G virus. These experiments show that the G protein is a VSV pathogenesis-related determinant in pigs, and may help explain field observations that outbreaks caused by VSV-NJ are generally more severe than those caused by VSV-IN. This information is useful in designing control and preventive measures against VSV infections.

Technical Abstract: We generated recombinant VSVs based on the Indiana (IN) serotype that contained either: 1) one copy of the IN glycoprotein gene (G), 2) two copies of G, one from each of the two different serotypes, IN and New Jersey (NJ), or 3) a single copy of the NJ-G instead of the IN-G. All recombinant viruses grew to similar titers in vitro, expressed the expected dglycoproteins, and incorporated them in the virions. The virus expressing the two glycoproteins was neutralized by antibodies to either the IN or NJ serotypes. Both proteins were co-immunoprecipitated by antibodies against the IN serotype in the presence of non-ionic detergents, indicating their association in functional heterotrimeric spikes. The pathogenesis of the viruses was examined in mice and pigs. Recombinant NJ-G and IN-G plus NJ-G viruses were attenuated in mice, as compared to the parental IN-G virus (LD50=7 pfu/mouse). The virus containing only NJ-G was the most attenuated (LD50>106 pfu/mouse), followed by the virus containing both IN-G and NJ-G (LD50=204 pfu/mouse). In pigs, the virus containing only NJ-G caused much more severe lesions and grew to higher titers than the parental IN-G virus. The virus containing both IN-G and NJ-G had intermediate phenotype. These experiments show that the G protein is a VSV pathogenesis-related determinant in pigs, and may help explain field observations that outbreaks caused by VSV-NJ are generally more severe than those caused by VSV-IN.

Last Modified: 7/25/2014
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