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United States Department of Agriculture

Agricultural Research Service

Title: VESICULAR STOMATITIS VIRUS GLYCOPROTEIN IS A DETERMINANT OF PATHOGENESIS IN SWINE, A NATURAL HOST

Authors
item Martinez, Isidoro - UNIVERSITY OF ALABAMA
item Rodriguez, Luis
item Jimenez, Carlso - UNIV NACIONAL COSTA RICA
item Pauszek, Steven
item Wertz, Gail - UNIVERSITY OF ALABAMA

Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 11, 2003
Publication Date: July 1, 2003
Citation: MARTINEZ, I., RODRIGUEZ, L.L., JIMENEZ, C.F., PAUSZEK, S.J., WERTZ, G.W. VESICULAR STOMATITIS VIRUS GLYCOPROTEIN IS A DETERMINANT OF PATHOGENESIS IN SWINE, A NATURAL HOST. JOURNAL OF VIROLOGY. 77L8039-8047, 2003.

Interpretive Summary: This study represents a first step in the development of a multivalent attenuated vesicular stomatitis virus (VSV) vaccine capable of protecting against both serotypes: New Jersey (VSNJV) and Indiana 1 (VSIN-1). Using recombinant DNA technology we obtained VSIV-1 that contained the VSNJV glycoprotein (Gnj), the main immunogenic component of the virus, in one of several forms: 1) one copy of the VSIV G gene (VSIV-GI), 2) two copies of the G gene, one from each serotype (VSIV-GNJGI), or 3) a single copy of the GNJ gene instead of the GI gene (VSIV-GNJ). We showed that the recombinant viruses expressed the expected glycoprotein and that the VSIV=GngG1 virus induced neutralizing antibodies against both serotypes in mice, demonstrating its potential use as a broad-range VSV vaccine. In mice, VSIV=Gnj and VSIV-GnjG1 viruses were attenuated. However, in swine, a natural host for VSV, the Gnj glycoprotein containing viruses caused more severe lesions and replicated to higher titers than the parental virus VSIV-G1. These observations implicate the glycoprotein as a determinant of VSV virulence in a natural host, and emphasize the difference between mice and swine regarding VSV pathogenesis.

Technical Abstract: There are two major serotypes of vesicular stomatitis virus, Indiana (VSIV) and New Jersey (VSNJV). We recovered recombinant VSIVs from engineered cDNAs that contained either: 1) one copy of the VSIV G gene (VSIV-GI), 2) two copies of the G gene, one from each serotype (VSIV-GNJGI), or 3) a single copy of the GNJ gene instead of the GI gene (VSIV-GNJ). The recombinant viruses expressed the appropriate glycoproteins, incorporated them into virions, and were neutralized by antibodies specific for VSIV (VSIV-GI), VSNJV (VSIV-GNJ) or both (VSIV-GNJGI), according to the glycoprotein(s) they expressed. All recombinant viruses grew to similar titers in cell culture. In mice, VSIV-GNJ and VSIV-GNJGI viruses were attenuated. However in swine, a natural host for VSV, the GNJ glycoprotein containing viruses caused more severe lesions and replicated to higher titers than the parental virus VSIV-GI. These observations implicate the glycoprotein as a determinant of VSV virulence in a natural host, and emphasize the differences between mice and swine regarding VSV pathogenesis.

Last Modified: 9/1/2014
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