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Title: Mutations in the Carboxi Terminal Region of E2 Glycoprotein of Classical Swine Fever Virus is Responsible for Viral Attenuation in Swine

Author
item RISATTI, GUILLERMO - UNIVERSITY OF CONN
item Holinka-Patterson, Lauren
item FERNANDEZ-SAINZ, IGNACIO - OAKRIDGE INST OF SCIENCE
item CARILLO, CONSUELO - USDA,APHIS,PIADC
item KUTISH, GERALD - UNIVERSITY OF CONN
item LU, ZHIQIANG - USDA,DHS,PIADC
item TULMAN, EDAM - UNIVERSITY OF CONN
item ROCK, DAN - UNIVERSITY OF ILLINOIS
item Borca, Manuel

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2006
Publication Date: 12/5/2006
Citation: Risatti, G.R., Holinka, L.G., Fernandez-Sainz, I., Carillo, C., Kutish, G.F., Lu, Z., Tulman, E.R., Rock, D.L., Borca, M.V. Mutations in the Carboxi Terminal Region of E2 Glycoprotein of Classical Swine Fever Virus is Responsible for Viral Attenuation in Swine. Conference of Research Workers in Animal Disease (CRWAD) annual meeting, Chicago, IL, December 3-5, 2006, page 138.

Interpretive Summary:

Technical Abstract: We have reported that chimeric virus 319.1 virus containing the E2 glycoprotein gene from Classical Swine Fever Virus (CSFV) vaccine strain CS with the genetic background of virulent CSFV strain Brescia (BIC virus) was attenuated in pigs. To identify the amino acids mediating 319.1 virus attenuation a series of chimeric viruses containing CS E2 residues in the context of the Brescia strain were constructed. Chimera 357 virus, containing CS E2 residues 691 to 881 of CSFV polyprotein was virulent, while chimera 358 virus, containing CS E2 residues 882 to 1064, differing in thirteen amino acids from BIC virus, was attenuated in swine. Single or double substitutions of those amino acids in BIC virus E2 to CS E2 residues did not affect virulence. Groups of amino acids were then substituted in BIC virus E2 to CS E2 residues. Mutants with six substitutions between residues 955-994 and between residues 975-1064, induced severe disease. A mutant virus (31 virus) with seven substitutions between residues 882-958, induced a delayed but lethal disease. Progressive introduction of CS residues into 31 virus yielded virulent viruses, but virulence was abrogated in mutants 42 virus and 43 virus containing 12 and 13 substitutions respectively. Importantly, 43 virus/358 virus protected swine from challenge with virulent BIC virus at 3 and 28 days post-infection.