The patent badge is an abbreviated version of the USPTO patent document. The patent badge does contain a link to the full patent document.

The patent badge is an abbreviated version of the USPTO patent document. The patent badge covers the following: Patent number, Date patent was issued, Date patent was filed, Title of the patent, Applicant, Inventor, Assignee, Attorney firm, Primary examiner, Assistant examiner, CPCs, and Abstract. The patent badge does contain a link to the full patent document (in Adobe Acrobat format, aka pdf). To download or print any patent click here.

Patent No.:

US 8961996 B1

PDF
Full Text
Expired
Date of Patent:
Feb. 24, 2015

Filed:

Oct. 27, 2010
Applicants:

Manuel Borca, Westbrook, CT (US);

Guillermo Risatti, Westbrook, CT (US);

Inventors:

Manuel Borca, Westbrook, CT (US);

Guillermo Risatti, Westbrook, CT (US);

Attorneys:
Primary Examiner:
Int. Cl.
CPC ...
A61K 39/12 (2006.01); G01N 33/569 (2006.01); A61K 39/187 (2006.01); C07K 14/005 (2006.01); C12N 7/00 (2006.01); C12Q 1/70 (2006.01); C12N 15/33 (2006.01); A61K 39/00 (2006.01);
U.S. Cl.
CPC ...
G01N 33/56983 (2013.01); A61K 39/12 (2013.01); A61K 39/187 (2013.01); A61K 2039/5254 (2013.01); C07K 14/005 (2013.01); C12N 7/00 (2013.01); C12N 2770/24322 (2013.01); C12N 2770/24362 (2013.01); C12Q 1/701 (2013.01); G01N 2333/183 (2013.01);
Abstract

E2 is one of the three envelope glycoproteins of Classical Swine Fever Virus (CSFV). E2 is involved in several functions including virus attachment and entry to target cells, production of antibodies, induction of protective immune response in swine, and virulence. Seven putative glycosylation sites in E2 were modified by site directed mutagenesis of a CSFV Brescia infectious clone (BICv). A panel of virus mutants was obtained and used to investigate whether the removal of putative glycosylation sites in the E2 glycoprotein would affect viral virulence/pathogenesis in swine. We observed that rescue of viable virus was completely impaired by removal of all putative glycosylation sites in E2, but restored when mutation N185A reverted to wild-type asparagine produced viable virus that was attenuated in swine. Single mutations of each of the E2 glycosylation sites showed that amino acid N116 (N1v virus) was responsible for BICv attenuation. N1v efficiently protected swine from challenge with virulent BICv at 3 and 28 days post-infection suggesting that glycosylation of E2 could be modified for development of CSF live-attenuated vaccines. Additionally, a new developed virus, contained deletions of putative glycosylation sites N1 in E2 and N1 in E0 (6b), called N1E0/2v, induce a solid protection against the challenge at 3 and 28 days post-inoculation.


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