Abstract: Genetically modified transgenic pigs or pig cells having at least one knocked out Transmembrane protease, serine (TMPRSS) gene. Expression of functional gene products of the at least one knocked out TMPRSS gene in the genetically modified transgenic pig or pig cells is reduced as compared to the non-genetically modified pig or pig cells. The at least one TMPRSS gene can be knocked out using CRISPR/Cas systems.

Abstract: The present disclosure provides for an immunogenic composition against epizootic hemorrhagic disease virus (EHDV). The immunogenic composition has been shown to be efficacious in inducing serum neutralizing antibodies against EHDV and intended to be used to prevent or reduce clinical symptoms associated with EHDV infection in susceptible animals. The disclosure provides for composition and methods that represent an improvement over previous strategies for treating and preventing EHDV.

Abstract: The present invention relates, in general, to attenuated swine influenza viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. In particular, the invention relates to attenuated swine influenza viruses having modifications to a swine NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. These viruses replicate in vivo, but demonstrate decreased replication, virulence and increased attenuation, and therefore are well suited for use in live virus vaccines, and pharmaceutical formulations.

Abstract: The present disclosure provides for an immunogenic composition against epizootic hemorrhagic disease virus (EHDV). The immunogenic composition has been shown to be efficacious in inducing serum neutralizing antibodies against EHDV and intended to be used to prevent or reduce clinical symptoms associated with EHDV infection in susceptible animals. The disclosure provides for composition and methods that represent an improvement over previous strategies for treating and preventing EHDV.

Abstract: The present invention relates, in general, to attenuated swine influenza viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. In particular the invention relates to attenuated swine influenza viruses having modifications to a swine NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. These viruses replicate in vivo, but demonstrate decreased replication, virulence and increased attenuation, and therefore are well suited for use in live virus vaccines, and pharmaceutical formulations.

Abstract: The present invention relates, in general, to attenuated swine influenza viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. In particular, the invention relates to attenuated swine influenza viruses having modifications to a swine NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. These viruses replicate in vivo, but demonstrate decreased replication, virulence and increased attenuation, and therefore are well suited for use in live virus vaccines, and pharmaceutical formulations.

Abstract: The present invention describes subunit vaccines containing Gn and Gc glycoproteins of the Rift Valley Fever Virus, including nucleic acids encoding such glycoproteins, host cells, vectors, and immunoreagents generated with the glycoproteins, methods of vaccination, methods of diagnosis, and kits.

Abstract: The present invention relates, in general, to attenuated swine influenza viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. In particular, the invention relates to attenuated swine influenza viruses having modifications to a swine NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. These viruses replicate in vivo, but demonstrate decreased replication, virulence and increased attenuation, and therefore are well suited for use in live virus vaccines, and pharmaceutical formulations.

Abstract: The present invention relates, in general, to attenuated swine influenza viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. In particular, the invention relates to attenuated swine influenza viruses having modifications to a swine NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. These viruses replicate in vivo, but demonstrate decreased replication, virulence and increased attenuation, and therefore are well suited for use in live virus vaccines, and pharmaceutical formulations.

Abstract: The present invention relates, in general, to attenuated swine influenza viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. In particular, the invention relates to attenuated swine influenza viruses having modifications to a swine NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. These viruses replicate in vivo, but demonstrate decreased replication, virulence and increased attenuation, and therefore are well suited for use in live virus vaccines, and pharmaceutical formulations.

Abstract: The present invention relates, in general, to attenuated swine influenza viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. In particular, the invention relates to attenuated swine influenza viruses having modifications to a swine NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. These viruses replicate in vivo, but demonstrate decreased replication, virulence and increased attenuation, and therefore are well suited for use in live virus vaccines, and pharmaceutical formulations.

Abstract: The present invention describes subunit vaccines containing Gn and Gc glycoproteins of the Rift Valley Fever Virus, including nucleic acids encoding such glycoproteins, host cells, vectors, and immunoreagents generated with the glycoproteins, methods of vaccination, methods of diagnosis, and kits.

Abstract: A specific, non-synonymous SNP in the Prnp gene encoding the bovine prion protein affects the susceptibility of bovine animals to bovine spongiform encephalopathy (BSE). Depending on the number of octapeptide repeat units present in the Prnp gene, the position of the SNP is either nucleotide 631 of exon 3 (codon 211) when the Prnp gene comprises six octapeptide repeat region sequences, nucleotide 607 of exon 3 (codon 203) when the Prnp gene comprises five octapeptide repeat region sequences, or nucleotide 655 of exon 3 (codon 219) when the Prnp gene comprises seven octapeptide repeat region sequences. Alleles of the bovine Prnp wherein the SNP at these positions is lysine (K) at the corresponding amino acids (i.e., 211, 203 or 219) in the bovine prion protein are all indicative of increased susceptibility to BSE in comparison to alleles which encode glutamic acid (E) at the same position.

Abstract: The present invention relates, in general, to attenuated swine influenza viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. In particular, the invention relates to attenuated swine influenza viruses having modifications to a swine NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. These viruses replicate in vivo, but demonstrate decreased replication, virulence and increased attenuation, and therefore are well suited for use in live virus vaccines, and pharmaceutical formulations.

Abstract: The present invention relates, in general, to attenuated swine influenza viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. In particular, the invention relates to attenuated swine influenza viruses having modifications to a swine NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. These viruses replicate in vivo, but demonstrate decreased replication, virulence and increased attenuation, and therefore are well suited for use in live virus vaccines, and pharmaceutical formulations.

Abstract: The present invention provides influenza A viruses that include a hemagglutinin subtype H2, a neuraminidase subtype N3, or the combination thereof. Included in the present invention are H2 hemagglutinins and N3 neuraminidases, and the polynucleotides encoding the polypeptides. Antibody to the polypeptides, and methods of using the viruses, polypeptides, polynucleotides, and antibodies are also provided.

Abstract: A specific, non-synonymous SNP in the Prnp gene encoding the bovine prion protein affects the susceptibility of bovine animals to bovine spongiform encephalopathy (BSE). Depending on the number of octapeptide repeat units present in the Prnp gene, the position of the SNP is either nucleotide 631 of exon 3 (codon 211) when the Prnp gene comprises six octapeptide repeat region sequences, nucleotide 607 of exon 3 (codon 203) when the Prnp gene comprises five octapeptide repeat region sequences, or nucleotide 655 of exon 3 (codon 219) when the Prnp gene comprises seven octapeptide repeat region sequences. Alleles of the bovine Prnp wherein the SNP at these positions is lysine (K) at the corresponding amino acids (i.e., 211, 203 or 219) in the bovine prion protein are all indicative of increased susceptibility to BSE in comparison to alleles which encode glutamic acid (E) at the same position.

Abstract: A specific, non-synonymous SNP in the Prnp gene encoding the bovine prion protein affects the susceptibility of bovine animals to bovine spongiform encephalopathy (BSE). Depending on the number of octapeptide repeat units present in the Prnp gene, the position of the SNP is either nucleotide 631 of exon 3 (codon 211) when the Prnp gene comprises six octapeptide repeat region sequences, nucleotide 607 of exon 3 (codon 203) when the Prnp gene comprises five octapeptide repeat region sequences, or nucleotide 655 of exon 3 (codon 219) when the Prnp gene comprises seven octapeptide repeat region sequences. Alleles of the bovine Prnp wherein the SNP at these positions is lysine (K) at the corresponding amino acids (i.e., 211, 203 or 219) in the bovine prion protein are all indicative of increased susceptibility to BSE in comparison to alleles which encode glutamic acid (E) at the same position.

Abstract: The present invention provides influenza A viruses that include a hemagglutinin subtype H2, a neuraminidase subtype N3, or the combination thereof. Included in the present invention are H2 hemagglutinins and N3 neuraminidases, and the polynucleotides encoding the polypeptides. Antibody to the polypeptides, and methods of using the viruses, polypeptides, polynucleotides, and antibodies are also provided.

Abstract: A specific, non-synonymous SNP in the Prnp gene encoding the bovine prion protein affects the susceptibility of bovine animals to bovine spongiform encephalopathy (BSE). Depending on the number of octapeptide repeat units present in the Prnp gene, the position of the SNP is either nucleotide 631 of exon 3 (codon 211) when the Prnp gene comprises six octapeptide repeat region sequences, nucleotide 607 of exon 3 (codon 203) when the Prnp gene comprises five octapeptide repeat region sequences, or nucleotide 655 of exon 3 (codon 219) when the Prnp gene comprises seven octapeptide repeat region sequences. Alleles of the bovine Prnp wherein the SNP at these positions is lysine (K) at the corresponding amino acids (i.e., 211, 203 or 219) in the bovine prion protein are all indicative of increased susceptibility to BSE in comparison to alleles which encode glutamic acid (E) at the same position.