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AssigneesThe United States of America as represented by the Secretary of Agriculture, University of Connecticut
InventorsManuel V. Borca, Douglas P. Gladue, Lauren G. Holinka-Patterson, Guillermo R. Risatti, Vivian K. O'Donnell
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African swine fever virus (ASFV) is the etiological agent of a contagious, often lethal viral disease of domestic pigs. The control of African Swine Fever (ASF) has been hampered by the unavailability of vaccines. Experimental vaccines have been derived from naturally occurring, cell culture-adapted, or genetically modified live attenuated ASFVs; however, these vaccines are only successful when protecting against homologous viruses. We have constructed a recombinant Δ9GL/ΔUK virus derived from the highly virulent ASFV Georgia 2007 (ASFV-G) isolate by deleting the specific virulence-associated 9GL (B119L) and the UK (DP96R) genes. In vivo, ASFV-G Δ9GL/ΔUK administered intramuscularly to swine even at relatively high doses (106 HAD50) does not induce disease. Importantly, animals infected with 104 or 106 HAD50 are solidly protected against the presentation of clinical disease when challenged at 28 days post infection with the virulent parental strain Georgia 2007.
A recombinant ASFV-G (African Swine Fever Virus-Georgia 2007 isolate) mutant, the mutant ASFV-G Δ9GL/ΔUK virus, comprising cDNA encoding mutant ASFV-G Δ9GL/ΔUK polypeptides wherein the mutant cDNA comprises two deletions, a deletion of 173 nucleotides resulting in a mutant 9GL protein comprising 58 fewer amino acids than the non-mutated, wild-type 9GL protein of ASFV-G, amino acids #11 to #68 being deleted, and a second deletion of 255 nucleotides resulting in a mutant UK protein comprising 85 fewer amino acids than the non-mutation, wild-type UK protein of ASFV-G, amino acids #1 to #85 being deleted.
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