Attenuated African Swine Fever Virus Strain Induces Protection Against Challenge With Homologous Virulent Parental Virus Georgia 2007 Isolate

摘要

African swine fever virus (ASFV) is the etiological agent of a contagious and often lethal viral disease of domestic pigs that has significant economic consequences for swine breeding. Control of ASF has been hampered by the unavailability of vaccines. Recombinant viruses harboring engineered deletions of specific virulence-associated genes induce solid protection against the challenge with parental viruses. Here we report the construction of a recombinant Δ9GL virus derived from the highly virulent ASFV Georgia 2007 (ASFV-G) isolate. In vivo, ASFV-G Δ9GL administered intramuscularly (IM) to swine at relatively high doses (104 HAD50) retains a virulent phenotype practically indistinguishable from the parental virus. Conversely, at low IM doses (102 or 103 HAD50), ASFV-G Δ9GL does not induce disease. Importantly, animals infected with 103 HAD50 are protected against the presentation of clinical disease when challenge at 28 days post infection with the virulent parental strain Georgia 2007.

主权项

1. A recombinant ASFV-G (African Swine Fever Virus-Georgia 2007 isolate) mutant, the mutant ASFV-G Δ9GL virus, comprising cDNA (SEQ ID NO:3) encoding a mutant ASFV-G Δ9GL protein wherein the mutant cDNA comprises a deletion of 172 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.