Abstract: Provided herein are details on the construction of a recombinant African Swine Fever Virus (ASFV) live attenuated vaccine for prevention of ASF caused by various strains of ASFV, such as the highly virulent Georgia 2007 isolate (“ASFV-G”). An exemplary vaccine comprises the ASFV-G?I1771 modified virus, a recombinant ASFV-G modified by deleting a portion of the I177L ORF rendering the I177L gene nonfunctional.

Abstract: Provided herein are details on the construction of a recombinant African Swine Fever Virus (ASFV) live attenuated vaccine for prevention of ASF caused by various strains of ASFV, such as the highly virulent Georgia 2007 isolate (“ASFV-G”). An exemplary vaccine comprises the ASFV-G?A137R modified virus, a recombinant ASFV-G modified by deleting a portion of the A137R ORF rendering the A137R gene nonfunctional.

Abstract: Methods are provided herein utilizing a stable cell line capable of efficient infection by African swine fever virus (ASFV) and also provides for the detection of the presence of virus in samples applied to the cells. Detection of the virus by means such as red blood cell rosetting is a surprising result given that the cell line is derived from African green monkeys. This cell line provides a marked improvement over the currently available testing strategies.

Abstract: Provided herein are details on the construction of a recombinant African Swine Fever Virus (ASFV) live attenuated vaccine for prevention of ASF caused by various strains of ASFV, such as the highly virulent Georgia 2007 isolate (“ASFV-G”). An exemplary vaccine comprises a deletion of multiple genes allowing for industrial-scale growth in stable cell lines.

Abstract: Provided herein are details on the construction of a recombinant African Swine Fever Virus (ASFV) live attenuated vaccine for prevention of ASF caused by various strains of ASFV, such as the highly virulent Georgia 2007 isolate (“ASFV-G”). An exemplary vaccine comprises the ASFV-G?A137R modified virus, a recombinant ASFV-G modified by deleting a portion of the A137R ORF rendering the A137R gene nonfunctional.

Abstract: Provided herein are details on the construction of a recombinant African Swine Fever Virus (ASFV) live attenuated vaccine for prevention of ASF caused by various strains of ASFV, such as the highly virulent Georgia 2007 isolate (“ASFV-G”). An exemplary vaccine comprises a deletion of multiple genes allowing for industrial-scale growth in stable cell lines.

Abstract: Methods are provided herein utilizing a stable cell line capable of efficient infection by African swine fever virus (ASFV) and also provides for the detection of the presence of virus in samples applied to the cells. Detection of the virus by means such as red blood cell rosetting is a surprising result given that the cell line is derived from African green monkeys. This cell line provides a marked improvement over the currently available testing strategies.

Abstract: Provided herein are details on the construction of a recombinant African Swine Fever Virus (ASFV) live attenuated vaccine for prevention of ASF caused by various strains of ASFV, such as the highly virulent Georgia 2007 isolate (“ASFV-G”). An exemplary vaccine comprises the ASFV-G?I1771 modified virus, a recombinant ASFV-G modified by deleting a portion of the I177L ORF rendering the I177L gene nonfunctional.

Abstract: Provided herein are details on the construction of a recombinant African Swine Fever Virus (ASFV) live attenuated vaccine for prevention of ASF caused by various strains of ASFV, such as the highly virulent Georgia 2007 isolate (“ASFV-G”). An exemplary vaccine comprises the ASFV-G?I1771 modified virus, a recombinant ASFV-G modified by deleting a portion of the I177L ORF rendering the I177L gene nonfunctional.

Abstract: Provided herein are details on the construction of a recombinant African Swine Fever Virus (ASFV) live attenuated vaccine for prevention of ASF caused by various strains of ASFV, such as the highly virulent Georgia 2007 isolate (“ASFV-G”). An exemplary vaccine comprises the ASFV-G?I1771 modified virus, a recombinant ASFV-G modified by deleting a portion of the I177L ORF rendering the I177L gene nonfunctional.

Abstract: The role of a specific E2 region containing a putative fusion peptide (FP) sequence was evaluated. FPs critically contribute to the interaction between proteins and the membrane system of the host cell. Reverse genetics utilizing a full-length infectious clone of the highly virulent CSFV strain Brescia (BICv) was used to evaluate how amino acid substitutions within this region of E2 may affect replication of BICv in cell cultures and affect virus virulence in swine. Interestingly, mutated virus FPi.c was completely attenuated when inoculated intranasally at a dose of 105 TCID50 in swine. Importantly, animals infected with FPi.c virus were protected against the virulent challenge with Brescia virus at 3 and 28 days after vaccination. Protection was evidenced by absence of clinical signs related with CSF as well as the absence of viremia produced by the challenge virulent virus.

Abstract: 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 ?9GL/?UK 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 ?9GL/?UK 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.

Abstract: The role of a specific E2 region, 869CKWGGNWTCV878, containing a putative fusion peptide (FP) sequence was evaluated. FPs critically contribute to the interaction between proteins and the membrane system of the host cell. Reverse genetics utilizing a full-length infectious clone of the highly virulent CSFV strain Brescia (BICv) was used to evaluate how amino acid substitutions within this region of E2 may affect replication of BICv in cell cultures and affect virus virulence in swine. A recombinant CSFV (FPi.c) containing mutations in three amino acid residues within the E2 protein area comprised CSFV amino acid residues 869-878 was constructed: W871T, W875D, and V878T. Interestingly, mutated virus FPi.c was completely attenuated when inoculated intranasally at a dose of 105 TCID50 in swine. Importantly, animals infected with FPi.c virus were protected against the virulent challenge with Brescia virus at 3 and 28 days after vaccination.