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: African swine fever virus (ASFV) is the etiological agent of a contagious and often lethal viral disease of domestic pigs. Control of 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. Among viral genes reported to be involved in virulence are components of the multi gene family (MGF). Here we report the construction of a recombinant ?MGF virus derived from the highly virulent ASFV Georgia 2007 (ASFV-G) isolate. In vivo, ASFV-G ?MGF administered intramuscularly (IM) to swine at either 102 or 104 HAD50 are completely attenuated; the inoculated animals are completely asymptomatic. Animals infected with 102 or 104 HAD50 of ASFV-G ?MGF are protected against the presentation of clinical disease when challenged at 28 days post infection with the virulent parental strain Georgia 2007.

Abstract: We have developed an ASFV Georgia strain adapted to grow in Vero cell line. The resulting virus, ASF-GVAV, efficiently grows in Vero cells although it still is able to significantly replicate in primary cell cultures of swine macrophages. ASF-GVAV virus was successfully used as parental virus to develop several recombinant ASF viruses. The development of an ASFV adapted to grow in an established cell line is a significant advance for research and development of vaccine candidate strains using genetic manipulation based in the process of homologous recombination. The GVAVS can be utilized as a basis for large scale production of ASF vaccines.

Abstract: 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 ?9GL virus derived from the highly virulent ASFV Georgia 2007 (ASFV-G) isolate. In vivo, ASFV-G ?9GL 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 ?9GL 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.

Abstract: African swine fever virus (ASFV) is the etiological agent of a contagious and often lethal viral disease of domestic pigs. Control of 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. Among viral genes reported to be involved in virulence are components of the multi gene family (MGF). Here we report the construction of a recombinant ?MGF virus derived from the highly virulent ASFV Georgia 2007 (ASFV-G) isolate. In vivo, ASFV-G ?MGF administered intramuscularly (IM) to swine at either 102 or 104 HAD50 are completely attenuated; the inoculated animals are completely asymptomatic. Animals infected with 102 or 104 HAD50 of ASFV-G ?MGF are protected against the presentation of clinical disease when challenged at 28 days post infection with the virulent parental strain Georgia 2007.

Abstract: 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 ?9GL virus derived from the highly virulent ASFV Georgia 2007 (ASFV-G) isolate. In vivo, ASFV-G ?9GL 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 ?9GL 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.