Evaluation in Swine of a Recombinant Georgia 2010 African Swine Fever Virus Lacking the I8L Gene
[3];
- US Dept. of Agriculture (USDA), Greenport, NY (United States). Agricultural Research Service (ARS). Plum Island Animal Disease Center; Mississippi State Univ., Mississippi State, MS (United States). Dept. of Pathobiology and Population Medicine; OSTI
- US Dept. of Agriculture (USDA), Greenport, NY (United States). Agricultural Research Service (ARS). Plum Island Animal Disease Center; Univ. of Connecticut, Storrs, CT (United States). Dept. of Pathobiology and Veterinary Science
- US Dept. of Agriculture (USDA), Greenport, NY (United States). Agricultural Research Service (ARS). Plum Island Animal Disease Center
- US Dept. of Agriculture (USDA), Greenport, NY (United States). Agricultural Research Service (ARS). Plum Island Animal Disease Center; Oak Ridge Inst. for Science and Education (ORISE), Oak Ridge, TN (United States)
- US Dept. of Agriculture (USDA), Greenport, NY (United States). Agricultural Research Service (ARS). Plum Island Animal Disease Center; Kansas State Univ., Manhattan, KS (United States). Dept. of Anatomy and Physiology
African swine fever virus (ASFV) is the causative agent of African swine fever, a disease currently causing significant economic losses in Europe and Asia. Specifically, the highly virulent ASFV strain Georgia 2010 (ASFV-G) is producing disease outbreaks in this large geographical region. The ASFV genome encodes for over 150 genes, most of which are still not experimentally characterized. I8L is a highly conserved gene that has not been studied beyond its initial description as a virus ORF. Transcriptional analysis of swine macrophages infected with ASFV-G demonstrated that the I8L gene is transcribed early during the virus replication cycle. To assess the importance of I8L during ASFV-G replication in vitro and in vivo, as well as its role in virus virulence in domestic swine, we developed a recombinant virus lacking the I8L gene (ASFV-G-ΔI8L). Replication of ASFV-G-ΔI8L was similar to parental ASFV-G replication in primary swine macrophage cultures, suggesting that the I8L gene is not essential for ASFV-G replication in vitro. Similarly, replication of ASFV-G-ΔI8L in swine intramuscularly inoculated with 102 HAD50 displayed replication kinetics similar to ASFV-G. In addition, animals inoculated with ASFV-G-ΔI8L presented with a clinical disease indistinguishable from that induced by the same dose of the virulent parental ASFV-G isolate. We conclude that deletion of the I8L gene from ASFV-G does not affect virus replication in vitro or in vivo, nor changes the disease outcome in swine.
- Research Organization:
- Oak Ridge Associated Univ., Oak Ridge, TN (United States)
- Sponsoring Organization:
- USDOE Office of Science (SC)
- Grant/Contract Number:
- SC0014664
- OSTI ID:
- 1816347
- Journal Information:
- Viruses, Journal Name: Viruses Journal Issue: 1 Vol. 13; ISSN VIRUBR; ISSN 1999-4915
- Publisher:
- MDPICopyright Statement
- Country of Publication:
- United States
- Language:
- English
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