Key result
Deletion of the I8L gene from the highly virulent ASFV-G strain did not affect virus replication in vitro or in vivo, nor did it change the clinical disease outcome in swine.
Why the study?
The highly conserved ASFV gene I8L had not been experimentally characterized beyond its initial description as a viral ORF, and its role during replication and virulence was unknown.
Does deletion of the I8L gene from ASFV-G affect virus replication or disease outcome in swine?
Does deletion of the I8L gene from ASFV-G affect virus replication or disease outcome in swine?
Deletion of the highly conserved I8L gene from ASFV-G does not affect viral replication or virulence in swine, indicating it is not essential for disease pathogenesis.
I8L deletion does not attenuate ASFV in swine; leaves open its utility for vaccine attenuation.
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.
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Vuono et al. (2020) studied African swine fever. Recombinant ASFV-G lacking the I8L gene (ASFV-G-ΔI8L) vs. Parental ASFV-G isolate was evaluated on Virus replication in vitro and in vivo, and clinical disease outcome. Deletion of the I8L gene from the highly virulent ASFV-G strain did not affect virus replication in vitro or in vivo, nor did it change the clinical disease outcome in swine.
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