Evaluation in swine of a recombinant African swine fever virus lacking the MGF-360-1L gene

Authors: RAMIEREZ-MEDINA, ELIZABETH - University Of Connecticut; VUONO, ELIZABETH - University Of Mississippi; RAI, AYUSHI - Oak Ridge Institute For Science And Education (ORISE); Pruitt, Sarah; SILVA, EDIANE - University Of Kansas; VELAZQUEZ-SALINAS, LAURO - University Of Kansas; Zhu, James; Gladue, Douglas; Borca, Manuel

Submitted to: Viruses
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/16/2020
Publication Date: 10/20/2020
Citation: Ramierez-Medina, E., Vuono, E., Rai, A., Pruitt, S.E., Silva, E., Velazquez-Salinas, L., Zhu, J.J., Gladue, D.P., Borca, M.V. 2020. Evaluation in swine of a recombinant African swine fever virus lacking the MGF-360-1L gene. Viruses. https://doi.org/10.3390/v12101193.
DOI: https://doi.org/10.3390/v12101193

Interpretive Summary: African swine fever virus (ASFV) causes a devastating disease in swine, called African swine fever (ASF), that is currently spreading across Europe and Asia. There is no available vaccine for ASF, and currently only experimental live attenuated vaccines are derived from deletions of individual genes in the ASFV genome. In this study we a delete a gene in ASFV, that that has never been deleted before and did not alter the pathogenesis of ASFV. We identified two cellular proteins that bind this gene giving insight into how ASFV interacts with cells.

Technical Abstract: The African swine fever (ASF) pandemic is currently affecting pigs throughout Eurasia, resulting in significant swine production losses. The causative agent, ASF virus (ASFV), is a large, structurally complex virus with a genome encoding more than 160 genes. The function of most of those genes remain unknown. Here we present the previously uncharacterized ASFV gene MGF360-1L, the first gene in the genome. Kinetic studies of virus RNA transcription demonstrated that the MGF360-1L gene is transcribed as a late virus protein. Essentiality of MGF360-1L to virus replication was evaluated by developing a recombinant ASFV lacking the gene (ASFV-G-'MGF360-1L). In primary swine macrophage cell cultures ASFV-G-'MGF360-1L showed similar replication kinetics as the parental highly virulent field isolate Georgia2007 (ASFV-G). Domestic pigs experimentally infected with ASFV-G-'MGF360-1L presented with a clinical disease undistinguishable from that caused by ASFV-G, demonstrating that MGF360-1L is not involved in virulence in swine, the natural host of ASFV.