Location: Location not imported yet.Title: Evaluation of the function of ASFV KP177R gene, encoding for structural protein p22, in the process of virus replication and in swine virulence
|RAMIREZ-MEDINA, ELIZABETH - University Of Connecticut
|VUONO, ELIZABETH - University Of Mississippi
|RAI, AYUSHI - Oak Ridge Institute For Science And Education (ORISE)
|VELAZQUEZ-SALINAS, LAURO - University Of Kansas
Submitted to: Viruses
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/19/2021
Publication Date: 5/26/2021
Citation: Ramirez-Medina, E., Vuono, E., Pruitt, S.E., Rai, A., Espinoza, N.N., Velazquez-Salinas, L., Gladue, D.P., Borca, M.V. 2021. Evaluation of the function of ASFV KP177R gene, encoding for structural protein p22, in the process of virus replication and in swine virulence. Viruses. https://doi.org/10.3390/v13060986.
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 were able to delete a structural protein in ASFV, however deletion of this structural protein did not have any effect on virus replication or virulence.
Technical Abstract: African swine fever virus (ASFV) causes a devastating disease of swine currently spread from Central Europe to Asia. ASFV is a large, structurally complex virus with a large dsDNA genome encoding for more than 160 genes, most of them still uncharacterized. p22, encoded by ASFV gene KP177R, is a structural virus protein located in the inner envelope of the ASFV particle. Although its exact function is unknow, p22 has being recently identified as interacting partner of several host proteins. Here we describe the development of a recombinant ASFV (ASFV-G-'KP177R) lacking the KP177R gene as a tool to evaluate p22 role in virus replication and virulence in swine. The recombinant ASFV-G-'KP177R demonstrated that the KP177R gene is non-essential for ASFV growth in primary swine macrophage, with virus yields similar to those of the parental highly virulent field isolate Georgia2010 (ASFV-G). In addition, experi-mental infection of domestic pigs with ASFV-G-'KP177R produced a clinical disease similar to that caused by the parental ASFV-G. Therefore, surprisingly, p22 does not seem to be involved in virus growth or virulence in swine.