Deletion of the EP296R Gene from the Genome of Highly Virulent African Swine Fever Virus Georgia 2010 Does Not Affect Virus Replication or Virulence in Domestic Pigs

Elizabeth A Vuono; Elizabeth Ramirez-Medina; Sarah Pruitt; Ayushi Rai; Nallely Espinoza; Edward Spinard; Alyssa Valladares; Ediane Silva; Lauro Velazquez-Salinas; Manuel V Borca; Douglas P Gladue

doi:10.3390/v14081682

Deletion of the EP296R Gene from the Genome of Highly Virulent African Swine Fever Virus Georgia 2010 Does Not Affect Virus Replication or Virulence in Domestic Pigs

Viruses. 2022 Jul 30;14(8):1682. doi: 10.3390/v14081682.

Authors

Affiliations

¹ Plum Island Animal Disease Center, ARS, USDA, Greenport, New York, NY 11944, USA.
² Department of Pathobiology and Population Medicine, Mississippi State University, P.O. Box 6100, Oxford, MS 39762, USA.
³ Oak Ridge Institute for Science and Education (ORISE), Oak Ridge, TN 37830, USA.

Abstract

African swine fever virus (ASFV) causes a lethal disease (ASF) in domestic pigs, African swine fever (ASF). ASF is currently producing a pandemic affecting pig production across Eurasia, leading to a shortage of food accessibility. ASFV is structurally complex, harboring a large genome encoding over 150 genes. One of them, EP296R, has been shown to encode for an endonuclease that is necessary for the efficient replication of the virus in swine macrophages, the natural ASFV target cell. Here, we report the development of a recombinant virus, ASFV-G-∆EP296R, harboring the deletion of the EP296R gene from the genome of the highly virulent field isolate ASFV Georgia 2010 (ASFV-G). The recombinant ASFV-G-∆EP296R replicates in primary swine macrophages with similar kinetics as the parental virus ASFV-G. Pigs experimentally infected by the intramuscular route with 10² HAD₅₀ show a slightly protracted, although lethal, presentation of the disease when compared to that of animals inoculated with parental ASFV-G. Viremia titers in the ASFV-G-∆EP296R-infected animals closely followed the kinetics of presentation of clinical disease. Results presented here demonstrate that ASFV-G-∆EP296R is not essential for the processes of ASFV replication in swine macrophages, nor is it radically involved in the process of virus replication or disease production in domestic pigs.

Keywords: ASF; ASFV; African swine fever; African swine fever virus; EP296R; virus virulence.

Publication types

Research Support, U.S. Gov't, Non-P.H.S.
Research Support, Non-U.S. Gov't

MeSH terms

African Swine Fever Virus*
African Swine Fever*
Animals
Gene Deletion
Sus scrofa
Swine
Virulence / genetics
Virus Replication

Grants and funding

This project was partially funded by the National Pork Board Project #21-137 and partially funded through an interagency agreement with the Science and Technology Directorate of the US Department of Homeland Security under Award Number 70RSAT19KPM000056.