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Research Project: Intervention Strategies to Control and Eradicate Foreign Animal Diseases of Swine

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Title: Evaluation of the function of ASFV gene E66L in the process of virus replication and virulence in swine

item Ramirez-Medina, Elizabeth
item VUONO, ELIZABETH - US Department Of Agriculture (USDA)
item RAI, AYUSHI - Oak Ridge Institute For Science And Education (ORISE)
item Espinoza, Nallely
item VALADARES, ALYSSA - Oak Ridge Institute For Science And Education (ORISE)
item SPINNARD, EDWARD - US Department Of Agriculture (USDA)
item Velazquez, Lauro
item Gladue, Douglas
item Borca, Manuel

Submitted to: Viruses
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/13/2023
Publication Date: N/A
Citation: N/A

Interpretive Summary: African swine fever virus (ASFV) causes a devastating disease in swine, called African swine fever (ASF), that is currently spreading across Europe, Asia and recently appeared in the Americas. Here we report on the function of a new gene in ASF where deletion of that gene is not necessary for the virus to replicate in cell cultures or to cause disease in swine.

Technical Abstract: African swine fever virus (ASFV) is the etiological agent of an economically important disease of swine currently affecting large areas of Africa, Eurasia and the Caribbean. ASFV has a complex structure harboring a large dsDNA genome which encodes for more than 160 proteins. One of the proteins, E66L, has recently been involved in arresting gene transcription in the infected host cell. Here, we investigate the role of E66L in the processes of virus replication in swine macrophages and disease production in domestic swine. A recombinant ASFV was developed (ASFV-G-DeltaE66L), from the virulent parental Georgia 2010 isolate (ASFV-G), harboring the deletion of the E66L gene as a tool to assess the role of the gene. ASFV-G-DeltaE66L showed that the E66L gene is non-essential for ASFV replication in primary swine macrophages when compared with the parental highly virulent field isolate ASFV-G. Additionally, domestic pigs infected with ASFV-G-DeltaE66L developed a clinical disease undistinguishable from that produced by ASFV-G. Therefore, E66L is not involved in virus replication or virulence in domestic pigs.