Abstract

African swine fever virus (ASFV) causes a devastating disease of swine that has caused outbreaks in Central Europe since 2007, spreading into Asia in 2018. 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 the ASFV gene KP177R, is an early transcribed, structural virus protein located in the ASFV particle. Although its exact function is unknown, p22 has recently been identified as an 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 the role of p22 in virus replication and virulence in swine. The recombinant ASFV-G-∆KP177R demonstrated that the KP177R gene is non-essential for ASFV replication in primary swine macrophages, with virus yields similar to those of the parental, highly virulent field isolate Georgia2010 (ASFV-G). In addition, experimental infection of domestic pigs with ASFV-G-∆KP177R produced a clinical disease similar to that caused by the parental ASFV-G. Therefore, and surprisingly, p22 does not seem to be involved in virus replication or virulence in swine.

Highlights

  • African swine fever virus (ASFV) Georgia (ASFV-G) was a field isolate kindly provided by Nino

  • KP177R Gene Is Conserved Across Different ASFV Isolates

  • The KP177R gene encodes for virus protein p22, originally described as an early transcribed transmembrane protein that is associated with the outer layer of the virus particle, as well as being transiently expressed on the surface of infected cells [23]

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Summary

Introduction

ASFV experimental vaccines developed through the deletion of specific genes from the virus genome have been shown to be effective in protecting against the current circulating strain in Europe and Asia [3,4,5,6,7,8]. The development of those vaccines was possible by identifying and characterizing virus genes involved in the process of virus virulence, 4.0/)

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