Assessment of the Effect of Deleting the African Swine Fever Virus Gene R298L on Virus Replication and Virulence of the Georgia2010 Isolate

African swine fever (ASF) is a lethal disease of domestic pigs that is currently challenging swine production in large areas of Eurasia. The causative agent, ASF virus (ASFV), is a large, double-stranded and structurally complex virus. The ASFV genome encodes for more than 160 proteins; however, the functions of most of these proteins are still in the process of being characterized. The ASF gene <i>R298L</i>, which has previously been characterized as able to encode a functional serine protein kinase, is expressed late in the virus infection cycle and may be part of the virus particle. There is no description of the importance of the <i>R298L</i> gene in basic virus functions such as replication or virulence in the natural host. Based on its evolution, it is proposed that there are four different phenotypes of <i>R298L</i> of ASFV in nature, which may have potential implications for <i>R298L</i> functionality. We report here that a recombinant virus lacking the <i>R298L</i> gene in the Georgia 2010 isolate, ASFV-G-∆R298L, does not exhibit significant changes in its replication in primary cultures of swine macrophages. In addition, when experimentally inoculated in pigs, ASFV-G-∆R298L induced a fatal form of the disease similar to that caused by the parental virulent ASFV-G. Therefore, deletion of <i>R298L</i> does not significantly affect virus replication and virulence in domestic pigs of the ASFV Georgia 2010 isolate.