INTRODUCTIONAfrican swine fever (ASF) is a highly contagious disease of domestic pigs and wild boars caused by a double-stranded DNA virus, African swine fever virus (ASFV) (1, 2). ASFV is the only member of the Asfarviridae family and replicates in the cytoplasm of cells of the myeloid lineage, primarily macrophages or monocytes, at an intermediate or late stage of differentiation (3). In East Africa, ASFV is maintained in a sylvatic cycle involving warthogs (Phacochoerus africanus) and soft ticks of the genus Ornithodoros (4). The virus can persist in warthogs and bushpigs with few clinical signs of disease, but case fatality rates in domestic pigs or wild boars infected with virulent isolates of ASFV can approach 100% (5 – 8). In 2007, ASFV was introduced to the Republic of Georgia (9) and spread to Russia, Eastern Europe, and European Union member countries. Following its introduction to China in 2018, the disease spread extensively there and in other countries in Southeast Asia, causing high economic losses (10 – 12). Vaccines are not widely available, thereby limiting the control of ASFV outbreaks. Ongoing efforts center on the targeted deletion of nonessential virus genes to construct modified live-attenuated vaccines (13 – 17).The ASFV genome varies between 170 and 193 kbp and encodes up to 170 proteins. Many of the virus genes are not essential for replication but play important roles in modulating the host’s antiviral defenses. Among these are inhibitors of the type I interferon response and inhibitors of apoptosis (1, 18). Apoptosis
Deletion of the gene for the African swine fever virus BCL-2 family member A179L increases virus uptake and apoptosis but decreases virus spread in macrophages and reduces virulence in pigs
