Abstract
African swine fever (ASF) is caused by the ASF virus (ASFV), a double-stranded DNA virus classified under the family Asfarviridae and genus Asfivirus. Although outbreaks have been occurring since 1909, ASF was first documented in Kenya in 1921. The three primary epidemiological cycles that contribute to the spread of ASF include ticks, wild boars, and domestic pigs. Numerous studies on acute ASF infection in pigs have demonstrated that the virus typically enters the body through the tonsils or dorsal pharyngeal mucosa and travels to the mandibular or retropharyngeal lymph nodes, where it spreads through viremia. Serious immunosuppression and apoptosis are hallmarks of ASFV infection, which mainly multiplies in monocytes and macrophages and enters cells via receptor-mediated endocytosis. The most distinctive ASF lesion found at autopsy is severe hemorrhagic splenomegaly, which is seen when the abdominal cavity of an animal with ASF is opened. ASF illness takes 3-15 days to incubate. ASF comes in four clinical forms: acute, subacute, chronic, and peracute. ASF can be diagnosed through laboratory analysis using techniques such as polymerase chain reaction, virus isolation, and serology assays. Domestic pigs may contract ASF disease directly from pigs or the body fluids of diseased pigs or indirectly through contact with virus-containing objects and exposure to virus-contaminated settings. Continued research and surveillance of ASF vaccine development are essential to support more effective prevention and control efforts, as well as to minimize the global economic and health impacts of this disease.