Evasive strategies by the organism

The interaction of ASF virus with the host cells and its immune system and the processes involved in pro ducing disease are still poorly understood; however, the complete genome sequence has indicated that some novel strategies may be employed to avoid the immune response, by direct and indirect effects of the virus on the cells of the immune system, in the absence of neutralizing antibody.

ASF virus replication in pig macrophages, and the release of immune mediators, may be important in aiding the virus to evade the immune system, in addition to being possible factors in the pathogenesis of the disease. Infection of pig macrophages does nor alter the expression of Fc receptors nor their ability to mediate ADCC of antibody-coated bovine erythrocytes but does modulate antibody-mediated phagocytosis and chemotaxis. A protein isolated from infected cells has been shown to have a strong immunosuppressive effect in vitro. Infection of these cells will cause the downregulation of the proinflammatory cytokines IL-8, IFNa and tumor necrosis factor a (TNFa) but not of TGF|3.

The ASF virus genome also encodes for a Bcl-2 homolog which may aid the survival of infected cells and maintain persistence. In contrast, lymphocytes in infected tissues have been found to be apoptotic. Thus ASF virus may downregulate inflammation, increase the survival of infected cells and cause apoptosis of surrounding effector cells.

Although virus-specific delayed-type hypersensitivity, antibody production and lymphoproliferation are readily demonstrable, there are reports that the more virulent isolates can interfere with the immune response to foot-and-mouth disease virus in pigs inoculated with this virus 3 days after infection with ASF virus.

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