Immune responses against African swine fever virus infection
Infection with African swine fever virus (ASFV) leads to a short haemorrhagic course of disease that, depending on the virus isolate, results in up to 100% lethality in domestic and Eurasian wild pigs. Consequently, ASFV infection in swine is of considerable economic significance. This chapter explains the basics of antiviral immunity in swine, focusing on the ‘knowns’ and ‘unknowns’ of the response against ASFV. In particular, monocytes and macrophages play an essential role as the main targets of infection and are crucial in viral persistence and dissemination. Furthermore, ASFV has developed several mechanisms to influence the antiviral and cell biological activity of infected monocytes, including down-regulation of cell surface receptors (e.g. CD14 and MHC-I) and modulation of interferon and cytokine/chemokine responses. ASFV infected pigs also develop virus-specific antibodies that can be used diagnostically, and while the neutralising effect of these antibodies has led to their involvement in protective immunity being controversially discussed, they may still exhibit protective functions through complement-mediated lysis and/or antibody dependent cell-mediated cytotoxicity. Indeed, T cells (presumably CD8+) also play a central role in the elimination of the virus, as can be seen in experiments where, after depletion of these cells, pigs previously primed with an avirulent ASFV become ill, while non-depleted animals are protected from highly virulent challenge. Nonetheless, despite these advances in our knowledge, much remains unknown about antiviral immunity generated during the course of a natural ASFV infection, or in response to attenuated virus strains or immunisation. Although such studies would undoubtedly be technically challenging, a deeper understanding of the immunity developed by the natural hosts (i.e. bushpigs and warthogs) against ASFV infection would teach us a lot about an effective protection from ASFV infection, and the involvement of both the innate and adaptive immune systems in this process.