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.