Humoral and cell immune mechanisms under African swine fever (review)

The evidences for protective immunity against African swine fever are symptomless infection in local populations of Phacochoerus africanus, Potamochoerus porcus, Hylochoerus spp. In Africa and experimentally produced avirulent strains of African swine fever virus (ASFV), preventing death in pigs inoculated with its virulent homolog. Serum or colostrum from convalescent animals can delay clinical symptoms, decline viremia and increase the survivors’ rate (R.C. Knudsen et al., 1987; D.H. Schlafer et al., 1984; D.V. Onisk et al., 1994). Humoral immune response is most probably due not to ASFV neutralization but the complement-mediated cytolysis (CMC) and antibody-mediated cell cytotoxicity (AMCC) (V.V. Makarov, 2013). Cell-mediated defense mechanisms, lyses of infected cells by N-killers and cytotoxic T-lymphocytes (CTL) lead to chronic or symptomless infection (S.G. Norley et al., 1983, 1984). An in vivo depletion of CD8+ T-lymphocytes by monoclonal antibodies was shown to stop protective immunity in pigs pre-immunized with an attenuated ASFV strain under next inoculation with the virulent homolog (C.A.L. Oura et al., 2005). Induction and defector activity of AMCC and CTL depend on the dose and biological features of ASFV strain (A.D. Sereda, 2010). High AMCC since day 3 and activity of cell-mediated mechanisms of immunity on day 6 after the ASFV inoculation provide a rapid decrease of the virus titers in blood, and, consequently, the absence of clinical symptoms (A.D. Sereda et al., 1992). Humoral and cell-dependent defense mechanisms act synergistically that must be taken into consideration when developing candidate recombinant vaccine against ASFV. ASFV candidate proteins involved in antigenic properties which can induce protective mechanisms against ASF are nominated. In pigs immunization with р54 and р30-32 combination caused a delay in appearance of ASF clinical symptoms after the inoculation with virulent isolate (P. Gómez-Puertas et al., 1998). CD2v (or GP 110-140) is a membrane protein of ASFV determining hemadsorption and identified as a serotype specific one (J.M. Rodriguez et al., 1993; A.D. Sereda et al., 1992; A. Malogolovkin et al., 2014). Therefore it should be considered crucial when constructing experimental protective facilities (H.H. Takamatsu et al., 2013). Thus, the investigations conducted to date show both humoral and cell effector mechanisms to be involved in defense against ASF.