African swine fever virus ASFV/NH/P68 is a naturally occurring, non-haemadsorbing and non-fatal isolate. Longitudinal clinical and immunological studies on 31 pigs inoculated oronasally or intramuscularly with this isolate defined two discrete groups of animals : those developing ASF chronic type lesions and those remaining asymptomatic. Animals developing lesions had viraemia and fever late after infection, NK activity levels close to that of control animals and high levels of anti-ASFV specific antibodies together with a marked hypergammaglobulinaemia involving IgG1, IgG2, IgM and IgA immunoglobulin isotypes. Pigs remaining asymptomatic after infection, on the other hand, did not have viraemia or fever after day 14 post-infection and had elevated NK cell activity, but normal plasma Ig concentrations and relatively low specific anti-virus antibody concentrations throughout the duration of the experiments. Importantly, the latter group of pigs virus were resistant to subsequent challenge with the highly virulent ASFV/L60 isolate and survived with no major changes in any of the parameters examined and referred to above. Finally, lymphoproliferative responses to the mitogens concanavalin A, phytohaemagglutinin and pokeweed mitogen were not depressed in either of the two clinically defined groups of pigs. Thus further studies with this infection model may provide new insights on mechanisms of protective immunity to ASFV.

To understand the mechanisms involved in protective immunity to African swine fever virus (ASFV) infection, the observation that infection with the avirulent Portuguese ASFV isolate OUR/T88/3 protects outbred pigs from challenge with the virulent Portuguese ASFV isolate OUR/T88/1 was exploited. It was demonstrated that pigs exposed to OUR/T88/3 and then depleted of CD8 + lymphocytes were no longer fully protected from OUR/T88/1 challenge. This indicated that CD8 + lymphocytes play an important role in the protective immune response to ASFV infection and that anti-ASFV antibody alone, from OUR/T88/3 infection, was not sufficient to protect pigs from OUR/T88/1 challenge. Inbred pigs of the cc haplotype infected with OUR/T88/3 were not always protected from OUR/T88/1 challenge and developed both viraemia and fever. Such viraemia was always correlated with increased numbers of circulating CD8b + lymphocytes, indicating a specific role for CD8b + lymphocytes in combating viraemia. These experiments indicate an important role for CD8 + lymphocytes, particularly CD8b + lymphocytes, in ASF protective immunity.

The pig is a useful model for the heterogeneity of the mammalian immune system and has also recently received attention as a possible source of organs for human transplantation. Here we report a detailed analysis of porcine lymphocyte phenotypes. Peripheral blood αβ T cells consisted of four subsets (CD4+8−, CD4+8lo, CD4−8lo and CD4−8hi) and γδ T cells of three (CD2−4−8−, CD2+4−8lo and CD2+4−8−). There were, in addition, a large proportion of non‐T‐non‐B lymphocytes with CD2+3−4−8lo surface immunoglobulin‐negative phenotype containing natural killer (NK) activity. A striking observation was the relatively low frequency of αβ T cells in the blood of young pigs. Similar phenotypes were also identified in the cells from peripheral lymphoid tissues, though the proportions of the γδ T cells and the non‐T‐non‐B lymphocytes in the lymph nodes and tonsil were much lower and the majority of the γδ T cells in the lymphoid tissues bore CD2 and/or CD8. In thymus, the small thymocytes were predominantly CD3−4+8+while the mature large thymocytes displayed phenotypes similar to those of peripheral T cells. Thus this work has directly defined porcine αβ and γδ T cells, demonstrated the T‐cell nature of the unique CD4+8+ subset of peripheral lymphocytes, revealed the high heterogeneity of the CD8+ cells, and established the phenotype of NK cells. The functional properties of these defined porcine lymphocyte subsets can now be experimentally determined in health and disease.

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