Abstract
African swine fever virus (ASFV) is a large double-stranded DNA virus which causes an acute haemorrhagic disease in domestic swine. The natural host reservoir is the bushpig (Potomochorus porcus), warthog (Phacochoerus aethiopicus) and soft ticks of the Ornithodoros species. ASFV is apathogenic in these hosts. One of the defining characteristics of ASFV induced haemorrhagic fever is massive lymphocyte apoptosis. This induction of apoptosis is most likely due to a combination of factors released from infected macrophage cells. Tumour necrosis factor alpha (TNFa) has been shown to induce apoptosis in lymphocytes but it is not solely responsible (Gomez del Moral et al. , 1999). Galectin-3 is a multi-functional protein expressed in macrophages. Previously transcription of galectin-3 has been shown to be up-regulated during ASFV infection. Porcine galectin-3 has been characterised as part of this project and the effect ASFV infection has on expression and localization of this protein has been investigated. The results show that ASFV infection induces secretion of galectin-3. It is possible that galectin-3 secreted from ASFV infected macrophage cells contributes to lymphocyte apoptosis. ASFV produces a large repertoire of proteins, a number of which have been shown to modulate host immune responses. Another aim of this project has been to investigate global host gene expression in response to early events in ASFV infection using a porcine micro array. In order to distinguish between the specific effects of virus entry and early viral gene transcription, host gene expression in cells infected with UV-inactivated virus was compared to gene expression in cells infected with untreated virus and mock-infected cells. The genes that were differentially-regulated included those from a number of signalling pathways. These included genes involved in the mitogen activated protein kinase (MAPK) pathway. This pathway is important in control of cell proliferation, survival, inflammation and cytokine synthesis. The manipulation of this pathway by ASFV is likely to facilitate virus replication and evasion of host defences.