Chapter 20 - Conclusions

Abstract

Historically, the primary epizootiological cycle of bluetongue virus (BTV) was between species of African antelope and vector Culicoides. The disease, bluetongue (BT), became evident only when susceptible European breeds of sheep were imported into Africa. Much has also been learned about the assembly and replication of BTV and other orbiviruses and of their inter-relationships and taxonomy. Such studies have benefited greatly from the detailed structural work on the viral core and through a synthesis of the information derived from structural, biochemical and cell biology studies. Advances in molecular epidemiology now mean that the geographical movements of BTV serotypes and strains can be closely tracked in time and space to help identify the origins of virus incursions, determine their routes of entry into new territories and even elucidate movement between individual farms, thus potentially enabling control responses to be better targeted. The knowledge of the mechanisms involved in causing and controlling cellular and tissue damage is rapidly increasing, providing a better understanding of the responses of different species (vertebrate and invertebrate) and different tissues to BTV infection. However, further work is necessary to determine the mechanisms that lead to the death of most BTV-infected mammalian cells but to persistence in insect cells and possibly some mammalian cells.