Abstract

This chapter reviews current knowledge concerning the BTV replication and transmission cycle within the ruminant host, as well as the immune mechanisms and antiviral responses. This includes considerations of organ tropism and the cellular targets for BTV infection within these organs. Bluetongue virus has evolved to optimize its transmission efficiency within the context of the insect vector)/ruminant (host) relationship. The BTV replication mechanisms and strategies within the ruminant host will therefore also be related to their consequences for transmission to the insect vector. Bluetongue virus-infected ruminants develop various antiviral host immune responses. These include serogroup-specific (BTV species-specific) antibodies that are directed against several of the more conserved virus proteins. VP7 is strongly immunodominant and raises group-specific antibodies that can be used for the diagnosis and identification of any BTV type and strain by ELISA. Neutralizing antibodies raised against one serotype of BTV generally provide protection only against challenge with BTV strains belonging to the same serotype, not against strains of heterologous serotypes, but a wider spectrum of cross-reactive neutralizing antibody responses and serotype cross-protection has been induced by sequential infection with two or more BTV serotypes. The recent spread of multiple BTV serotypes in southern Europe, the damage and losses caused by the BTV-8 epidemic in northern Europe and the recent spread of several exotic BTV types to the United States are all likely to renew interest in the immunobiology of BTV infection in the mammalian host.

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