Rhabdoviruses and mechanisms of type I interferon antagonism.

The Novirhabdovirus genus includes typical rhabdoviruses from fish, such as viral hemorrhagic septicemia virus, which infects numerous marine and freshwater fish species. Rhabdoviruses that infect plants are separated into the genera Cytorhabdovirus and Nucleorhabdovirus, based on their sites of replication and morphogenesis. The leader RNA of rhabdoviruses is the prime target candidate for recognition by retinoic acid-inducible gene I (RIG-I). Defective interfering (DI) particle RNAs are generated notoriously in fast-replicating rhabdoviruses like vesicular stomatitis virus (VSV). Rhabdoviruses are being recognized by nucleic acid pattern receptors, although most of their RNA is shielded by N protein, and at the latest when they start gene expression by synthesis of leader RNA. The crucial point is therefore to limit the consequential interferon (IFN) production and the expression of IFN-stimulated genes (ISGs) as long and as far as possible by expression of “IFN antagonists.” This chapter analyzes the rhabdoviruses with respect to type I IFN antagonism. Characterization of the mechanisms involved in IFN escape of rhabdoviruses will help to better explain how self and nonself are distinguished and how host signaling networks are connected and regulated and how they function. Furthermore, studies on rhabdoviruses like VSV in its vector host, and of other rhabdoviruses of fish, insects, and plants, will undoubtedly provide further intriguing insights into the host defense mechanisms and the intricate relationship with viruses.