Induced mechanisms are by definition imperceptible or less active in uninfected, unstressed, or untreated plants, but can be activated by pathogen infection, stress, or chemical treatment to inhibit the replication and movement of virus in the host. In contrast, defenses that are pre-existing or serve to limit virus propagation and spread in otherwise susceptible hosts are considered to be "basal" in nature. Both forms of resistance can be genetically determined. Most recessive resistance genes that control resistance to viruses appear not to depend upon inducible mechanisms but rather maintain basal resistance by producing nonfunctional variants of factors, specifically translation initiation factors, required by the virus for successful exploitation of the host cell protein synthetic machinery. In contrast, most dominant resistance genes condition the induction of broad-scale changes in plant biochemistry and physiology that are activated and regulated by various signal transduction pathways, particularly those regulated by salicylic acid, jasmonic acid, and ethylene. These induced changes include localized plant cell death (associated with the hypersensitive response, HR) and the upregulation of resistance against many types of pathogen throughout the plant (systemic acquired resistance, SAR). Unfortunately, it is still poorly understood how virus infection is inhibited and restricted during the HR and in plants exhibiting SAR. Resistance to viruses is not always genetically predetermined and can be highly adaptive in nature. This is exemplified by resistance based on RNA silencing, which appears to play roles in both induced and basal resistance to viruses. To counter inducible resistance mechanisms, viruses have acquired counter-defense factors to subvert RNA silencing. Some of these factors may affect signal transduction pathways controlled by salicylic acid and jasmonic acid. In this chapter, we review current knowledge of defensive signaling in resistance to viruses including the nature and roles of low molecular weight, proteinaceous, and small RNA components of defensive signaling. We discuss the differences and similarities of defenses and defensive signaling directed against viral versus nonviral pathogens, the potential role of RNA silencing as an effector in resistance and possible regulator of defensive signaling, crosstalk and overlap between antiviral systems, and interference with and manipulation of host defensive systems by the viruses themselves.