The Rpv3 locus determines the ability to operate an isolate-specific hypersensitive response (HR) against Plasmopara viticola in grapevines that carry a resistant Rpv3 (+) haplotype. Artificial infection was performed on leaf discs of Rpv3 (+) and Rpv3 (-) grapevines with two distinct isolates of the pathogen (avrRpv3 (+) and avrRpv3 (-)). The plant response, including the establishment of HR and changes in expression of 33 genes, was compared to the development of the pathogen. HR was induced exclusively in the Rpv3 (+) host upon inoculation with the avrRpv3 (+) isolate of the pathogen, which is assumed to use avrRpv3 (+) effectors that are recognised by/through the plant Rpv3 (+) gene product. The limitation imposed on pathogen growth was the result of inducible responses elicited by the Rpv3 (+)-avrRpv3 (+) interaction. This host reaction relied on transcriptional induction of the HR-associated gene HSR1 and salicylic acid-induced pathogenesis-related (PR) genes PR-1 and PR-2 during the initial 24-48 h post-inoculation. These events had no parallel in the Rpv3 (-) host or upon infection with the avrRpv3 (-) isolate. The emerging model for Rpv3-mediated defence, which is dependent upon race-specific recognition, associated with up-regulation of PR-1 and PR-2 genes, and enforced by localised HR-type necrosis, is compatible with the cascade of events initiated by the products of NB-LRR and LRR-kinase receptor-like genes, such as those residing in the Rpv3 locus.