We have shown that adaptation of a virus to a new host occurs by few changes in viral genome. The increase in viral fitness correlates with deep changes in the patterns of host's gene expression, illustrating that the subtle but dynamic interplay between the pathogen and the plant shifts as the virus adapts to its host. Under the experimental conditions imposed, it may be speculated that natural selection may had favored viral genomes that avoided plant defense mechanisms as suggested by the observation of stress-related genes not being activated after infection with the evolved virus (Table 2 ). Therefore, perhaps as a consequence, increases in the strength of symptoms, virus accumulation and transmissibility have been observed. These phenotypic changes are associated to a few genomic changes fixed in the viral genome. In particular, the development of symptoms is associated to a single substitution in the viral VPg protein, whereas ulterior mutations in other viral components simply magnify symptoms. Our starting hypothesis was that viral adaptation occurs throughout the integration of viral replication processes within host physiology and circuitry of genetic and metabolic interactions. Necessarily, this integration has to affect the patterns of host's gene expression. Our experiments directly test this hypothesis, supporting its validity and, furthermore, pinpointing some physiological processes that may be targeted by the virus as it improves its fitness. The obvious follow-up of this study is to dissect the physiological processes and identify, whenever possible, the precise steps and proteins that are getting targeted by the virus during its adaptation.