The above phenotypic changes have a correlate at the genetic level. Full-genome sequencing of TEV-At17 indicates that six changes have occurred during adaptation (first six rows in Table 1 ); three of them were non-synonymous. The first non-synonymous change, A1047V, affected the P3 protein. P3 localizes in nucleus and nucleoli in association with the NIa protein and participates in virus amplification through its interaction with the CI protein [20] . In other potyviruses, P3 is also involved in systemic movement [25, 26] . The second mutation is a T1210M replacement in the 6K1 peptide. This short peptide has been implicated in plant pathogenicity since its deletion results in symptomless infections [20] . Finally, the third amino acid replacement observed is L2013F in the VPg domain of the NIa protein. VPg is covalently attached to the 59 end of the viral RNA and has essential functions in the viral replication and, relevant for the problem in hand, it has been reported as a key determinant in host-genotype specificity for systemic movement or replication [20] and it has been recently demonstrated that the proper interaction between the translation initiation factor eI4B and VPg is necessary for TEV infection [27] . In conclusion, these three mutations may explain the observed improvement in virus amplification and pathogenicity. The relevance of the three synonymous substitutions observed is not as clear, although their adaptive value cannot be ruled out.