To investigate the role of salicylic acid (SA) in the hypersensitive response (HR) its accumulation was compromised during different phases of lesion development by differential expression of a salicylate hydroxylase gene (SH-L). Constitutive suppression of SA accumulation was achieved by expression of a gene fusion between the CaMV35S promoter (35S) and SH-L. Using the H2O2-responsive AoPR1 promoter to drive SH-L SA accumulation could be compromised at an early stage, on lesion formation and possibly prior to visible necrosis, whilst use of the salicylate-responsive PR1a promoter reduced SA accumulation at a later stage as lesions expand. TMV infection of 35S-SH-L and AoPR1-SH-L, but not PR1a-SH-L, tobacco resulted in significantly greater rates of lesion growth than in wild-type tobacco. TMV was detected in asymptomatic tissue surrounding lesions only in 35S-SH-L and AoPR1-SH-L lines; subsequently these transgenic lines exhibited a 'spreading-necrosis' originating from the lesion which entered the stem and eventually other leaves, a phenotype which could be correlated with the presence of TMV particles. Analysis of TMV-infected and 'temperature-shifted' tobacco indicated that both 35S-SH-L and AoPR1-SH-L, but not PR1a-SH-L, transgenics exhibited delayed cell-death compared to wild-type infections. We propose that the SH-L phenotypes indicate that early SA accumulation is a major factor in preventing viral escape, via mechanism(s) which may include influencing the rate of host-cell death and, possibly, an effect on viral function.