How and why would a virus become a pathogen?

We are addressing this question by trying to understand the basis of pathogenesis of a lethal parasite of CMV, the D satRNA. D satRNA attenuates CMV symptoms in most hosts, but specifically induces systemic necrosis in tomato.

We are interested in the cellular and molecular mechanisms involved in this lethal disease that result in a run-away systemic necrosis. We are using molecular biological, genomic, functional genomic, genetic, biochemical and cell biological approaches to understand the mechanisms of virus-induced plant lethality and host specificity of plant death (Xu and Roossinck, 2000; Xu et al., 2003; Xu et al., 2004).

We know that we can change only 3 nt of the D satRNA, and change it from a pathogen to an attenuating satRNA. We have studied the changes in the transcriptome that are associated with infection by these two closely related satRNAs and find that expression of 400 genes is either enhanced or reduced (Irian et al., 2007).