Arrest in viral transport as the basis for plant resistance to infection

After initial inoculation, most viruses spread in host plants via two mechanisms: local, cell-to-cell movement and systemic movement. Cell-to-cell movement occurs through intercellular connections, plasmodesmata (PD), between epidermal (EP) cells and mesophyll (MS) cells, or MS cells and MS cells. Systemic movement is more complex, comprising three distinct stages: viral entry into vascular system from MS cells in the inoculated leaf, long distance transport through the vasculature, and viral egress from the vascular tissues into MS cells within uninoculated, systemic organs. Generally, local movement is a relatively slow process (e.g., 5-15 μm/hr, see Gibbs, 1976), which, in some hosts, may be further restricted by limitations in the viral replication rate. On the other hand, long distance movement through the vascular system is rather rapid (e.g., 50-80 mm/hr, see Gibbs, 1976), occurring with the flow of photoassimilates and, in many if not all cases, not requiring viral replication (Wintermantel et al. 1997; Susi et al. 1999). Studies to date show that these two processes are mediated by different sets of viral proteins, implying that cellular machineries, especially those for the PD transport that viruses utilize in their two modes of movement are quite different from each other.