Plant viruses spread cell-to-cell by exploiting and modifying plasmodesmata, coaxial membranous channels that cross cell walls and interlink the cytoplasm, endoplasmic reticulum and plasma-membranes of contiguous cells. To facilitate viral spread, viruses encode for one or more movement proteins that interact with ER and ER derived membranes, bind vRNA and target to Pd. Mounting evidence suggests that RNA viruses that do not spread as virions employ the same basic mechanism to facilitate cell-to-cell spread. In light of the research reviewed here, we propose a general functional model for the cell-to-cell spread of these viruses. This model posits that MPs have multiple functions: one function involves directing virus induced beta-1,3-glucanases which accumulate in ER derived vesicles to the cell wall to hydrolyze Pd associated callose in order to gate open the Pd; independently, the MPs form ER-associated protein rafts which transport bound vRNA by diffusion along ER to adjacent cells via the ER component of the plasmodesmata. The driving force for spread is the diffusion gradient between infected and non-infected adjacent cells.