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Logically, most plant viruses being vector-transmitted, the majority of viral transport mechanisms associated to the transmission step have been approached through the study of virus-vector relationships. However, in the case of non-vector vertical transmission through the seeds, some viruses have evolved specific patterns to colonize either the gametes or the embryo, thereby connecting viral transport within the plant to that in between plants. Moreover, though it may appear counter intuitive and has been largely overlooked, some specific virus accumulation within cells or organs, as well as specific control of multiple infections of single cells, can also directly affect the success and efficiency of vector transmission, again connecting viral transport mechanisms inside and outside the host plants. This work summarizes the data available on viral transport outside the plant in various vectors, and also highlights a few available examples and proposes hypotheses for illustrating the concept that some viral trafficking within plants is specifically intended to prepare ulterior acquisition by the vectors.

Macromolecular cell-to-cell transport in plants occurs through complex intercellular channels, the plasmodesmata. Plant viruses pirate these natural plant communication channels for their own spread from an infected cell to a neighboring healthy cell. Viral movement proteins are the major agents in promoting this process. is the most extensively studied plant virus and can therefore be viewed as a model system for cell-to-cell transport. In this chapter we summarize knowledge about mechanistic properties of the movement protein of and discuss the potential involvement of other viral and cellular components in the intercellular transport process.

Plant viruses move from cell to cell through plasmodesmata, which are complex gatable pores in the cell wall. While plasmodesmata normally allow the diffusion of only small molecules, they can be biochemically or structurally modified by virus-encoded movement proteins to enable the passage of either infectious ribonucleoprotein complexes or entire virus particles. In the latter case, the movement protein forms a transport tubule inside the plasmodesmal pore or at the surface of isolated cells. In this review, we describe the functional relevance of the tubules in the transport of viruses, speculative models for this movement mechanism, as well as the host components that seem to contribute to this type of transport.

Viral long distant transport is an essential step for systemic infection. Because the process involves different types of highly differentiated vascular-associated cells, the virus systemic movement is regulated differentially at each tissue interface. In this chapter, we review current knowledge about viral systemic transport process in non-Arabidopsis hosts. We especially focus on viral and host factors participating in viral systemic transport. We also briefly overview the effect of RNA silencing, the host innate immunity, on viral systemic movement.

Viroids are small, noncoding and nonencapsidated RNAs that infect plants. To establish systemic infection, viroid genomes or their derivatives must interact directly with cellular factors. There is increasing evidence that subcellular localization and systemic trafficking of viroid RNAs are regulated, likely via interactions between viroid RNA elements and specific cellular proteins. Here we summarize recent progress on the characterization of viroid structures and host proteins that may play important roles in trafficking. We also discuss critical issues that need to be addressed in future investigations.

In plants, RNA interference constitutes an important defense mechanism against viruses, transposons, and transgenes. Viruses, on the other hand, use suppressors to counteract silencing. In contrast to mammalian systems, silencing in plants spreads systemically through the whole organism. Since also viruses spread and consequently produce suppressors systemically, a race between silencing and virus replication occurs. Apparently, successful viruses win the race, but only until they reach the tissue around the meristem. There, the silencing mechanism is most capable by efficiently amplifying the silencing signal, bona fide 21-nt siRNA, leading to the well-known phenomenon of meristem exclusion.

The model plant has been established as a host for representatives of many of the major groups of plant viruses. These viruses use a variety of strategies to replicate and traffic their genomes within compatible host plants. The development of as a host for these diverse viruses provides opportunities to apply genetic and reverse genetic approaches to the complex interactions that are not feasible or practical in many of their agronomically important hosts. In this chapter, we summarize the amazing array of viruses that have been shown to infect one or more ecotypes, describe natural variation in the ability of these ecotypes to support systemic infections, and discuss host genes that have been identified through a variety of approaches that are involved in movement or limit virus spread in .