Update on Virus-Host Interactions during Movement Virus-Host Interactions during Movement Processes

Plant viruses must invade and infect as much of their hosts as possible to maximize their chances of successful perpetuation. They move cell to cell via plasmodesmata (PD), which they modify to a greater or lesser extent, and to distant parts of the plant through the vascular system. Plant viruses encode one or more nonstructural proteins specifically required for movement within their hosts and many also require their capsid (coat) protein(s). Classically, a viral movement protein (MP) is defined by its ability to increase the plasmodesmal size exclusion limit (SEL) and to move cell to cell; however, other viral proteins that do not themselves move may be essential for the movement process. Viruses that infect plants have developed a variety of strategies to move from cell to cell and are heavily dependent on endogenous host transport systems during movement, as with all aspects of their life cycles. Rather than attempt to cover all reported virus-host interactions during movement, in this short review, we would like to focus on some common themes that appear in the literature regarding each of the steps involved in viral cell-to-cell movement. These are the use of the endoplasmic reticulum (ER)/actin network as an intracellular transport pathway, recognition of adhesion sites at the cell periphery, modification of PD by alteration of the cell wall structure, heat shock protein (Hsp) 70-class chaperones as potential translocation factors, and regulation of movement. We will discuss how the movement processes of different viruses may utilize these steps in different ways or may not involve all of these steps. Other reviewers have covered different aspects of short and long distance movement processes, such as the role of the cytoskeleton and the requirement for suppression of host defense responses (for example, Reichel et al., 1999; Oparka, 2004; Waigmann et al., 2004; Voinnet, 2005).