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Plant virus diseases occur worldwide in cultivated plant species as well as many native (weed) plants. A plant virus is dependent on host and vector for its “survival”. The efficiency and extent of spread of infection within a plant are important factors for allowing the virus to be accessible to its vector(s), which in turn allows for dispersal of the virus to new plants and crops. If dispersal by a vector, such as an insect, is not part of the virus’ infection cycle, it may adapt alternative, and seemingly clever, approaches. For example, Tomato mosaic virus is not dispersed in nature by a recognized vector but its ability to persist in the environment allows it to be transmitted from soil bound decaying plant tissues, and virus occurred in clouds and fog which may have served as a source of virus for transmission to spruce trees ( Castello et al. 1995 ). Plant viruses appear to represent extreme ends of a life spectrum; they are genetically and structurally simple infectious agents but their obligatory and intimate relationship with a host plant is quite complex.

The ability of a plant virus to systemically infect its hosts can be considered the consequence of a series of interactions between the viral genome and its gene products with the host. Once a virus enters the cell, it must be able to express each of its proteins, replicate its genome, move from one cell to another, and then gain access to the host vascular system to move out of the initially infected leaf to other parts of the plant. At each step of this process, there must be a basic level of compatibility between the virus and its host; otherwise, the infection process ends prematurely. ( 2002 ) discusses how mismatches between host and virus at different points of the infection process can define the host range of a virus. For example, stringent requirements for cell-to-cell movement in the plant can provide one important barrier that limits the host range of a virus. A virus may be able to replicate in an individual cell, but its cell-to-cell movement protein may be non-functional in that host, thereby limiting its movement into adjacent cells. In this instance, there would be no visible response of the plant to the inoculation of the virus.

Over the last years RNA silencing in plants and its animal counterpart RNA interference (RNAi) have become intensively studied biological systems. While initially being discovered as a side effect of transgene expression in plants and a process by which transgenic virus resistance could be obtained, it has since been implicated in natural virus resistance and basic biological processes such as development, gene regulation and chromatin condensation. RNA silencing related mechanisms are not only limited to plants, but also play a role in a variety of eukaryotic organisms. Due to the biochemical dissection of components of the silencing pathway in several model organisms, such as Arabidopsis thaliana, Caenorhabditis elegans and Drosophila melanogaster , the general understanding of how RNA silencing works has greatly increased in recent years. The revelation of a striking level of conservation of the RNA silencing pathway between most eukaryotic organisms strengthens its importance. Nowadays, RNA silencing induced by double stranded RNA (dsRNA) molecules such as short hairpins, short interfering RNAs (siRNAs) and long dsRNAs has developed into a standard tool in gene function studies (gene knock-down). It is being applied in large automated genome screens, where a majority of genes of certain organisms (e.g. C. elegans and Homo sapiens ) are knocked-down and analyzed using different assays depending on the research interests. In plants RNA silencing is used as a generally applicable antiviral strategy.

Plants are constantly challenged by a wide array of pathogens, including viruses. For any specific plant species most viruses cannot surmount basal defenses that include physical barriers like a waxy layer covering the plant and post-transcriptional gene silencing (PTGS). However, in those instances when a virus is able to infect a plant, host survival relies on quick recognition of the invading virus and rapid signaling of a defense response. One form of resistance termed gene-for-gene type of resistance relies on the interaction of a plant R gene and a pathogen-encoded avirulence ( Avr ) gene. If a plant has a specific R protein that can recognize a pathogen Avr product, the plant will mount a defense response and thwart an infection. Therefore, plant R proteins have a dual role. Not only must they recognize a pathogen directly or indirectly, they must also initiate signaling that leads to a defense response. One of the earliest defense responses is the hypersensitive response (HR), a type of programmed cell death (PCD) that occurs at the pathogen’s infection site. HR is correlated with the signaling of an R -gene-mediated disease resistance response and containment of the pathogen at the infection site (For details, see Chapter A5). Following HR, a systemic acquired resistance (SAR) response results in an enhanced resistance to further infection by a variety of pathogens. In this chapter we will discuss the major advances in understanding how R proteins recognize different viruses and the intricacies of the defense-signaling network that leads to HR and SAR.

Viruses that cause economically important diseases spread systemically in the plant. However, in several laboratory test or indicator plants, the virus after multiplying in several hundred cells around the point of entry, does not continue to spread and remains in a local infection. Several types of local infections are known ( Loebenstein et al. 1982 ): (a) self-limiting necrotic local lesions such as Tobacco mosaic virus (TMV) in Datura strammonium , where lesions reach their maximum size three days after inoculation; (b) chlorotic local lesions, such as Potato virus Y (PVY) in Chenopodium amaranticolor , where infected cells lose chlorophyll; (c) ring-like patterns or ringspots that remain localized, such as Tetragonia expansa infected with Tomato spotted wilt virus (TSWV); (d) starch lesions, such as TMV in cucumber cotyledons, where no symptoms are observed on the intact leaf, but when it is decolorized with ethanol and stained with iodine, lesions become apparent; (e) microlesions (with a mean size of 1.1 x 10^−2 mm_2), such as the U_2 of TMV on Pinto bean leaves; and (f) subliminal symptomless infections not detectable as starch lesions., as in TMV-infected cotton cotyledons, where virus content is 1/200,000 of that produced in a systemic host ( Cheo, 1970 ). The localized infection is an efficient mechanism whereby plants resist viruses, though most viral resistance genes are not associated with the hypersensitive response (HR), but affect virus multiplication or movement as a result of incompatible viral and host factors.

During the co-evolution of plants and their pathogens, the pathogens developed a wide variety of strategies to infect and exploit their hosts. In response to this pressure, plants countered by deploying a range of defense mechanisms. Some of these are conceptually simple, for example defenses based on physical barriers such as the cell wall or cuticle, or resistance engendered by pre-existing antimicrobial compounds ( Osbourn 1996 ). However, certain resistance mechanisms, most particularly those that are inducible, are complex in nature and have proved to be more difficult to understand, particularly with respect to resistance to viruses.

Plants resist viral infections either via an active mechanism, involving the participation of resistance ( R ) genes and subsequent signal transduction pathways, or in a passive manner, which entails the absence of essential host factors required for replication or movement of the virus. An active resistance response involves strain-specific recognition of a virus-encoded elicitor, through direct or indirect interaction with the corresponding R gene product. This in turn activates downstream signaling, which leads to prevention of viral spread and confers resistance against the pathogen. An R gene-mediated recognition of virus often turns on defense responses such as the accumulation of salicylic acid (SA), the expression of pathogenesisrelated ( PR ) genes, and the development of a hypersensitive response (HR) on the inoculated leaves. The HR is defined by necrotic lesion formation at the site of infection and is thought to help prevent multiplication and movement by confining the virus to the region immediately surrounding the necrotic lesions.

The concepts of an RNA surveillance defense operating against plant viruses and plant viruses expressing counter-defense molecules came to a confluence in late 1998, with the publication of three seminal papers ( Anandalakshmi et al. 1998 ; Brigneti et al. 1998 ; Kasschau and Carrington, 1998 ). These studies demonstrated that specific viral-encoded proteins, shown to enhance pathogenicity when expressed from viral vectors, could suppress the silencing of a reporter transgene. A fourth paper also published in 1998, demonstrated that infection by Cucumber mosaic virus (CMV) could suppress the silencing of reporter transgenes, but did not delimit a specific viral-encoded protein ( Béclin et al. 1998 ). These studies all led to the idea that some viruses are able to counter an inherent defense mechanism in plants based on targeting the viral RNA sequence. Subsequent work has identified many such potential counter-defense molecules in different viruses. These are referred to as silencing suppressors, since it is in such assays that a role for all these proteins in suppressing an RNA surveillance system has been demonstrated. The connection between a role for these proteins in suppressing the silencing of a transgene and inhibition of plant defense mechanisms preventing natural virus infection has only limited direct experimental support. Here we will describe the work that led to the concept of plant viruses expressing counter-defense proteins and the experimental evidence that silencing suppressors are involved in countering some plant defense measures.

Dark green islands (DGIs) have been an enigma since they were first documented before the nature of viruses was known (reviewed in Allard, 1914 ). In 1898 Beijerinck identified the casual agent of tobacco mosaic disease as a contagious solution a “ contagium vivum fluidum ” and described dark green blotches on the upper leaves of infected plants ( Goldstein, 1926 ). When a mosaic virus infects a plant, these discrete regions of dark green tissue occur only on leaves that are systemically infected when immature. Leaves that are fully developed at the time of infection do not develop DGIs. A variety of tools and plant-virus models have been used in the years since Beijerinck’s report to compare the dark green tissue with the surrounding yellow tissue. These experiments and observations have been aimed at determining the nature and causes of DGIs.

Without the equivalent of a copper or fungicide spray, virtually all realistic control measures for plant virus diseases in the field fall into two categories ( Fraser, 1990 ), (i) preventing the virus and the plant from coming in contact in a manner that can initiate an infection (Chapter 14), and (ii) biologically based interference with virus replication, spread or symptom induction. The intimate interaction of virus and cell is demanding on any potential anti-viral and, thus far, none are inexpensive. “Curing” a plant virus disease usually is economical only for propagation stock, accomplished by long term plant culture at elevated temperature (“thermotherapy”), chemotherapy or plant micropropagation. Preventing virus-plant contact may involve clean stock programs and/or at least minimal applications of pesticides to control virus vectors ( Jones, 2004 ). Biologically based interference is considered in Chapters 1, 6 and 13 and here.