Virus and Host Plant Interactions


Plant viruses use the host pathways for cellular and tissue communication in order to spread through the plant leading to the onset of symptoms and reduced productivity. A successful virus infection represents the exploitation of the host plant to massively amplify the viral genome in a form that can be transmitted to neighbouring uninfected plants or progeny plants.

Keywords: movement of viruses in plants; tissue specificity; seed transmission; virus‐induced symptoms

Figure 1.

The relationship between the distribution of symptoms and the phylotactic organization of leaves. A CAWV‐infected turnip plant is used to illustrate how sink, but not source tissues, are susceptible to virus invasion. (a) Aerial view of a growing turnip plant. Leaf 1 is the oldest leaf and leaf 6, the youngest. After inoculation of the virus on to leaf 1, local chlorotic symptoms showed the primary infection foci. (b) The virus moved from leaf 1, bypassed leaf 2 (not shown) and entered the basal portion of leaf 3, which had not made the transition from sink to source. The tip portion of leaf 3 had made the transition and could not be invaded. Leaves 4 (not shown), 5 and 6 were all sink tissues at the time of invasion and show complete symptom coverage.

Figure 2.

Effects on plasmodesmata during the passage of virus from cell to cell. Virus MPs affect plasmodesmata in two principal ways: (a) without any observable alterations in ultrastructure but by causing a change in the functional SEL, or (b) with major changes in ultrastructure. In the latter, the desmotubule (D) is lost and replaced by a tubule (T) composed of MP. Virus particles (VP) translocate through the tubule from the infected to the uninfected cell. The formation of the tubule is often associated with a distortion of the cell wall (CW) around the tubule. ER, endoplasmic reticulum; PM, plasma membrane.

Figure 3.

Virus symptoms are modulated, in part, by the RNA silencing pathway. Virus symptoms show a range of morphological effects, which in this case (a Turnip mosaic virus infection of Arabidopsis) include stunting, exaggerated lobeing of the leaves and defects in flower development. Most of these effects are replicated by the transgenic expression of the virus's suppressor of gene silencing, P1/HC‐Pro (b and c), and are phenocopied in mutant plants in the gene silencing pathway. This is illustrated as the consequences of transgenic P1/HC‐Pro expression and mutations in DICER (dcl1‐9 and dcl1‐7) on the narrow sepal (s) phenotype (D) observed in infected plants. Modified from Kasschau et al. , with permission from Elsevier.

Figure 4.

Biochemical changes associated with a Cucumber mosaic virus (CMV) lesion on a cucurbit cotyledon. (a) The virus‐induced lesion is seen after staining the tissues for starch accumulation using iodine. (b) The sequence of biochemical changes following virus multiplication is recorded as changes relative to the maximal activity within or adjacent to the lesion. The earliest responses are seen as increases in photosynthetic electron transport, protein synthesis and anaplerotic enzyme (nicotinamide adenosine disphosphate (NADP)‐dependent malic enzyme) activity. The last response is seen as a loss of chlorophyll associated with the onset of chlorosis. (Modified from Tésci et al. ).



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Further Reading

Dunoyer P and Voinnet O (2005) The complex interplay between plant viruses and host RNA‐silencing pathways. Current Opinion in Plant Biology 8: 415–423.

Hull R (2002) Matthew's Plant Virology, 4th edn. London: Academic Press.

Kurata T, Okada K and Wada T (2005) Intercellular movement of transcription factors. Current Opinion in Plant Biology 8: 600–605.

Lucas WJ (2005) Plant viral movement proteins: agents for cell‐to‐cell trafficking of viral genomes. Virology 344: 169–184.

Maule A and Wang D (1996) Seed transmission of plant viruses: a lesson in biological complexity. Trends in Microbiology 4: 153–158.

Maule AJ, Escaler M and Aranda MA (2000) Programmed responses to virus replication in plants. Molecular Plant Pathology 1: 9–15.

Nagy PD and Pogany J (2006) Yeast as a model host to dissect functions of viral and host factors in tombusvirus replication. Virology 344: 211–220.

Roth BM, Pruss GJ and Vance VB (2005) Plant viral suppressors of RNA silencing. Virus Research 102: 97–108.

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Whitham SA and Wang Y (2004) Roles for host factors in plant viral pathogenicity. Current Opinion in Plant Biology 7: 365–371.

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Maule, Andrew J(Apr 2007) Virus and Host Plant Interactions. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0000758.pub2]