PLANT VIRUSES

FIGURE 245 Internal structures of aphids that are involved into the circulative transmission of luteovirus. The circulative pathway, indicated by arrows, requires that the virus be actively transported from the hemolymph into the salivary system. It appears the luteovirus read-through domain is required for virus transport through the membranes of aphid salivary glands, but is not required for systemic infection of plants and influences virus accumulation in plants. A viral nonstructural 17-kDa protein is required for systemic infection. ASG, accessory salivary gland, HG, hindgut; MG, midgut; PSG, principal salivary gland. (From Chay, C.A., Gunasinge, U.B., Dinesh-Kumar, S.P., Miller, W.A., and Gray, S.M., Virology, 219, 57, 1996. With permission.)

FIGURE 246 Proposed receptor-mediated endocytotic pathway of circulative nonpropagative viruses across hindgut epithelial cells. Accessible or protruding capsid protein domains bind to receptors on the apical plasmalemma of hindgut epithelial cells. The process of virus uptake or the environment within cytoplasmic transport vesicles might strip off the receptor-binding domain. The vesicle membrane fuses with the basal plasmalemma of the cell and virus is released into the hemocoel. (Reprinted from Trends Microbiol., 4, 259-264, 1996. Gray, S.M., Plant virus proteins involved in natural vector transmission. © 1996, with permission of Elsevier Science.)

FIGURE 247 Three models of interaction between a noncirculative virus, the virally-encoded helper component and vector material lining the cuticle in the food canal. Most experimental evidence supports either model A or model B. In model A, the helper component directly facilitates virus binding by first attaching to sites in the food canal; the virus then binds to the helper component. In B , the helper component indirectly facilitates binding of virus directly to the cuticle. Helper component first binds to a specific site causing a conformational change that allows virus to bind. In C, helper component interacts directly with the virus causing a conformational change in the virus. This exposes sites on the virus that can interact directly with binding factors on the cuticular lining of the food canal. The release of the virus, regardless of the binding process, occurs during the intermittent phases of feeding when the vector expels digestive secretions into the plant. The model proposes that proteases in the digestive secretions expose sites on the virus capsid that are involved in binding the virus to a helper component or to the vector. (Reprinted from Trends Microbiol., 4, 259-264, 1996. Gray, S.M., Plant virus proteins involved in natural vector transmission. © 1996, with permission of Elsevier Science.)

FIGURE 248 Types of graft used for virus transmission. (A) Wedge graft, used with herbaceous plants such as tomato; the cuts are made with a razor or thin sharp knife to avoid bruising the delicate stems. (B) Bottle graft; the base of the scion is kept in water until a union is formed and is removed later. (C) Tongue-cut approach, used with strawberry runners; the graft is later fitted with crepe rubber (not shown). (D) Shield bud graft, used with woody plants. The bud (eye) is inserted under the bark of the stock ready for tying. (E) Spliced-approach graft. The components are sliced to expose the cambium in equal patterns. The shoots of rooted plants are pared to expose their cambium and the cut surfaces bound together. (After an arrangement by Gibbs, A. and Harrison, B., Plant Virology, The Principles, John Wiley & Sons, New York, 1976, 35. Adapted from Garner, R.J., The Grafter's Handbook, 3th ed., Faber and Faber, London, 1967, 103, 106, 110, 115, and 151. With permission by Mrs. I.L. Garner.)

FIGURE 249 Progression of tobacco mosaic virus (in black) through a medium-sized, young tomato plant. Based on tests of Dwarf Champion plants about 15 in. high, growing in 6 in. pots in an unheated greenhouse. (From Samuel, G., Ann. Appl. Biol., 21, 90, 1934. With permission.)

FIGURE 250 Turnip plant inoculated with cauliflower mosaic virus (CaMV) showing parameters influencing bilateral and basipetal accumulation of virus in leaves of systemically infected plants. The virus moves over long distances in plants within the phloem vasculature, i.e., from an older source leaf that exports photoassimilates to younger leaves. Leaves and leaf sectors that export photoassimilates are shaded. The inoculated leaf is indicated as leaf number 0. Black areas indicate immature (sink) parts of a leaf. (From Leisner, S.M., Turgeon, R., and Howell, S.H., Mol. Plant Microbe Interact., 5, 41, 1992. With permission.)

FIGURE 251 Translocation of curly-top virus in tobacco. Fig. 12. and 13. Two tobacco plants, each produced by grafting scions of Nicotiana tabacum, to a stock of N. glauca. The stem of the stock was "ringed" by removing bark in a ring-like area. Pith and internal phloem were also removed through a small hole. In Fig. 13 the ring was incomplete since some bark with phloem remained. In each plant the upper scion was inoculated with the virus and developed symptoms. In Fig. 12 the virus was unable to pass into the lower scion which remained healthy. In Fig. 13 the narrow phloem bridge allowed the virus to pass into the lower scion which developed symptoms. Fig. 14 and 15, cross-sections of the ringed parts of the stems in Fig. 12 and 13, respectively; xylem is indicated by hatching. Fig. 16, section of complete stem. (From Esau, K., Am. J. Bot., 43, 739, 1956. With permission.)

FIGURE 252 Translocation of curly-top virus in a sugar-beet plant with three crowns. Crown I was inoculated with the virus and developed symptoms. Crown II was shaded but not inoculated and developed symptoms. In the absence of light it did not form food and received its supply of food from the root. Virus appeared to have entered crown II from the root. Crown III was not treated in any way and remained free of symptoms. Arrows indicate prevailing direction of food movement. (Diagram by M. Shenkovsky, from Esau, K., Am. J. Bot., 43, 739, 1956. With permission.)

FIGURE 253 Flow-pattern of virus movement to sink leaves. Viruses (black hexagons) move short distances through nonvascular cells and long distances through phloem vascular cells. They move from cell to cell through plasmodesmata in vascular tissues and encounter a number of different cell types when entering and exiting the conductive (sieve element) cells of phloem vasculature. (Reprinted from Trends Microbiol., 1, 314-317, 1993. Leisner, S.M. and Howell, S.H., Longdistance-movement of viruses in plants. © 1993, with permission of Elsevier Science.)

FIGURE 254 Two mechanisms by which virus-encoded movement proteins mediate cell-to-cell spread of viruses. The TMV-like mechanisms (above) involve transient modification of plasmodesmal width to allow transport of either (a) the ribonucleoprotein complex or (b) free RNA to the adjacent cell. The CPMV-like mechanism (below) involves formation of a tubule through which virions are transported to the adjacent cell; this tubule appears to modify plasmodesmal structure permanently. (Reprinted from Trends Microbiol., 1, 105-108, 1993. McLean, B.G., Waigmann, E., Citowsky, V., and Zambryski, P., Cell-to-cell movement of plant viruses. © 1993, with permission from Elsevier Science.)

FIGURE 255 Ectodesmata - possible routes for virus entry. (From Stevens, W.A., Virology of Flowering Plants, Blackie & Sons, Glasgow, 1983, 95. With permission of Kluwer Academic Publishers.)

FIGURE 256 Effect of mosaic disease upon the sugar beet leaf. (1) Mosaic pattern on leaf. Green areas are shaded, yellow areas are left blank. (2) Mesophyll from a green area. It shows a loose arrangement of cells and numerous chloroplasts. (3) Mesophyll from a yellow area. It shows compact arrangement of cells like a young leaf. This underdevelopment is one of the expressions of hyperplasia. The chloroplasts are few. The deficiency in chloroplasts makes the tissue appear yellow. (4) Cell from green mesophyll with numerous chloroplasts. (5) Cell from yellow mesophyll. The chloroplasts have become partly or completely disorganized. (From Esau, K., Am. J. Bot., 43, 739, 1956. With permission.)

FIGURE 257 Transverse sections of tobacco leaves showing xylem proliferation and cell enlargement (hypertrophy) resulting from virus infection. (From Stevens, W.A., Virology of Flowering Plants, Blackie & Sons, Glasgow, 1983, 28. With permission of Kluwer Academic Publishers.)

FIGURE 258 Clearing of veins. (A) Transverse section of young diseased leaf, showing hyperplasia of cells and degeneration of chloroplasts in mesophyll adjacent to phloem (ph). (B) Transverse section of a young healthy leaf. (C) Parenchyma cell from a large vein of a young healthy leaf. (D). Healthy mesophyll cell from region adjacent to phloem of small bundle. (E) Diseased mesophyll cell from region adjacent to phloem of small bundle, showing degenerated chloroplasts. Original magnification: A and B, x 450; C-E, x 1060. (From Esau, K., Phytopathology, 23, 679, 1933. With permission.)

FIGURE 259 Vascular anatomy of a galled vascular bundle in a sugarcane leaf infected with Fiji disease virus. Only the distribution of xylem and phloem tissues is shown and a section of the bundle through the galled area has been removed to expose the tissues in transverse section. The galls appear to result from virus-induced cell proliferation. The proliferating cells develop into abnormal phloem (gall-phloem) and xylem (gall-xylem). Virus particles and viroplasms are confined to these tissues. (From Hatta, T., and Francki, R.I.B., Physiol. Plant Pathol., 9, 321, 1976. With permission.)

FIGURE 260 Changes in French bean leaf cell ultrastructure during local lesion production by TMV. (1) Healthy leaf mesophyllic cell. (2) Initial stages of infection. (3) Cell destruction in region near local lesion. (4) Complete loss of organelles in necrotic area of lesion. (After photomicrographs by Spencer, C. and Kimmins, W.C., Can. J. Microbiol., 47, 2049, 1969; from Stevens, W.A., Virology of Flowering Plants, Blackie & Sons, Glasgow, 1983, 29. With permission of Kluwer Academic Publishers.)

FIGURE 261 Structural abnormalities in chloroplasts associated with virus infections. (From Strobel, G.A. and Mathre, D.E., Outlines of Plant Pathology, 1st edition, by Van Nostrand Reinhold, New York, 1970, 282. © 1970. Reprinted with permission of Brooks/Cole, a division of Thomson Learning. Fax 800-730-2215.)

FIGURE 262 Sequence of changes in the chloroplasts of Chinese cabbage following infection with turnip yellow mosaic virus. (1) Chloroplast with scattered vesicles; (2) Swollen chloroplast, vesicles scattered. (3) Vesicles aggregated, endoplasmic reticulum (ER) associated with vesicles. (4) Chloroplasts aggregate together in area of vesicles. (5) Virus particles appear in space between chloroplasts. (After photomicrographs by Hatta, T., and Matthews, R.E.F., Virology, 59, 383, 1974; from Stevens, W.A., Virology of Flowering Plants, Blackie & Sons, Glasgow, 1983, 30. With permission of Kluwer Academic Publishers.)

FIGURE 263 Peripheric membraneous vesicle induced by TYMV in chloroplasts. The diagram is based on the assumption that the vesicle membranes are derived from chloroplast membranes by invagination. A and B indicate membrane faces; fracture paths within the membranes are indicated by a dotted line. (From Hatta, T., Bullivant, S., and Matthews, R.E.F., J. Gen. Virol., 20, 37, 1973. With permission.)

FIGURE 264 Various cytoplasmic inclusions induced by plant viruses. (From Stevens, W.A., Virology of Flowering Plants, Blackie & Sons, Glasgow, 1983, 35. With permission of Kluwer Academic Publishers.)

FIGURE 265 Fracture of intracellular membranes in a living plant tissue by sharp-pointed viral inclusions. The abundant growth of thread-shaped, needle-like, spindle-shaped virus inclusions (of a crystalloid or paracrystalloid kind) may hamper the normal course of cell division in virus-diseased plants. (From Goldin, M.I., in Viruses of Plants, Proc. Internat. Conf. Plant Viruses, Beemster, A.B.R. and Dijkstra, J., Eds., North-Holland Publishing Company, Amsterdam, 1966, 158. With permission of S. Chirkov, Russian Academy of Sciences, Moscow.)

FIGURE 266 Cytoplasmic banded bodies in parenchyma cells. (From Stevens, W.A., Virology of Flowering Plants, Blackie & Sons, Glasgow, 1983, 36. With permission of Kluwer Academic Publishers.)

FIGURE 268 All members of the potyvirus family that have been investigated cytologically, induce the formation of intracellular cytoplasmic inclusions called "pinwheels." These formations, constituted by a type of protein encoded by the viral genome which assembles into regular sheets around an axis, were originally described as cylindrical. Some, at least during the initial stages of their development, may be conical in shape. (From Cornuet, P., Éléments de Virologie Végétale, © INRA, Paris. With permission.)

FIGURE 267 Cell with inclusion bodies characteristic of tobacco mosaic virus. The bodies are of two kinds: an amoeboid x-body and a body of crystalline striated material. The relative size of the bodies may be judged from their comparison with the nucleus. (From Esau, K., Am. J. Bot., 43, 739, 1956. With permission.)