1. PHYSIOLOGICAL EFFECTS OF VIRUSINFECTED PLANTSSUBMITTED BY:ROUF AHMADL-2011-BS-249-M
2. INTRODUCTION: Plant cells serve for an infecting virus as biochemical andmolecular environment. Achieved by the use of the host cells protein synthesizingsystem for the production of non-structural proteins (NSP)(nucleic acid replicating enzymes, and the coat protein(CP) of the virus). The latter serves, together with viral nucleic acid (NA)molecules for the formation of new infective viral particles. These processes are in many virus-host systems not fullycompatible with the host cells physiological balanceand, therefore, incite various symptoms of cellulardegeneration, in the extreme cellular death.
3. Various physiological changes in virusinfected plants can be discussed as under:-A.Nucleic Acids and Proteins(i) DNA Virus infection may well have some effect on host-cell DNAsynthesis, but such effects are likely to be fairly small anddifficult to establish because (i) DNA content per cell may increase for some time in anormal expanding leaf; (ii) minor DNA fractions, which might be affected by virusinfection, may be difficult to isolate and identify; and (iii) any effect might be very transitory and, thereforedifficult to detect in asynchronous infections
4. (ii) Ribosomes and ribosomal RNA Effects of virus infection on ribosomal RNA synthesis andthe concentration of ribosomes may differ with thevirus, strain of virus, time after infection, and the host andtissue concerned. In addition, 70 S and 80 S ribosomesmay be affected differently In TMV-infected leaves viral RNA may come to representabout 75% of the total nucleic acids without having anymarked effects on the main host RNA fractions except tocause a reduction in 16 S and 23 S chloroplast ribosomalRNAs (Fraser 1987b).
5. (iii) Proteins The coat protein of a virus such as TMV can come to representabout half the total protein in the diseased leaf. This can occurwithout marked effects on the overall content of host proteins. Many other viruses multiply to a much more limited extent.Effects on host protein synthesis are not necessarily correlatedwith amounts of virus produced. A reduction in the amount of the most abundant host protein-ribulose bisphosphate carboxylase-oxygenase (rbcs)-is one ofthe commonest effects of viruses that cause mosaic andyellowing diseases (e.g, TYMV, Reid and Matthews, 1966; wheatstreak mosaic Potyvirus, White and Brakke 1983).
6.  Fraser (1987b) estimated that TMV infection reduced hostprotein synthesis by up to 75% during the period of virusreplication. Infection did not alter the concentration of hostpolyadenylated RNA, nor its size distribution. Thissuggested that infection may alter host protein synthesis atthe translation stage rather than interfering withtranscription. Many viruses infecting vertebrates inhibit host-celltranslation by a variety of mechanisms, bringing aboutconditions that favor translation of viral mRNAs(Schneider and Shenk, 1987).
7. 2. Lipids The sites of virus synthesis within the cell almost alwayscontain membrane structures. TYMV infection alters the ultrastructure of chloroplastmembranes, and rhabdovirus particles obtain their outermembrane by budding through some host-cell membrane. There have been a few studies on the effects of virusinfection on lipid metabolism (e.g., Trevathan et al., 1982)but none of these has illuminated the mechanism bywhich viruses change and use plant membrane systems
8. 3. Carbohydrates Some viruses appear to have little effect on carbohydrates in theleaves, while others may alter both their rate of synthesis andrate of translocation. Following may be fairly common effects:(i) a rise in glucose, fructose, and sucrose in virus - infectedleaves;(ii) a rise in these sugars caused by mild strains of a given viruscompared with severe train; and(iii)effect of infection on mesophyll cells, not yet understood, mayreduce translocation of carbohydrates out of the leaves.
9. 4. Cell Wall Compounds Although cytological studies have demonstratedultrastructural changes in the cell walls in many virusinfections. Eighty-five percent of detectable peroxidase activity and22% of the acid phosphatase are located in the cell wall ofhealthy tobacco leaves (Yung and Northcote, 1975), Elevated peroxidase activity has been reported as aresponse of tobacco and many other hosts to virusinfection (Matthews, 1981).
10. 5. Respiration For many host – virus combinations where necrosis doesnot occur, there is a rise in respiration rate, which maybegin before symptoms appear and continue for a time asdisease develops. In chronically infected plants, respirationis often lower than normal. In host-virus combinations where necrotic local lesionsdevelop, there is an increase in respiration as necrosisdevelop . This increase is accounted for, at least in part, byactivation of the hexose monophosphate shunt pathway(Matthews 1981; Fraser, 1987b).
11. 6. Photosynthesis In a tobacco mutant in which some islands of leaf tissue had nochlorophyll, TMV replication occurred in white leaf areas in theintact plant. However, replication did not occur if the white tissue wasdetached and floated on water immediately after inoculation(R, E. F. Matthews, unpublished). Detached white tissue supplied with glucose supported TMVreplication, indicating that the process of photosynthesis itselfis not necessary for replication of this virus, Nevertheless, virus infection usually affects the process ofphotosynthesis. Reduction in carbon fixation is the mostcommonly reported effect in leaves showing mosaic or yellowsdiseases. This reduction usually becomes detectable some daysafter infection
12.  Photosynthetic activity can be reduced by changes inchloroplast structure, by reduced content ofphotosynthetic pigments or ribulose bisphosphatecarboxylase, or by reduction in specific protein associatedwith the particles of photosystem II (Naidu et al .. 1986).7.Transpiration In chronically virus-infected leaves transpiration rate andwater content have been found to be generally lower thanin corresponding healthy tissues.
13. 9. Hormones Virus infections tend to decrease auxin and gibberellinconcentrations and increase that of abscisic acid. Stimulation ofethylene production is associated with necrotic or chloroticlocal responses.10.Low-Molecular-Weight Compounds There are numerous reports on the effects of virus infection onconcentration of low-molecular-weight compounds in variousparts of virus-infected plants. Some of these effects can bebriefly discussed as: a. Amino Acids and Related Compounds The most consistent change observed has been an increase inone or both of the amides, glutamine and asparagine. The iminoacid pipecolic acid has been reported to occur in relatively highconcentrations in several virus-infected tissue (e.g. Welkie et al1967)10. Low-Molecular-Weight Compounds10. Low-Molecular-Weight Compounds
14.  In Chinese cabbage leaves infected with TYMV, sampled 12-20days after inoculation, a rise in virus phosphorus wasaccompanied by a corresponding fall in nonvirus-insolublephosphorus, suggesting that this virus uses phosphorus at theexpense of (but not necessarily directly from) some insolublesource of phosphate in the leaf (Ma thews et al 1963).c. Leaf Pigments Virus infection frequently involves yellow mosaic mottling, or ageneralized yellowing of the leaves. Such changes are obviouslydue to a reduction in leaf pigments. Many workers have measured the effects of virus infection onthe amounts of pigments in leaves. Frequently it appears toinvolve a loss of the chlorophylls, giving the Yellowishcoloration due to carotene and xanthophyll, but the latterpigments are also decreased in some diseases.b. Compounds Containing Phosphorus
15.  The reduction in amount of leaf pigments can be dueeither to an inhibition of chloroplast development or dueto the destruction of pigments in mature chloroplastsd. Flower Pigments Virus infection usually appears to affect only the vacuolaranthocyanin pigments. The pigments residing inchromoplasts may not be affected. For example, the brownwallflower (Cheiranthus cheirii), which contains ananthocyanin, cyanin, and a yellow plastid pigment(Gairdncr 1936), breaks to a yellow color when infected byturnip mosaic Potyvirus (TuMV). A preliminary chromatographic examination of brokenand normal parts of petals infected with several virusesshowed that the absence of color was due to the absence ofparticular pigments rather than to other factors, such aschange in pH within the vacuole