Physiological effects of virus infected plants
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  • 1. AN ASSIGNMENTONPHYSIOLOGICAL EFFECTS OF VIRUS INFECTEDPLANTSSUMITTED BY:ROUF AHMADL-2011-BS-249-MSUBMITTED TO:Prof. Dr. S.S. KANGDeptt. of Plant pathology
  • 2. INTRODUCTION:Plant cells serve for an infecting virus as biochemical and molecular environment which canby the viral genome be determined to sustain the replication of the virus. This is achieved bythe use of the host cells protein synthesizing system for the production of non-structuralproteins (NSP), including nucleic acid replicating enzymes, and the coat protein (CP) of thevirus. The latter serves, together with viral nucleic acid (NA) molecules for the formation ofnew infective viral particles. The processes incited by a virus may disturb the biochemicalbalance of the host cells since host cell components including its energy conferring systemshave to be used for the synthesis of viral components.These processes are in many virus-hostsystems not fully compatible with the host cells physiological balance and, therefore, incitevarious symptoms of cellular degeneration, in the extreme cellular death.Various external symptoms indirectly illustrate the complicated interactions betweenvirus and host cells. They may occur in the whole host plant or may be localized on plantparts near the original infection sites. Virus symptoms may be specific to certain plant organslike the flowers (flower break symptoms) or to certain tissues like the phloem. Variousdistinct regular or irregular patterns of chlorotic or necrotic tissues develop on leavesindicating that the distribution of systemically spread virus is not really uniform throughoutthe plant. The effects of systemically spread virus are obviously regulated by more or lessbalanced interactions between the host metabolism, the virus and environmental factors.Hypersensitivity phenomena occur which lead to sudden cell death immediately upon theinitial cell infection. These examples indicate highly complex interactions which have largelynot been elucidated. The external symptoms are produced by infected tissues relatively late,at a time when viral propagation is already completed in the respective tissue. On the cellularlevel degeneration symptoms caused by the infection are observed e.g. in form of chloroplastsenescence (lipid accumulation, vacuolization).Various physiological changes in virus infected plants can be discussed as under:-A. Nucleic Acids and Proteins(i) DNAIt is widely assumed that the small RNA viruses have little effect on host-cell DNAsynthesis, but there are very few, if any, definitive experiments bearing on the question.
  • 3. Virus infection may well have some effect on host-cell DNA synthesis, but such effects arelikely to be fairly small and difficult to establish because (i) DNA content per cell mayincrease for some time in a normal expanding leaf; (ii) minor DNA fractions, which might beaffected by virus infection, may be difficult to isolate and identify; and (iii) any effect mightbe very transitory and, therefore difficult to detect in asynchronous infections. Using a radioautographic technique to assay for DNA synthesis in individual cells, Atchison (1973) foundthat there was a drop in DNA synthesis in the terminal 1 mm of French bean roots about thetime they were invaded by tobacco ring spot virus. This was soon followed by a transientdrop in the mitotic index.(ii) Ribosomes and ribosomal RNAEffects of virus infection on ribosomal RNA synthesis and the concentration ofribosomes may differ with the virus, strain of virus, time after infection, and the host andtissue concerned. In addition, 70 S and 80 S ribosomes may be affected differently.In TMV-infected leaves viral RNA may come to represent about 75% of the totalnucleic acids without having any marked effects on the main host RNA fractions except tocause a reduction in 16 S and 23 S chloroplast ribosomal RNAs (Fraser 1987b). However,under some conditions cytoplasmic ribosomal RNA synthesis is also inhibited. A reduction inchloroplast ribosomes without a marked effect on cytoplasmic ribosomes is a fairly commonfeature for mosaic diseases (e.g., BSMV in barley, Brakke et al 1987b; TYMV) .In Chinese cabbage leaves chronically infected with TYMV the concentration of 70 Sribosomes in the yellow-green islands in the mosaic is greatly reduced compared to that indark green islands in the same leaf (Reid and Matthews. 1966). here is little effect on theconcentration of cytoplasmic ribosomes in such yellow-green islands of tissue. The extent ofthis reduction depends very much on the strain of TYMV, and it also becomes more severewith time after infection. Loss of 70 S ribosomes more or less parallels the loss ofchlorophyll, "white" strains causing the most severe loss.A somewhat different result is obtained if the effect of TYMV infection with time in ayoung systemically infected leaf is followed. Chloroplast ribosome concentration fallsmarkedly about the time virus concentration reaches a maximum. About the same time thereis a significant increase in cytoplasmic ribosome concentration, which is mainly due to thestunting effect of infection. On the other hand, if the effects of virus infection on these
  • 4. components for the plant as a whole are considered, a different picture emerges. Infectionreduces both cytoplasmic and chloroplast ribosomes.These results emphasize the fact that infection of a growing plant with a virusintroduces an additional time-dependent variable into a system in which many normalinteracting components are changing with time. Analyses made on only one or twocomponents of the system, or at some particular time, arc unlikely to give much in sight intovirus replication and the nature of the disease process. Very little is known about any effectsof virus infection on host tRNAs, nuclear RNAs, or mitochondrial ribosomal RNAs.(iii) ProteinsThe coat protein of a virus such as TMV can come to represent about half the totalprotein in the diseased leaf. This can occur without marked effects on the overall content ofhost proteins. Many other viruses multiply to a much more limited extent. Effects on hostprotein synthesis are not necessarily correlated with amounts of virus produced. A reductionin the amount of the most abundant host protein-ribulose bisphosphate carboxylase-oxygenase (rbcs)-is one of the commonest effects of viruses that cause mosaic and yellowingdiseases (e.g, TYMY, Reid and Matthews, 1966; wheat streak mosaic Potyvirus, White andBrakke 1983).Fraser (1987b) estimated that TMV infection reduced host protein synthesis by up to75% during the period of virus replication. Infection did not alter the concentration of hostpolyadenylated RNA, nor its size distribution. This suggested that infection may alter hostprotein synthesis at the translation stage rather than interfering with transcription. Manyviruses infecting vertebrates inhibit host-cell translation by a variety of mechanisms, bringingabout conditions that favor translation of viral mRNAs (Schneider and Shenk, 1987). Themechanisms used by plant viruses are beginning to be studied. For example, Stratford andCovey (1988) found that there were changes in the levels of specific translatable mRNAs inresponse to infection of turnip leaves with CaMV. More such changes were found with asevere strain. In particular the mRNA encoding the precursor to the small subunit of the wasmarkedly decreased following infection with the severe strain.It is known that the coat protein of TMV, and some other viruses, can encapsulatesome host RNAs in vivo. Sleat et al (1988b) transformed tobacco seedlings to expresschloramphenicol acetyl transferase (CAI) mRNA. Transformed plants that also contained the
  • 5. TMV origin of assembles quench 3 to the CAT gene showed a threefold suppression of CAYactivity compared with plants without the origin of assembly sequence. Thus it is possiblethat the coating of host mRNAs in viral coat protein may be a mechanism for the shutting offof specific host mRNAs during virus replication.Saunders et al. (1989) used another approach to the same problem. They generated alibrary of cDNA clones corresponding to the host RNAs isolated from turnip leaves infectedwith CaMV during the early vein-clearing stage. Hybridization was used to selected clonesthat represented RNAs whose levels had been raised or lowered by infection. For example,one RNA that was greatly reduced in amount was Identified as the mRNA for the ribulose1,5-bisphosphate carboxylase small subunit polypeptide. Overall, the findings of Stratfordand Covey (1988) and Saunders et al (1989) suggest that there are few major changes in hostgene expression during infection with CaMV .2. LipidsThe sites of virus synthesis within the cell almost always contain membranestructures. TYMV infection alters the ultrastructure of chloroplast membranes, andrhabdovirus particles obtain their outer membrane by budding through some host-cellmembrane. There have been a few studies of the effects of virus infection on lipidmetabolism (e.g., Trevathan et al., 1982) but none of these has illuminated the mechanism bywhich viruses change and use plant membrane systems.3. CarbohydratesSome viruses appear to have little effect on carbohydrates in the leaves, while othersmay alter both their rate of synthesis and rate of translocation. These changes may beillustrated in a simple manner.Leaves that have been inoculated several days previously with a virus that does notcause necrotic local lesions are harvested in the morning or after some hours in darkness,decolorized, and treated with iodine. The local lesions may show up as dark-staining areasagainst a pale background, indicating a block in carbohydrate translocation. On the otherhand, if the inoculated leaves are harvested in the afternoon on after a period ofphotosynthesis, decolorized and stained with iodine, the local 1esions may show up as pale
  • 6. spots against the dark-staining background of uninfected tissue .Thus, virus infection candecrease the rate of accumulation of starch when leaves are exposed to light.From the few diseases that have been examined in any detail, it is not possible tomake very firmly based generalizations about other carbohydrate changes, but the followingmay be fairly common effects: (i) a rise in glucose, fructose, and sucrose in virus - infectedleaves; (ii) a greater rise in these sugars caused by mild strains of a given virus comparedwith severe strain; and (iii) effect of infection on mesophyll cells, not yet understood, mayreduce translocation of carbohydrates out of the leaves.4. Cell Wall CompoundsAlthough cytological studies have demonstrated ultrastructural changes in the cellwalls in many virus infections, the biochemical basis of such changes would be difficult tostudy. Future work may show that virus infection has effects on various activities in the cellwall compartment, which is not metabolically inert. Eighty-five percent of detectableperoxidase activity and 22% of the acid phosphatase are located in the cell wall of healthytobacco leaves (Yung and Northcote, 1975), Elevated peroxidase activity has been reportedas a response of tobacco and many other hosts to virus infection (Matthews, 1981).5. RespirationMany studies have been made of the effects of virus infection on rate, and pathwaysof respiration, but it is not possible to relate the results to the processes involved virusreplication. In summary for man many host – virus combinations where necrosis does notoccur, there is a rise in respiration rate, which may begin before symptoms appear andcontinue for a time as disease develops. In chronically infected plants, respiration is oftenlower than normal. In the one systemic disease so for examined in detail, there is nodetectable change in the pathway of respiration. In host-virus combinations where necroticlocal lesions develop, there is an increase in respiration as necrosis develop . This increase isaccounted for, at least in part, by activation of the hexose monophosphate shunt pathway(Matthews 1981; Fraser, 1987b).6. PhotosynthesisIn a tobacco mutant in which some islands of leaf tissue had no chlorophyll, TMVreplication occurred in white leaf areas in the intact plant. However, replication did not occur
  • 7. if the white tissue was detached 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 itself is not necessary for replicationof this virus, Nevertheless, virus infection usually affects the process of photosynthesis.Reduction in carbon fixation is the most commonly reported effect in leaves showing mosaicor yellows diseases. This reduction usually becomes detectable some days after infection.Photosynthetic activity can be reduced by changes in chloroplast structure, by reducedcontent of photosynthetic pigments or ribulose bisphosphate carboxylase, or by reduction inspecific protein associated with the parti les of photosystem II (Naidu et al .. 1986). However,such changes appear to be secondary, occurring some time after infection when much virussynthesis had already taken place. In tobacco plants infected with various strains of TMV,electron transport rates were reduced when loss of chlorophyll occurred. In inoculated laves,photosystem II appeared to be irreversibly damaged in inoculated leaves even when nomacroscopic symptoms were apparent (van Kooten et al 1990). A variety of effects oflocalized and systemic TMV infection in tobacco were observed in experiments with isolatedchloroplasts. However, some enzyme activities were little affected (Montalbini and Lupattelli1989).Some effects on photosynthesis are known that appear to be closely linked in time tothe early period of maximum virus production. In chloroplasts isolated from Chinese cabbageleaves infected with TYMV, the Hill reaction and cyclic and noncyclic photophosphorylationwere all increased compared with healthy leaved during the phase of active virusmultiplication (on an equal chlorophyll basis (Goffeau and Bove, 1965). At a late stage ofinfection, photosynthetic activity way lower than in controls measured on chloroplastsisolated from whole plants in young Chinese cabbage leaves infected with TYMV there was asubstantial diversion of a the products of photosynthetic carbon fixation away from sugarsand into organic acids and amino acids. This change was most marked during the period ofvirus increase and returned to the normal pattern when virus replication was near completion(Bedbrook and Matthews, 1973). An increase in the activity of the enzymesphosphoenolpyruvate carboxylase and aspartate aminotransferase followed a similar timecourse.Magyarosy (et al (1973) found a similar shift from the production of sugars to aminoacids and organic acids in squash plants systemically infected with squash mosaic
  • 8. Comovirus. They isolated chloroplasts from healthy and diseased leaves and snowed thatboth produced a similar pattern of carbon fixation products and that the total carbon fixedwas about the same. They concluded that the virus-induced production of amino acids wastaking place in the cytoplasm.In summary, during the period of rapid replication, virus infection may cause ondiversion of the early products of carbon fixation away from sugars and. into pathways waysthat lead more directly to the production of building blocks for the synthesis of nucleic acidsand proteins. The most general result of virus infection is a reduction in photo photosyntheticactivity. This reduction arises from a variety of biochemical and physical changes. Therelative importance of different factors varies with the disease.7. TranspirationIn chronically virus-infected leaves transpiration rate and water content have beenfound to be generally lower than in corresponding healthy tissues. The reported effects overthe first 1-2 weeks after inoculation vary. Results are difficult to compare and interpretbecause different viruses and host species have been used together with different conditionsof growth and different tissue sampling procedures.Bedbrook (1972) used the cobalt chloride paper method (Stahl, 1894) to estimaterelative transpiration rate and to give a measure of stomatal opening. He compared, in intactChinese cabbage plants, dark green islands in leaves showing mosaic patterns due to TYMVinfection and various islands of tissue fully invaded by the virus. In darkness or low lightintensity, stomata in darker green and pale green islands were closed, while those in islandsof more severely affected lamina were open. In plants that had been held in full daylight thedark and pale green islands were transpiring rapidly. Transpiration from severely affectedislands was much less. These and other experiments showed that TYMV infection lowers theresponsiveness of the stomata to changes in light intensity, the lowered response being mostmarked with strains causing the greatest reduction in chlorophyll. Because of diminishedtranspiration, the temperature of sugar beet leaves in susceptible plants infected withBNYVV was 2-3°C higher than that of a tolerant variety (Xeller et al 1989).8. Activities of Specific EnzymesMuch of the work dealing with the effect of virus infection on specific enzymes isdifficult to interpret for the following reasons: (i) where differences have been found, it has
  • 9. usually been assumed that virus infection alters the amount of enzyme present and littleconsideration has been given to the possibility that infection may affect enzyme activitiesthrough changes in the amount of enzyme inhibitors or activators released when cells aredisrupted; (ii) the difficulty of deciding on an appropriate basis for expressing enzymeactivity has often been ignored; and (iii) much of the work was done before the widespreadexistence of isoenzymes was recognized.There have been many studies involving the use of polyacrylamide gel electro-phoresis to fractionate and assay isoenzymes and to study the consequences of virus infectionon these patterns. It is relatively easy to generate data by this means. It is much less easy toprovide meaningful interpretations of any observed changes. There are several reasons forthese difficulties:1. In the healthy plant there may be a continually changing developmental sequence ofisoenzymes2. Electrophoretically· distinct isoenzymes may be determined genetically or may bedifferent conformational forms derived by posttranslational modification from thesame primary structure.3. The pattern of isoenzymes in the normal host may differ in closely related genotypes,and the effects. of virus infection may differ with these.4. Isoenzymes may be distributed in several subcellular sites. For example, a differentset of peroxidase isoenzymes was associated with the cell wall and with the solublefraction in extracts of normal maize root tips. Virus infection may affect various sitesin different ways.5. Virus-induced cell death may lead to changes in isoenzyme patterns that do not differsignificantly from those induced by entirely unrelated causes of necrosis.6. The observed effect of virus infection may depend on the substrate used forisoenzyme assay.7. Aggregation states (e.g., monomer = dimer) may affect the kinetic properties of anenzyme, for example, aspartate aminotransferase.Studies have been reported that involve representatives of all the major groups of
  • 10. enzymes (oxidoreductases and so on), but none of these has taken the preceding variablesadequately into account.9. HormonesThere is little doubt that virus infection influences hormone activities in infected plantand that hormones play some part in the induction of disease. Quantitative effects ofinfection on concentration have been shown for all the major groups of plant hormones(reviewed by Fraser, 1987b). Virus infections tend to decrease auxin and gibberellin isconcentrations and increase that of abscisic acid. Stimulation of ethylene production isassociated with necrotic or chlorotic local responses.10. Low-Molecular-Weight CompoundsThere are numerous reports on the effects of virus infection on concentration of low-molecular-weight compounds in various parts of virus-infected plants. The analyses give riseto large amounts of data, which vary with different hosts and viruses, and which areimpossible to interpret in relation to virus replication. Some of these effects can be brieflydiscussed as:a. Amino Acids and Related CompoundsThe most consistent change observed has been an increase in one or both of theamides, glutamine and asparagine. The imino acid pipecolic acid has been reported to occurin relatively high concentrations in several virus-infected tissue. A general deficiency insoluble nitrogen compounds compared with healthy leaves may occur during periods of rapidvirus synthesis.b. Compounds Containing PhosphorusPhosphorus is a vital component of all viruses and as such may come to representabout one-fifth of the total phosphorus in the leaf. In spite of this we still have no clearpicture for any virus of the source of virus phosphorus, or the effects of infection on hostphosphorus metabolism.In Chinese cabbage leaves infected with TYMV, sampled 12-20 days afterinoculation, a rise in virus phosphorus was accompanied by a corresponding fall in nonvirus-insoluble phosphorus, suggesting that this virus uses phosphorus at the expense of (but not
  • 11. necessarily directly from) some insoluble source of phosphate in the leaf (Ma thews et al1963).c. Leaf PigmentsVirus infection frequently involves yellow mosaic mottling, or a generalizedyellowing of the leaves. Such changes are obviously due to a reduction in leaf pigments.Many workers have measured the effects of virus infection on the amounts of pigments inleaves. Frequently it appears to involve a loss of the chlorophylls, giving the Yellowishcoloration due to carotene and xanthophyll, but the latter pigments are also decreased in somediseases. Changes in chloroplast pigments are probably often secondary changes, since manyviruses appear to multiply and accumulate in other parts of the cell, and since closely relatedstrains of the same virus may have markedly different effects on chloroplast pigments eventhough they multiply to the same extent.The reduction in amount of leaf pigments can be due either to an inhibition ofchloroplast development or due to the destruction of pigments in mature chloroplasts. Thefirst effect probably predominates in young leaves that are developing as virus infectionproceeds. The rapidly developing chlorosis frequently observed in local lesions when maturegreen leave are inoculated with a virus must be due to destruction of pigments alreadypresent. In systemically infected leaves, TYMV reduced the concentration of all sixphotosynthetic pigments to a similar extent. This was due to a cessation of net synthesis, andsubsequent dilution by leaf expansion.Dark green islands of tissue in Chinese cabbage leaves showing mosaic symptomshad essentially normal concentrations of pigments. Small leaves near the apex of largeChinese cabbage plants are shielded from light and contain little chlorophyll. When suchcream-colored leaves, about 2 cm long, were excised and exposed to light, those from healthyplants became uniformly dark green, while those from TYMV-infected plants developed aprominent mosaic pattern of dark green islands and yellow areas within 24 hours. Thus, inyoung expanding leaves chlorophyll synthesis is inhibited in those islands of tissue in whichTVMV is replicating.
  • 12. d. Flower PigmentsIn view of the work that has been done on the genetics and biochemistry of normalflower coloration, surprisingly little is known about the biochemistry of the flower-breakingprocess, which is such a conspicuous feature of many virus diseases. In tobacco plantsinfected with TMV, the normal pink color of the petals may be broken by white stripes orsectors. We have found the virus present only in the white areas. However, presence orabsence of Virus may not be the only cause for color breaks. In sweet peas (Lathrusodoratus) infected with what was presumably a single virus-bean yellow mosaic Potyvirus-apale pink flower sometimes became flecked with both darker pink and white areas.Virus infection usually appears to affect only the vacuolar anthocyanin pigments. Thepigments residing in chromoplasts may not be affected. For example, the brown wallflower(Cheiranthus cheirii), which contains an anthocyanin, cyanin, and a yellow plastid pigment(Gairdncr 1936), breaks to a yellow color when infected by turnip mosaic Potyvirus (TuMV).A preliminary chromatographic examination of broken and normal parts of petals infectedwith several viruses showed that the absence of color was due to the absence of particularpigments rather than to other factors, such as change in pH within the vacuole (R. E. F.Matthews, unpublished).Kruckelmann and Seyffert (1970) examined the effect of TuMV infection on severalgenotypes of Matthiola incana R. Br. Infection brought about both white stripes and pigmentintensification. Observations on a set of known host genotypes have shown that virusinfection affected only the activities of genes controlling the quantities of pigments produced.It appeared to have no effect on the activities of genes modifying anthocyanin structure.
  • 13. REFRENCES:Brakke M K, Ball E M and Langenberg W G (1987) A non capsid protein associated withunencapsidated virus RNA in barley infected with stripe mosaic virus. J. Gen. Virol. 69:481-91.Kooten O V, Meurs C and Van Loon L C V(1990) Photosynthetic electron transport in tobacco leavesinfected with tobacco mosaic virus. Physiologia Plantarum.80:446-52.Montalbini P and Lupattelli M (1989) Effect of localizedand systemictobacco mosaicvirus infectionon some photochemical and enzymatic activities of isolatedtobacco chloroplasts.physiol and mol. Plant pathol.34: 147-62,Mathews R E F. Plant virology 3rdedition.Rebecca Stratford ,Simon N. Covey (1988 ) Segregation of cauliflower mosaic virus symptom geneticdeterminants.virol.172:451-59.Reid M S and Matthews R E F (1966) On the origin of the mosaic induced by turnip yellowmosaic virus virology 28:563-70.ALL AND W. G. LANGENBERGON K. BRAKKE,* E. M. BALYung KH and Northcote D H (1975) some enzymes present in the walls of mesophyll cells of tobaccoleaves. Biochem J.151(1):141-4.