The most obvious symptom of systemic virus infection is the mosaic pattern of the leaves. Yellowing, chlorosis is also frequent and characteristic sign of the altered photosynthetic activity. Virus infection effects photosynthesis in a complex manner, depending on the particular host-virus combination. The symptoms are basically different in the incompatible or the compatible host-virus interaction.
Hafiz Muhammad Rizwan Mazhar
Department of Plant Pathology, University of Agriculture, Faisalabad-Pakistan
Photosynthetic changes in incompatible host-virus interaction Virus infection often causes local lesions in resistant plants. The development of local lesions in hypersensitive reaction (HR) was described in details by electron micros- copy, based on the time course of the appearance of symptoms. The ultrastructure of the lesion and the surrounding cell layers and the role of the active zone in the localisation of the infection was highlighted (Israel and Ross, 1967).
In tobacco mosaic tobamovirus (TMV) infected N. glutinosa leaves the size and number of the starch grains increased in the chloroplasts following the infection (Weintraub and Ragetli, 1964). One day after the infection plasmolysis occurred, and first the cytoplasm and later the chloroplast membranes completely disappeared.
In the remains of the chloroplasts large vesicles were formed, the number of mitochondria increased and their structure changed. Finally the whole cell structure collapsed and its content disin-tegrated. All these alterations were consequences of the loss of osmotic regulation, and have been related to the so-called ‘starch-lesions’ described by Holmes (1931).
Photosynthetic changes in compatible host-virus interaction For the synthesis of virions the parasite uses the metabolites and energy of the host plant, which are produced in the course of photosynthesis. It is evident that the phy- siological processes of the virus and the plant are linked in complex ways, the structure and the function of the chloroplasts are disturbed (Zaitlin and Hull, 1987).
Changes in the ultrastructure of chloroplasts
The chlorosis of leaf tissues in the compatible host parasite interactions can be traced back to different causes. The number, size or chlorophyll content of the chloroplasts may decrease.Their shape, inner membrane structure may alter to some degrees, some of their metabolites may accumulate. Often the starch grains enlarge, or accumulate for example in the case of the cauliflower mosaic caulimovirus (CaMV) infected cabbage plants (Conti et al., 1972).
Effect of virus infection on CO2-fixation and on some biosynthetic processes
In several virus-host interactions the disturbances of CO2-fixation and of related metabolic ways, or the alteration in ratio of certain products was reported. At the early stage of systemic TMV infection (virus replication) more CO2molecules assimilated by the photosynthetic processes (Doke and Hirai, 1970a). As the infection had been progressed this tendency inverted: CO2-uptake was decreasing in the infected.
The same changes as well as the increase of res-piration were observed in tobacco leaves infected with tobacco etch potyvirus (TEV).The enzyme activity of phosphoenol-pyruvate-carbox-ylase (PEP-carboxylase) increased in the leaves of chinese cabbage infected with TYMV.
In contrast, in tobacco leaves infected with TSWV activity loss of PEP-carboxylase was measured and it was explained as the early senescence induced by the virus infection.
Changes in the chlorophyll protein complexes and chloroplast proteins
Virus infected monocotyledons (e.g. barley infected with BSMV or WSMV) contained reduced amount of chlorophyll protein complexes compared to the healthy controls.
Effect of virus infection as a biotic stress factor on photosynthesis
Stress has been described by Osmond et al. (1987) as all parameters that suppress the maximum, potential genomial value of growth and reproduction of a plant. Plants adopt to stress conditions in two ways, either by tolerance or avoidance. In the case of tolerance the plant’s reaction to a moderate stress is the upregulation, while against a severe stress the down regulation of metabolic processes.
At the cellular level the damage in the membranes and the fluorescence of chlorophyll built in the thylakoid membranes indicated the post stress conditions. In the early phase of virus infection both the non-photochemical quenching of fluorescence and the predominantly reduced state of QAthe primary electronacceptor of PSII, indicated the development of symptoms and the rapid chloroplast destruction due to photoinhibitory conditions (Balachandran et al., 1997).
The build up of carbohydrates and the brakeup of the equilibrium between synthesis and brakedown probably blocks the gen regulation, which effects the level of chlorophyll-protein complexes and photosynthetic metabolic enzymes.