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Viral diseases of local economic crops
 

A virus is a nucleoprotein that has the ability to cause disease. It multiplies only in living cells and it is too small to be seen individually with a light microscope.


Coconut - a local economic crop

In economic terms, viruses are only of importance if they are likely to spread to crops during their commercial lifetime, which of course varies greatly between very short extremes in horticultural production and very long extremes in forestry.

Some estimates put total worldwide damage due to plant viruses as high as US$ 6 x 10 10 per year.

The importance of plant viruses in relation to crop production can be realised from the fact that among the various factors responsible for low yields, viral diseases are prominent.

Plant virus may damage leaves, stems, roots, fruits, seed or flowers and may cause economic losses by reduction in yield and quality of plant products.

The severity of individual viral diseases may vary with the locality, the crop variety, and from one season to the next.

All viruses are parasitic in cells and cause a multitude of diseases in all forms of living organisms, from single-celled microorganisms to large plants and animals.

The total number of viruses known to date exceeds 2000, and new viruses are described almost every month. About one fourth of all known viruses attack and cause diseases in plants.

One virus may infect one or dozens of different species of plants, and each species of plant is usually attacked by many different kinds of viruses. A plant may also be infected by more than one kind of virus at the same time.

Viruses cause diseases by upsetting the metabolism of the cells, but not by consuming cells or killing them with toxins. Plant viruses differ greatly in their shape and size. Nearly half of them are elongate and almost as many are spherical. There are a number of routes by which plant viruses may be transmitted:

Seeds: These may transmit virus infection either due to external contamination of the seed with virus particles, or due to infection of the living tissues of the embryo.

Transmission by this route leads to early outbreaks of disease in new crops, which are usually initially focal in distribution, but may subsequently be transmitted to the remainder of the crop by other mechanisms.

Vegetative propagation/grafting: These techniques are cheap and easy methods of plant propagation but provide the ideal opportunity for viruses to spread to new plants.

Vectors: Many different grows of living organisms can act as vectors and spread viruses from one plant to another, which are Bacteria (e.g. Agrobacterium tumefaciens), Fungi, Nematodes, Arthropods: Insects - aphids, leafhoppers, plant hoppers, beetles, thrips, etc. and Arachnids - mites.

Mechanical: Mechanical transmission of viruses is the most widely used method for experimental infection of plants and is usually achieved by rubbing virus-containing preparations into the leaves, which in most plant species are particularly susceptible to infection.

However, this is also an important natural method of transmission. Virus particles may contaminate soil for long periods and may be transmitted to the leaves of new host plants as wind-blown dust or as rain-splashed mud.

Pollen transmission: Virus transmitted by pollen may result in reduced fruit set, may infect the seed and the seedling that will grow from it, and in some cases can spread through the fertilised flower and down into the mother plant. Which thus become infected with virus.

Such plat-to-plant transmission of virus through pollen is known to occur, for example in sour cherry infected with prunus necrotic ringspot virus.

Transmission of plant viruses by insects is of particular agricultural importance. Extensive areas of monoculture and the inappropriate use of pesticides, which kill natural predators, can result in massive population booms of insects such as aphids.

Plant viruses rely on a mechanical breach of the integrity of a cell wall to directly introduce a virus particle into a cell.

This is achieved either by the vector associated with transmission of the virus or simply by mechanical damage to cells. Insects, which bite or suck plant tissues, are, of course, the ideal means of transmitting viruses to new hosts.

However, in other cases (e.g. many plant rhabdoviruses) the virus may also infect and multiply in the tissues of the insect (propagative transmission) as well as those of host plants.

In these cases, the vector serves as a means not only of distributing the virus, but also of amplifying the infection.

Initially, most plant viruses multiply at the site of infection, giving rise to localised symptoms such as necrotic spots on the leaves. Subsequently, the virus may be distributed to all parts of the plant either by direct cell-to-cell spread or by the vascular system, resulting in a systemic infection involving the whole plant.

However, the problem these viruses face in reinfection and recruitment of new cells is the same as they face initially - how to cross the barrier of the plant cell wall.

Plant cell walls necessarily contain channels called plasmodesmata, which allow plant cells to communicate with each other and to pass metabolites between them.

However, these channels are too small to allow the passage of virus particles of genomic nucleic acids. Many plant viruses have evolved specialised movement proteins, which modify the plasmodesmata and allowing the passage of intact virus particles to pass from one cell to another.

The symptom a virus causes at the primary site of infection is called primary symptom. Symptoms caused by its spreading throughout the rest of the plant are called secondary symptoms.

The most obvious symptoms of virus infected plants are usually those appearing on the foliage, but some viruses may cause striking symptoms on the stem, fruit and roots, with or without symptom development on the leaves.

The most common types of plant symptoms produced by virus infections are mosaic, mottle, vein clearing, vein banding, yellows, ring spots, chlorosis, dwarfing and stunting, tumours or galls, bunchy top, witches broom, rosette, enation and necrosis.

Virus infections can usually be recognised by mosaic-like leaf patterns of light and dark green. The infection spreads often over the whole leaf beginning at the leaf veins. Leaves that had been infected during their development are usually deformed or involute.

Frequently, lightened leaf areas, called chlorosis, develop around the primary site of infection. Withered areas are called necrosis. Chlorosis is caused by a breakdown of the chlorophyll resulting in a decreased rate of photosynthesis.

Heavy infections are characterised by a complete local loss of chlorophyll. Affected areas have a yellowish look as only the carotenoids remain. Some viruses multiply within the plant without causing symptoms. This phenomenon is called latent infection.

In contrast, wound tumour virus causes the development of tumours. The symptoms of most viruses are dependent on both virus and host, and do thus present an important diagnostic feature. Plant viruses face special problems at initiating an infection.

The outer surfaces of plants are composed of protective layers of waxes and pectin, but more significantly, each cell is surrounded by a thick wall of cellulose overlying the cytoplasmic membrane.

To date, no plant virus is known to use a specific cellular receptor of the type that animal and bacterial viruses use to attach to cells.

Rather, plant viruses rely on a mechanical breach of the integrity of a cell wall to directly introduce a virus particle into a cell. This is achieved either by the vector associated with transmission of the virus or simply by mechanical damage to cells.

After replication in an initial cell, the lack of receptors poses special problems for plant viruses in recruiting new cells to the infection.

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