Plant viruses mainly come in the form of single-stranded ss and double-stranded ds RNA viruses, as well as single-stranded and DNA-containing retroviruses [ 17 ]. Due to a wide diversity of their genetic material, the reproductive cycle and life pattern often vary from virus to virus Fig. Viruses are composed of a nucleic acid molecule and a protective protein coat capsid.
Capsid can sometimes contain a combination of proteins and lipids, which form a lipoprotein membrane. The typical size of a plant virus is 30 nm [ 19 ]. A — plant viruses and viroids : replication and translation strategies. B - schematic representation of infection of neighboring cells by a virus viroid via plasmodesmata. C - symmetric and asymmetric mechanisms of viroid replication. The virion enters the cytoplasm of the plant cell via passive transport through wounds caused by mechanical damage to the cuticle and cell wall, since it is unable to pass through these structures on its own.
Upon entering the cell, the virus uncoats. DNA-containing viruses also need to penetrate the nucleus in order to start transcription and mRNA synthesis. All viruses encode at least two types of proteins: replication proteins, which are required for the synthesis of nucleic acid, and structural proteins, which form the capsid.
In some cases, there are also proteins that are responsible for virion motility; they ensure transport of virus particles between the plant cells. Viral replication proteins bind to cellular proteins to form a complex that produces multiple copies of the viral genome which interact with structural proteins to form new virions, which are then released from the cell. This is the standard viral life cycle. Plant viruses can be transmitted vertically from parents to offspring and horizontally from diseased plants to healthy ones.
Viruses utilize small intercellular channels called plasmodesmata to penetrate neighboring cells Fig. Viruses often express the proteins that ensure virion motility by modifying channels to facilitate the transmission of the infection to a neighboring cell [ 20 ]. This is how a local infection of a plant takes place. In order to infect an entire plant, a virus must enter its vascular system, where it then moves passively through the sieve tubes of the phloem with the flow of substances: this is how it can infect cells distant from the primary site of the infection [ 19 , 20 ].
Some viruses are very stable and resistant to heat, can remain viable for a long time in plant cells and the products derived from them [ 21 , 22 ], and can spread through passive mechanical transport from one plant to another [ 23 ]. However, most plant viruses actively spread from infected plants to healthy ones using a carrier organism vector.
Carriers are divided into a mechanical vector, in which the agent does not propagate, and a biological one, in which part of the viral life cycle takes place [ 24 ].
The main vectors of plant viruses are arthropods, nematodes, and fungi that feed on plants [ 25 ]. Plant viruses pose a serious threat to a wide range of crops, while the economic losses caused by viruses are second only to the losses caused by other pathogens [ 26 ]. Moreover, some viruses can infect more than 1, different plant species comprising more than 85 families [ 27 ]. Viruses manifest themselves in a different way depending on the stage of crop production: they can inflict colossal damage at the stage of crop growth, while at the stage of harvesting, storage, and transportation, the damage from a viral infection is minimal.
It should be also noted that, in some cases, plants are found infected with viruses in the absence of any obvious symptoms [ 29 ]. The symptoms of viral diseases can be divided into five main types: growth suppression reduced growth of the entire plant or its leading shoots ; discoloration mosaic, chlorotic rings, leaf chlorosis, variegation ; deformations leaf wrinkling, corrugation, threadlike leaves ; necrosis; and impaired reproduction flower sterility, parthenocarpy, shedding of flowers and ovaries [ 2 ].
There is another type of infectious agents: viroids, which are circular RNAs that cause various diseases in plants and animals. Taxonomically, they belong to viruses families Pospiviroidae and Avsunviroidae. In contrast to viruses, viroids lack a protein envelope capsid and present covalently linked ssRNA molecules — nucleotides long, which is times shorter than the viral genome.
Viroids do not encode proteins and cannot replicate autonomously. It is considered that the viroid can employ the DNA-dependent RNA polymerase, endoribonuclease, and DNA ligase 1 which is usually silent of the host cell for its replication [ 30 ]. Viroids replicate via a rolling-circle mechanism, with members of the families Pospiviroidae and Avsunviroidae replicating through an asymmetric and symmetric pathway, respectively Fig.
The molecular mechanism of the pathogenic action of viroids is not fully understood. It is believed that viroids can alter the phosphorylation state of gene products via binding to cellular kinases [ 31 ], affect the expression of the genes associated with growth, stress, development, and protection [ 32 ], induce the proteins associated with pathogenesis during an infection [ 33 ], cause post-transcriptional suppression of gene expression by RNA interference, impair splicing [ 34 ], and induce demethylation of rRNA genes.
It is surprising that the substitution of one nucleotide at a certain position alters the pathogenicity of the viroid significantly [ 35 ]. The RNA molecule of Pospiviroidae family members has five domains: a central domain C containing the central, conserved region, which plays an important role in viroid replication; a pathogenicity domain P implicated in the manifestation of disease symptoms; a variable domain V , which is, apparently, responsible for viroid adaptation; and the transport domains T1 and T2 in cases of co-infection with two viroids, they can exchange with these domains, which can contribute to their evolution.
Viroids of the family Avsunviroidae lack the central conserved region but contain the sequences involved in the formation of the ribozyme structures necessary for self-cleavage of RNA strands [ 36 ]. The main symptoms of viroid diseases are reduced growth of the entire plant or its parts, discoloration chlorosis, anthocyanosis , and deformation of various organs [ 2 ].
Thus, viruses and viroids represent a rather large group of pathogens that cause plant diseases and can result in serious damage to crops in the absence of management and preventive measures, especially when infected at early stages of plant growth.
Bacteria are found almost everywhere and can be pathogenic to animals, plants, and fungi [ 37 ]. Bacterial genetic information is encoded in the DNA in the form of a chromosome; more than one chromosome can be found in a cell.
A bacterial cell can contain extrachromosomal mobile genetic elements: plasmids that can carry important virulence factors or, on the contrary, biological control factors. Bacteria can also contain a prophage, which represents bacteriophage DNA integrated into the genome. Most bacteria divide by binary fission, usually with simultaneous duplication of both chromosomal DNA and extrachromosomal elements.
Division of a bacterial cell requires the presence of the membrane potential [ 38 ]. Bacteria can contain more than one plasmid, since some of them can be lost during division. For instance, Pantoea stewartii can harbor up to 13 different plasmids [ 39 ]. Although bacteria usually transfer plasmids within their population [ 40 ], horizontal transfer of genetic information remains quite common in the prokaryotic world.
Bacteria have a cell membrane which separates the cytoplasm from the external environment. Bacteria are divided into Gram-positive and Gram-negative organisms depending on the cell wall structure [ 41 ]. The cell wall of Gram-positive bacteria consists of a membrane and a thick peptidoglycan layer. The main component of the latter is multilayered murein.
Peptidoglycan also contains proteins, lipids, and teichoic and teichuronic acids. The cell wall of Gram-negative bacteria has two membranes with a peptidoglycan layer between them. The outer membrane contains lipopolysaccharides and porins but lacks teichoic and lipoteichoic acids.
Due to the presence of a cell wall, bacteria need secretion systems to pump out xenobiotics, as well as release various proteins and virulence factors Fig. The secretion systems are divided into several groups based on their structure. There are at least six different types of secretion systems typical of Gram-negative bacteria, four types found in Gram-positive bacteria, and two types present in both groups [ 42 ]. The secretion systems also play a key role in the virulence of phytopathogenic bacteria.
It should be noted that, during the division of a bacterial cell, an asymmetry between mother and daughter cells can be observed, where the mother cell retains most of the secretion system transporters, while the daughter cell receives a smaller part of transporters and is forced to synthesize them de novo [ 43 ]. A — bacterial secretory systems that are used to infect plant cells and tissues. B - development of bacterial infection: 1 — penetration through the stomata due to phytotoxins, 2 — secretion of phytotoxins to modify the physiology, immune system, and metabolism of plants, 3 — secretion of phytotoxins for degradation of the cell wall and cytotoxic effect on plant cells, 4 — surface colonization and formation of biofilms, 5 — damage to plant cells due to ice nucleation and formation of crystals.
C - development of fungal infection: 1 — penetration into an intact cell at the site of appressorium attachment through the combined effect of mechanical force and enzymes that destroy the plant cell wall, 2 — penetration of the fungus through stomata, 3 — secretion of phytotoxins to modify plant physiology, immune system, and metabolism in biotrophic fungi 4 — penetration of the fungus through the wound; 5 — secretion of phytotoxins for degradation of the cell wall and cytotoxic effect on plant cells.
Bacterial pathogens contain several types of genes: virulence genes, which play a major role in infection and contribution to virulence, and disease-specific genes, which are important for disease manifestation Fig.
There are a series of genes that are required for host recognition, pathogen attachment to the plant surface, formation of infectious structures, as well as penetration and colonization of the host tissue. Pathogenic factors may either remain attached to the bacterial surface or can be released to the external environment. Pathogenic bacteria cause many serious plant diseases around the world, although not as many as fungi or viruses; however, the economic damage from bacterial diseases is relatively less severe than that from fungi and viruses [ 44 ].
Bacteria wreak havoc at all stages of crop production. Furthermore, due to the increase in the average annual temperature, there is reason to believe that the damage from bacterial spot and economic loses will only continue to grow in the coming years [ 45 ].
The main symptoms of bacterial diseases are wilting, necrosis, chlorosis, rot, overgrowth galls , and scab. They cause phytoplasmosis and growth retardation. Like mycoplasmas, a related genus of bacteria, phytoplasmas are apparently one of the most primitive and autonomously reproducing living organisms [ 46 ]. The genome of phytoplasmas is 0.
Phytoplasmas exhibit gliding motility [ 49 ], while representatives of the genus Spiroplasma have a spiral shape and move in a twisting motion [ 50 ].
Cultivation of phytoplasmas in axenic cultures is quite difficult, which indicates their greater dependence on the host metabolism [ 51 ]. Phytoplasmosis significantly decreases both crop yield and its quality. There is only one known case of positive phytoplasmosis, which leads to an economically useful effect: it is phytoplasmosis of poinsettia, a popular seasonal ornamental plant. Fungi are characteristic representatives of the domain Eukaryota.
Unlike bacteria, they have a complex cell structure with a distinct nucleus and mitochondria. Fungal genome is much smaller than that of most eukaryotes but much larger than prokaryotic. Fungi have a cell wall, which usually consists of chitin, mannan, and chitosan, and also includes various proteins, lipids, and polyphosphates. Fungi form a mycelium: a system of thin branching hyphae, which sometimes lacks intercellular septa and forms a syncytium.
Fungi are found in all ecological niches and can cause significant harm. Fungi appear to be evolutionarily much older than plants; the duration of their coexistence can be compared to the evolutionary age of higher plants [ 53 ]. However, fungi sometimes disrupt the delicate balance of the mutually beneficial cooperation by turning into plant pathogens classified as biotrophs, hemibiotrophs, and necrotrophs.
As a rule, pathogenic fungi enter plants through damaged leaves and stomata. These fungi exhibit specificity and interact with the host via special biotrophic hyphae in the interphase region where biomolecules synthesized by the plant are absorbed [ 57 ]. Haustoria move from the base of the appressorium through the destroyed areas and penetrate the lumen.
As a rule, haustoria contain a large number of mitochondria and ribosomes with a well-developed endoplasmic reticulum; haurtorium is usually separated from the plant cell by invagination of the host plasmalemma [ 58 ]. At the same time, one can assume that an increased pressure of plant defense can cause a transition from biotrophy to necrotrophy [ 53 ]. Phytopathogenic fungi are the most dangerous plant pathogens to cause harm at all stages of crop production.
The most common way to fight fungi is considered to be treatment with fungicides. The use of fungicides is associated with serious environmental and medical risks, namely the emergence of resistance and horizontal transfer of resistance genes, with the occurrence of species with multiple resistance [ 59 ].
At least chemical compounds with different mechanisms of action are used as fungicides in world agriculture; however, there have been cases of resistance among various types of phytopathogens against almost all major classes of fungicides recorded to date [ 60 ]. The main symptoms of fungal diseases include wilting, spotting, mold mycelium and sporulation of the fungus on the surface of affected organs , pustules accumulation of fungal spores , overgrowth, deformations, mummification shrinkage, darkening, and compaction of the infected tissue , and rot [ 2 ].
To date, more than 10, fungal species associated with plants have been discovered, and it is not surprising that fungal infections cause more harm than the diseases caused by other pathogenic microorganisms [ 61 ]. Plant viruses, like those infecting humans and other animals are spread by some sort of contact. Some are spread by vectors such as aphids and thrips. Shown here is rose mosaic virus. Some are carried by single celled organisms such as Polymyxa betae which transmits Beet necrotic yellow vein virus by infecting plant roots.
If plant leaves become damaged by cultivation or animals feeding, sap containing virus may be transmitted another plant. This has been observed with cucumber mosaic virus. Although rare, nematodes and fungi are also implicated. Parasitic plants can spread viruses. Tobacco mosaic virus can even survive in dead infected tobacco leaves in cigarettes. All virus diseases will be transferred from infected parent plants through new bulbs, corms, tubers, stolons, and cuttings.
As we know from human virus epidemics, animal viruses are almost impossible to control except by avoiding exposure, mounting our own immune system to fight off the infection or by vaccination. Some viruses do not infect the growing tip of a plant the meristem and this is often used to advantage by growers. The unaffected tissue from the meristem of a plant can be tissue-cultured and can result in virus-free plants. There are many virus diseases not yet in Australia, so quarantine is an important method of preventative control.
Symptoms along with other criteria are used to identify virus diseases. An advanced array of symptoms can be recognized today as expressions of viral diseases in plants. Some of these would include abnormal leaf color, abnormal vein patterns of leaves, mottling in leaves [ figure 1 ], [ figure 2 ], spotting patterns in leaves, and abnormal leaf shape [ figure 4 ], and [ figure 7 ]. There are also abnormalities of flower color, fruit size, shape and color.
Viruses can be spread from plant to plant by several means. Some of these would include transmission from the parent plant to an offspring through the genetic structure of the plants. In some cases, the organism creating the wound can also be carrying the virus and then introduce it to the plant. Viruses are often transmitted from one plant to another by vectors , e. Sap-feeding insects like leafhoppers, planthoppers, aphids, and whiteflies can transfer viruses from one plant to another.
Gardeners can also transfer viruses from an infected plant to a healthy plant when pruning or propagating, if care is not taken to sterilize tools between cuts. Gardeners typically know viruses by their descriptive names that reference the disease they cause, in part because their full scientific classification is somewhat complicated.
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