HOST PARASITE INTERACTION

HOST PARASITE INTERACTION

13.      HOST PARASITE INTERACTION

13.1.    Recognition and entry processes of different pathogens
The germination or multiplication of an infective propagule in or on a potential host through to the establishment of a parasitic relationship between the pathogen and the host. The process of infection is influenced by properties of the pathogen, the host and the external environment like temperature, moisture, light, aeration, nutrient availability and pH.
While some parasites colonize the outside of the plant (ectoparasites), pathogens may also enter the host plant by penetration, through a natural opening (like a stomatal pore) or via a wound. The symptoms of the diseases produced by these pathogens result from the disruption of respiration, photosynthesis, translocation of nutrients, transpiration, and other aspects of growth and development. 
The "infection process" can be divided into three phases: pre-entry, entry and colonization. The initial contact between infective propagules of a parasite and a potential host plant is called inoculation. Pathogens use a variety of stimuli to identify a suitable entry point. Several fungi use topographical on the plant surface to guide them towards a likely stomatal site. Once the hypha reaches a stoma, volatile compounds escaping from the pore appear to provide a signal for the formation of a specialized penetration structure, the appressorium. Sugars, amino acids and minerals secreted by plants at the leaf surface can non-specifically trigger spore germination or provide nutrition for the pathogen. Some pathogenic spores will not germinate in the absence of these substances.
Just as glycans are major components of the outermost surface of all animal and plant cells, so too are oligosaccharides and polysaccharides found on the surface of all bacteria and viruses. Thus, most (if not all) interactions of microbial pathogens with their hosts are influenced to an important degree by the pattern of glycans and glycan-binding receptors that each expresses. This holds true at all stages of infection, from initial colonization of host epithelial surfaces to tissue spread, to the induction of inflammation or host-cell injury that results in clinical symptoms.
Many pathogens have to breach the barriers of plant waxes, cutin and suberin that cover plants as well as plant cell walls before establishing a parasitic relationship with their hosts, the physical and chemical characteristics of this adhesion are often required for successful penetration, particularly where this is achieved by the exertion of mechanical force. Products of degradative enzymes acting on host tissues are through specialized structures called haustoria. some of these, such as degradative enzymes, are also involved sources of nutrition for necrotrophic pathogens but the subtler biotrophic pathogens feed in this process.
13.2.    Adhesins and Invasion
Most microorganisms express more than one type of adherence factor or “adhesion.” Adhesion may be mediated through terminal sugars or internal carbohydrate motifs. The specific carbohydrate ligands for bacterial attachment on the animal cell are often referred to as adhesion receptors and they are quite diverse in nature
In a number of cases, the key adhesive factor is an assembly of protein subunits that project from the bacterial surface in hair-like threads known as pili or fimbriae. Such pili are usually composed of a repeating structural subunit providing extension and a different “tip adhesin” that actually mediates the host-cell interaction. Often the structural genes and enzymes for pilus assembly are encoded in a bacterial operon. Colonization of the host after penetration. For certain pathogens, the epithelial attachment is a two-step process, in which a microbial glycosidase acts upon a target cell polysaccharide to modify its structure into a novel glycan, which then serves as the adhesion receptor. Glycan–lectin interactions play pivotal roles in enabling certain pathogens to penetrate or invade through epithelial barriers, whereupon they may disseminate through the bloodstream to produce deep-seated infections.
13.3.    Viral Infection
The specific binding of a virus particle to a target receptor on the host-cell surface is a prerequisite for viral entry and the subsequent intracellular replication steps in the viral life cycle. In the attachment part, virus attached to the host cell receptor and gain entry into the cell. In the eclipse stage, the virus is busy with replication. Viral titer decreases when there are no infectious particles present during the replication process. The virus is detected in the external medium only when released. In the burst or released part, new progeny virus gathered and is then released.
Virus attachment protein (VAP) attaches to the receptor of the host cell. The virus can enter the host cells through three different routes. The three different routes are Direct penetration, Fusion (direct penetration), Endocytosis. A process by which materials from outside the cell, such as proteins, are absorbed by cells through engulfing of these materials with their cell membrane is known as endocytosis. All cells of the body use endocytosis due to those important substances are large polar molecules which cannot pass through the plasma membrane.
Clathrin molecule mediates the major route for endocytosis in most cells. Clathrin is a large protein which helps in the formation of a coated pit on the inner surface of the cell’s plasma membrane. A coated vesicle is formed in the cytoplasm of the cell when this pit buds into the cell. 
The virus needs to be spread so that it can continue reproducing and ensuring the survival of the virus species. The effectiveness of viral transmission depends on virus concentration and the route of transmission. The higher the viral concentration, the higher the chances of transmission. Some modes of virus transmission include respiratory secretions and salivary pathways.
13.4.    Pathogen recognition
Plants use a vast array of signals originate from micro-organisms and the environment to recognise pathogens and elicit plant defence responses in which Elicitors (specific and nonspecific), Hypersensitivity, a phytoalexin, etc. are involved. Non-specific elicitors of biotic and abiotic origin induce host defences in a broad range of host species. Abiotic elicitors such as heavy metal ions or UV light can induce stress responses in exposed tissues, which may provide an additional barrier to invading pathogens whereas biotic elicitors include cell wall fragments released from fungi and bacteria, hydrolytic enzymes of plant or pathogen origin, some peptides, glycoproteins and polyunsaturated fatty acids. These elicitors induce defence responses in a range of host species. 
Specific elicitors enable defence against a very specific pathogen and are conditioned by avirulence genes in that pathogen. Avirulence genes determine the pathogen's host range but are only able to function in the presence of another set of genes, the 'hypersensitive response and pathogenicity' (Hrp) gene cluster. Some Hrp gene products are involved in distinguish the pathogen from host recognition, thus playing a role in both virulence and avirulence.These are encoded by avirulence genes, and these peptides are believed to bind to receptor peptides, encoded by host resistance genes. Recognition of the avirulence gene products by the host triggers signal transduction pathways that cause a massive shift in gene transcription and plant cell metabolism, and local and systemic signals are released that prime the rest of the plant against further infection
For a biotroph to form a successful infection, it must establish basic compatibility with its host. Incompatibility between a host and a pathogen results in the recognition of the pathogen and activation of defence mechanisms, while compatibility results in infection. At various points pathogen is identified by the host. At the cell membrane, cell wall, by physical responses of the plant, and by pathogenesis-related proteins etc.
At cell membrane level a change in membrane permeability after exposure to a pathogen causes fluxes in ions, such as K+, H+, Ca2+ and oxidative burst which involves the generation of reactive oxygen species, such as hydrogen peroxide results in changes to gene activation and triggers signals that affect gene expression respectively that results in the defence processes. At the site of infection ROS (reactive oxygen species) are also produced that capable of killing micro-organisms directly. Like cell membrane defence process cell wall also responsible for the pathogen identification. At cell wall level attempts of a pathogen to penetrate a host cell  Preparations for the reinforcement of the cell wall get begin which is responsible for improving the host cell resistance. It’s characterized by intensification of cytoplasmic streaming and the accumulation of host cytoplasm around the site of attempted penetration. 
Besides at the level of the cell wall and cell membrane Hypersensitive cell death is another widespread mechanism used by hosts to prevent the spread of a pathogen. Besides this Phytoalexins are also to prevent pathogen infection. Phytoalexins are low molecular weight antibiotics produced by many (but not all) plants in response to infection. There are many biotic and abiotic elicitors of phytoalexin production. Phytoalexins inhibit the growth of bacteria and fungi in vivo and in vitro. They include pterocarpans, sesquiterpenes, crypto phenols, isocoumarins, isoflavonoids, and others. 
In the reference of physical response shown by the host after the pathogen infection the ability to repairing wounds can help protect the plant from further infection by other pathogens. Cork cells, which have thick, suberized cells walls can create a barrier to further colonization by the pathogen. 
Pathogenesis-related proteins also play a major role in prevention to pathogens these are responsible for disrupt pathogen nutrition. Chitinase and glucanases enzyme accumulate in the vacuoles, and glucanase is also sometimes secreted into the intercellular space. They dissolve the fungal cell wall, fragments of which then elicit hypersensitive cell death.
The success of defence responses is increased if activated in combination. Passive mechanisms, coupled with rapid active responses and slower follow-up defences provide a broad defence front to the plant. The specific interaction between host and pathogen is, of course, crucial to the success of the plant's resistance or the pathogen's invasion and is mediated by the many pathways involved in producing or detecting elicitors, enhancers, suppressors and secondary signals.
13.5.    Alteration of host cell behaviour by pathogens 
A cell transmutes a stimulus on the outside of the plasma membrane into changes in the cell's physiological program by means of intracellular signalling pathways. These are usually triggered by the ligation of an external ligand, to a receptor on the cell surface. This ligation causes activation of the receptor, commonly by phosphorylation and or conformational changes, resulting in activation of second messengers within the cytosol. These second messengers are often protein kinases, which then phosphorylate other kinases to continue a cascade that ultimately results in the activation of effector molecules, such as transcription factors or actin filaments, and causing a change in the cell's behaviour. It should be emphasized that the activity of an intracellular pathway is normally determined by a balance of both positive and negative regulation. Many prokaryotic and eukaryotic pathogens, including Leishmania, have evolved various strategies to exploit host cell signalling regulatory mechanisms by distorting this balance between positive and negative influences.
In another way, we see that certain viruses have the ability to enter a cell and follow one of two alternative courses. They both multiply in a normal manner and are eventually released from the cell, or they may be dormant in the cell and eventually transform the cell into a malignant cell. It is believed that the transformation process involves the integration of viral nucleic acid into the host chromosome. pathogens express effector proteins that are adapted to allow them to infect certain plant species, these effectors often enhance pathogen virulence by suppressing the basal host defences. There are many examples which give a description of alteration behaviour of the host cell by the pathogen. These are as following: 
•    Damage or destroy host cells, Example HIV, Salmonella. Epithelial cells in the intestine take up the organism (pathogen) which  posses  host specific ligand that fit onto the receptor proteins of host and destroys the brush border of microvilli because of this host creates a ruffled surface which causes the detachment of  invaded cells from intestinal wall and creates inflamed lesions followed by secretion of large amounts of watery fluid into the lumen of the gut causes diarrhoea.  
•     Toxic waste production eg. Vibrio cholera. It is harmless but produce harmful exotoxins (toxins released from the cell) that causes loss of chloride and hydrogen carbonate ions from the intestinal cells and Osmotic loss of up to 10 liters of water per day which results into the impaired absorption of water and salt from the gut and causes severe watery diarrhoea and death from dehydration. 
•    Body's own immune response to the presence of microorganisms which produce the symptom example: Mycobacterium tuberculosis. The body tries to destroy the invading bacteria this causes inflammation and damage to the surrounding cells occur because of these lesions may become hard or spongy, leaving holes in the lungs, sometimes damaging the blood vessels. 
Some bacteria will cause all the above three; some require a large number of bacteria for a disease; some will only cause disease with a few numbers of bacteria. Microorganisms may enter the lymphatic system via tissue fluid and are carried around the body. The ability of bacteria to cause disease relies on location which tissue is colonized infectivity and can easily a bacterium can enter the host cell and spread toxin within the body and causes disease. 
Suppression of immune mechanisms causes infection. Viruses are known to replicate in the cells of the lymphoreticular system, these viruses, therefore, can affect the immune system. Viruses or virus-like particles have been found in the thymus, lymph nodes, spleen, bone marrow, stem cells, plasma cells, lymphocytes, macrophages, monocytes, polymorphonuclear leukocytes and Kupffer cells. The nature and extent of the immunologic alteration depend on the organ or cell type infected and the species of virus causing the infection.
13.6.    Viral-Induced cell transformation
Viral transformation is the change in growth, phenotype, or indefinite reproduction of cells caused by the introduction of inheritable material. The term can also be understood as DNA transfection using a viral vector. Viral Transformation and Oncogenesis focused on the process of viral-encoded gene products contribute to the establishment and maintenance of viral-induced malignancies. virus replication cycle contains six phases. These are Attachment, penetration, uncoating, replication and expression, assembly and release.
Viral infection is of cytocidal, persistent and transforming type. Viral transformation is most commonly understood as transforming infections. In order for a cell to be transformed by a virus, a bacteriophage lands on a cell and pins itself to the cell. The phage can then penetrate the cell membrane and inject the viral DNA into the host cell. it can be immediately taken up by the host's genome. The viral DNA will replicate along with the original host DNA during cell replication causing two cells to now be infected with the virus. The process will continue to propagate more and more infected cells because of cell lysis (releasing the virus from the infected cell by bursting its membrane and this kills the infected cell). This process is in contrast to the lytic cycle where a virus only uses the host cell's replication machinery to replicate itself before destroying the host cell. 
Viral transformation disrupts the normal expression of the host cell's genes in favour of expressing a limited number of viral genes. The virus also can disrupt communication between cells and cause cells to divide at an increased rate.
Viral transformation can easily be detected by physiological, biochemical and genetic responses or changes of the host cell. In physiological changes, high saturation density, anchorage-independent growth, loss of contact inhibition, loss of orientated growth, immortalization, disruption of the cell cytoskeleton are included.
While biochemical changes the Viral genes are expressed through the use of the host cell replication machinery, therefore, many viral genes have promoters that support binding of many transcription factors found naturally in the host cells. These transcription factors along with the virus own proteins can repress or activate genes from both the virus and the host cell genome. Many viruses can also increase the production of the regulatory proteins of the cell. 
Furthermore in the reference of genetic changes that occur in the host cell in a variety. In the case of lysogeny, the viral DNA can either be incorporated into the genetic material of the host cell or can persist as a separate genetic vector. either case can lead to damage of the chromosomes of the host cell.
13.6.1.    Pathogen-induced disease in animals and plants
Infectious diseases are a major cause of death, disability, and social and economic disorder for millions of people throughout the world. Prevention and treatment strategies for infectious diseases derive from a thorough understanding of the complex interactions between specific viral or bacterial pathogens and the animal host.
13.6.2.    Bacterial-induced disease in plants
Bacterial induce diseases in a wide range of plants. Symptoms can range from mosaics, resembling viral infections, to large plant abnormalities, such as galls or distorted plant parts. Hormone disruption can produce characteristic abnormal growths on roots, stems, and floral structures (phyllody) and sometimes abnormal flower colors (virescence). The most common symptoms are spots on leaves or fruit, blights or dead-ending of tissue on leaves, stems or tree trunks, and roots of any part of the plant, usually roots or tubers. Wilts can also occur, due to plugging of vascular tissue. Symptoms may vary with photoperiod, plant variety, temperature and humidity, and infective dose. In some cases, symptoms may disappear or become inconsequential with further growth of the plant. 
13.6.3.    Bacterial diseases of animals
Besides plants bacteria are also responsible for the causing of diseases in animals in a wide range. These are Anthrax, Leptospirosis, Anaplasmosis, Tularemia etc. the  description of these diseases are as follow:
13.6.3.1. Anthrax
It’s an infectious disease caused by a bacterium called Bacillus anthracis, which can change into spores that can last for a long time in the environment before germinating. It is carried by wild and domestic animals in Asia, Africa and parts of Europe.
There are two main types of anthrax. The Cutaneoushrax starts as a skin bump that ulcerates, which is not generally a serious illness. The second type is inhalational anthrax, is normally less common and symptoms begin as a flu-like illness which progresses to pneumonia, respiratory failure and septicaemia, which can lead to shock and death. There is also a third type, intestinal anthrax, but this is a very rare form of food poisoning and results in fever and severe gut disease.
13.6.3.2. Leptospirosis
It is a bacterial disease that affects humans and animals. It is caused by bacteria of the genus Leptospira. Symptoms of leptospirosis include high fever, severe headache, chills, muscle aches, and vomiting, and may include jaundice (yellow skin and eyes), red eyes, abdominal pain, diarrhoea, or a rash. If the disease is not treated, the animal could develop kidney damage, meningitis, liver failure, and respiratory distress. In rare cases, death occurs. Treatment is done with antibiotics.
13.6.3.3. Anaplasmosis
Anaplasmosis is a type of tick fever that is caused by the invasion of red blood cells by the rickettsial blood parasite Anaplasma ovis. In cattle, the disease is caused by A. marginale or A. centrale. Transmission is through insect vectors, especially horse flies, ticks and flies. Ticks are the natural vectors and a range of tick species has been shown to be capable of transmitting infection, e.g. Boophilus, Dermacentor, Rhipicephalus, Ixodes, Hyalomma, Argas and  Ornithodoro.
13.6.3.4. Tularemia
It is caused by the bacterium Francisella tularensis found in animals, especially rodents, rabbits, and hares.
Symptoms of tularemia could include sudden fever, chills, headaches, diarrhoea, muscle aches, joint pain, dry cough and progressive weakness.
13.6.3.5. Bovine tuberculosis
There are three types of TB (Bovine Tuberculosis) these are human, avian, and bovine. Human TB is rarely transmitted to non-humans, avian TB is typically restricted to birds, and bovine TB – or cattle TB – is the most infectious, capable of infecting most mammals. Bovine TB is caused by the bacterium Mycobacterium bovis, which is part of the Mycobacterium tuberculosis complex.
13.7.    Virus-induced injury in plants
Virus infections are the cause of numerous plant disease syndromes that are generally characterized by the induction of disease symptoms such as developmental abnormalities, chlorosis, and necrosis. There are many types of plant virus, and some are even asymptomatic. Under normal circumstances, plant viruses cause only a loss of crop yield. Most plant viruses have small, single-stranded RNA genomes. However, some plant viruses also have double-stranded RNA or single or double-stranded DNA genomes. These genomes may encode only three or four proteins these are replicas, a coat protein, a movement protein, in order to allow the cell to cell movement through plasmodesmata, and sometimes a protein that allows transmission by a vector. Plant viruses can have several more proteins and employ many different molecular translation methods.
Plant viruses are generally transmitted from plant to plant by a vector, but mechanical and seed transmission also occurs. Vector transmission is often by an insect (for eg. aphids), but some fungi, nematodes, and protozoa have been shown to be viral vectors. In many cases, the insect and virus are specific for virus transmission such as the beet leafhopper that transmits the curly top virus causing disease in several crop plants.
13.8.    Virus-induced injury in Animals
The cytopathic effect (degeneration of the cell due to viral infection) experienced by the cells is on the cellular level. These injuries may include Detachment from substrate, Membrane permeability (changes in permeability hinders the transport of materials required for the cell),Lysis (cell death by bursting its membrane), Shape alteration (the shape of the cell is changed which might affect its functions eg. RBC) Apoptosis (cell death caused by a series of morphological changes that bring about the breakdown of the various functions of the cell),  Membrane fusion or Synchytrium. (a structure containing many nuclei).Virus-induced injuries can cause some serious damage such as the shutdown of cellular functions in the host. For example, the polio virus shuts down the cellular functions of the neurons in the CNS and PNS (peripheral nervous system), resulting in cell death which leads to paralysis or even death.
Another kind of injury would be immunopathological (immune system or response related). Here, the immune system is impaired due to infection of the immune cells such as the WBC. The body becomes relatively weak because its own WBCs are fighting each other. However, due to the weakening of the body’s immune system, the body itself will try to enhance its immune response by, for example, increasing body temperature to try to kill the virus, thus causing haemorrhagic fevers.
13.9.    Cell-Cell fusion in both normal and abnormal cell
Membrane fusion is a fundamental requirement in numerous developmental, physiological, and pathological processes in eukaryotes. So far, only a limited number of the viral and cellular Fuso gene, proteins that fuse membranes, have been isolated and characterized. The basic building blocks of all organisms are cells, whose outer surfaces are lipid bilayer-based plasma membranes. The plasma membrane normally functions as a barrier between the inner contents of individual cells and between the cells and the extracellular space. In prokaryotes, it is not known whether membrane fusion occurs in processes where two bacteria are united; for example, during conjugation contrast, cell fusion has been identified as an important stage of development in most eukaryotes from yeast to humans. cell fusion is used to unite gametes and other cells, to alter cell differentiation states, and to resculpt organs. membrane fusion is essential for the progression of different pathological events such as viral entry into host cells and, possibly, tumour progression.
Despite the diversity in the organisms and cell types that utilize cell fusion in normal physiology and pathology, most fusion reactions occur via a common stereotypic sequence of events starting with cell-cell recognition, alignment, and adhesion. This is followed by an actual fusion event that merges the two cells together by the tethering of plasma membranes, the formation of aqueous pores between the membranes, and expansion of these pores to clear the membranes from the fusing cells junction. In addition to viral-host membrane fusion, some viral fusogens mediate fusion between virus-infected cells and adjacent noninfected cells. Diverse triggers activate specific viral envelope glycoproteins that serve as fusogens. Activated fusogens fuse the viral envelope with either plasma or endosomal membranes, delivering the viral genome into the cytoplasm of the host cells.
13.10.    Viral Fusogens to Fuse Membranes
Viral fusogens unite membranes. There are five principles that appear to be shared by most of the studied viruses First, the prefusion structures of oligomeric viral glycoproteins are localized to one of the fusing membranes (the virus). Second, fusion triggering involves processing, receptor binding, exposure to low pH, or some combination thereof. Third, triggering elicits diverse conformational changes involving coiled-coils and or β sheets exposing and inserting amphiphilic fusion domains into the opposing membrane. Fourth, diverse viral fusogens establish remarkably similar hairpin rod-like structures. Fifth, hairpin formation, interactions between the fusion domains and membranes, and, likely, lateral protein-protein interactions drive membrane rearrangements into a hemifusion intermediate followed by fusion pore formation and expansion.


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