MICROBIOLOGY PAPER

VIRUS IN PLANTS AND ANIMALS

By:

Annisa Farah Dilla (100210103060)

Yessi Rizki Meirina           (100210103062)

BIOLOGY EDUCATION STUDY PROGRAM

DEPARTMENT OF MATHEMATIC AND SCIENCE EDUCATION

FACULTY OF TEACHER TRAINING AND EDUCATION

2012

INTRODUCTION

           

            Viruses cause a number of economically important diseases in animals and birds. Some viruses of animals can cause human infection or can mutate to give rise to human infection. The SARS virus, which came from an animal source, led to an outbreak of human infection and highlights the significance of viruses that are harboured in animals. Influenza viruses, which persist in their natural bird host, can sometimes infect humans. The study of animal viruses contributes to our understanding of viral infection in general.

Virology is the study of everything connected with virus.Virologi plant is one of the virology branch in particular studying the virus that infects plants tumbuhan.Virus was first discovered in 1576, as the pathogen that causes symptoms of discoloration of the tulips, which was originally become symptomatic in a solid color stripe (spotting line). Then in 1886, Prof. Adolf Meyer conducted an experiment to study the etiology of diseases caused by virus mosaic symptoms on tobacco plants (tobacco mosaic virus / TMV). In 1892 Dimitrii Ivanowski found that tobacco mosaic pathogens can pass through the sieve bakteri.and 1898, Martinus Beijerinck concluded based on the experiments that pathogen is not the kind of tobacco mosaic disease-carrying fluid life. And findings have paved the way to the development of subsequent virologic, so he called the father of Virology.

Viruses are microscopic parasites that infect cells biologis.Virus organism can only reproduce in living material to invade living cells and use because the virus does not have the equipment to their reproduction. Within the cellular host cell, viruses are obligate parasites and their hosts out to be not powerless. Commonly virus contains small amounts of nucleic acid (DNA or RNA, but not a combination of both) is covered with a sort of protective material consisting of proteins, lipids, glycoproteins, or combinations of them all.Genom virus encodes a protein that is used to contain genetic material and protein needed in the life cycle.
            The term usually refers to virus particles that infect the cells of eukaryotes (multicellular organisms, and many types of single cell organisms), while the term bacteriophage or phage is used for this type of attack the cell types of prokaryotes (bacteria and other organisms that are not core cell) .

Viruses are often debated status as a living because he can not run independently of its biological function. Because of its distinctive characteristics of this virus is always associated with certain diseases, both in humans (eg influenza virus and HIV), animals (eg bird flu virus), or plants (eg tobacco mosaic virus / TMV. Plant viruses, such as viruses and bacteria that attack animals, plants have special characteristic, Virus properties in some respects different from the virus that attacks the animal or bakteri. One of difference is the mechanism of virus penetration into host cells. Viruses of plant can only enter the cell occurring plants through wounds caused mechanically or by insects is due to virus vector.

VIRUSES IN PLANTS

Plants in disease when the plants are attacked by pathogens (parasites) or influenced by abiotic agents (fisiopath).Plants viruses do not have the tools to penetrate the cell wall penetration. The other way, most of the viruses that attack animals and bacteria can penetrate directly through cell membranes, such as bakteriofage ( viruses that attack bacteria) has a penetration tool that can penetrate the bacterial cell membrane. In the laboratory, plant viruses can be transmitted in several ways, namely by connecting (grafting) with the healthy plants and diseased plants through tissue culture of virus-infected explants. Some plant viruses can be transmitted mechanically by rubbing the extract on the surface of the leaves of diseased plants that have been sprinkled karbondurum. In the field of plant virus transmission occurs through vectors (insects, nematodes and fungi).

Some plant viruses also spread by seed from parent plants infected with the virus. Unlike the defense system in animals can make antibodies to prevent infection virus.Mekanisme such defense was not the case in plants. Diseased plants will always contain the virus for life, so it will always carry on breeding crops mainly vegetative propagation. Plant viruses can infect all parts of the host plant except the root meristem and apical shoot.Beberapa virus that only attacks the plants there are certain parts of the plant host.In general, the virus can not pass the new plants are propagated by seed.In general, plant diseases can be classified or grouped as follows:

·                     Plant diseases  infections (parasitic)
a. Diseases caused by fungi
b. Diseases caused by prokaryotes (bacteria and micoplasma)
c. Diseases caused by parasites of higher plants
d. Diseases caused by viruses and viroids
e. Diseases caused by nematodes
f. Diseases caused by protozoa

·                     Non-infective diseases, or abiotic (fisiopath) is a disease caused by:
a. Temperature is too high or too low
b. Deficiency or excess soil moisture
c. Deficiency or excess light
d. Lack of oxygen
e. Air pollution
f. Difesiensi nutrient
g. Nutrients poisoned
h. Acidity or salinity
i. Toxicity of pesticides
j. Technical culture is wrong

Among plant viruses, the most common forms are:

·                     Isometric: it seems the ball and (depending on species) of approximately 18nm in the diameter. The example here shows tobacco necrosis virus, Necrovirus genus with 26 nm diameter particles.

·                     Rod-shaped: about 20-25 nm in diameter and from about 100 to 300 nm long. It looks stiff and often have a clear central canal (depending on the staining method used). Some viruses have two or more different lengths of these particles and contain components of different genomes. The example here shows the tobacco mosaic virus, genus Tobamovirus with particles 300 nm long.

·                     Filamentous: usually about 12 nm in diameter and more than a flexuous rod-shaped particles. They can be up to 1000 nm in length, or even longer in some cases. Some viruses have two or more different lengths of these particles and contain components of different genomes. The example here shows the Potato Virus Y, Potyvirus genus with a particle length of 740 nm.

·                     Geminate: twin isometric particles about 30 x 18 nm. These particles are diagnostic for virus in the family Geminiviridae which is widespread in many plants, especially in the tropics. The example here shows the Maize streak virus, Mastrevirus genus.

·                     Bacilliform: Short round-ended rod. These come in various forms to about 30 nm wide and 300 nm long. This example shows virus Cacao swollen shoot, Badnavirus genus with 28 x 130 nm particles.

           Therefore, for the occurrence of plant diseases, at least be in contact and there interaction between two components (plants and pathogens). If at the time of contact and for a few moments later a state of very cold, very hot, very dry, or some other extreme, it may not be able to attack the pathogen or the plant may be able to withstand the attack, although there has been contact between the two, the disease is not developed. It appears that all three components must also be there to be progression of the disease. However, each of the three components may exhibit a tremendous diversity, and if one component is changed, it will affect the level of disease in individual plants or in plant populations.

           Interaction of all three components have been generally described as a triangle, commonly called the disease triangle (disease triangle). Each side is proportional to the total number of properties of each component that allows the disease. For example, if the plants are resistant, generally at a disadvantage or with the wide spacing of the disease and the disease triangle will be small or nonexistent, whereas if the plants are vulnerable, susceptible to the growth rate or the spacing of the meeting, the sides will host the length and number of potential diseases will increase. By the same token, more virulent pathogens, in abundance and in an active state, then the pathogen will grow longer and larger number of potential illness.

           Also more favorable circumstances that help the pathogen, for example temperature, humidity and wind that can reduce the level of host resistance, then the environment will become longer and larger number of potential diseases.

      Persistence of virus in the host called infection .Infection that began at the site of entry of virus called a local virus. Through plasmodesmata, the infection will spread slowly into the surrounding cells. When it reaches the organ transport networks, together with the virus into the phloem asimilation and spread passively to the young plants and fruit growing as well. There, the virus re-entering the parenchymal tissue and slowly move from cell to cell. This process is reflected in a beautiful pattern of a particular line or a centralized clear-ringed spots on leaf veins. In the mosaic, a growing group of cells of certain cells that are infected, the meristematic later developed into a hospital network islands, bordered by groups of cells that apparently healthy.

      The viruse in radiates through the entire system of the host and the infection becomes systemic. Most rapidly after two days, local symptoms become visible in the entry of the virus and systemic symptoms will appear after about 5-14 days or even weeks after the entry of the virus in the plant is growing. The grace period between the entry of the virus and the first symptoms appear to so-called incubation period.

      Effect of virus infection on macromolecular synthesis were observed in decreased synthesis of nucleic acids, proteins, and it carbohydrat. while, virus infection on host plant photosynthesis can be observed on the effect of the reduced rate of viral infection on host plant photosynthesis.

      Virus replication involves the organization of cells and metabolites in the host for the virus to multiply in host cells. Understanding of viral replication, it is known how the virus can induce disease host plants through molecular and biochemical processes. Three ways a virus can induce disease on host plants, namely

·                     the use of plant metabolism for the synthesis of the virus, so the plant will experience a scarcity of food metabolites, such as amino acids, energy (ATP), nucleotides, and enzymes.

·                     the accumulation of virions or part of the virus, such as envelope protein subunit, another component of the viral genome and the virus that causes pathological reaction in the host plant.

·                     the impact of non-typical structure of the polypeptide encoded by the genes of  the virus.

.     Virus infections in general will reduce the vegetative and generative growth of host plants. Many studies have shown that viral infections reduce plant growth, reduce yield and yield plant components.Some mechanism of virus leads to reduced plant growth indicated by ternatut symptoms (stunting). Three physiological mechanisms that can lead to inhibition of plant growth, namely

ü    changes in plant growth hormone activity,

ü    reduction of photosynthesis that plants can be utilized, and

ü    reducing the ability of plant nutrients in the decision.

      The emergence of viral diseases can be influenced by host plant, virus, and the environment. Disease occurs when the virus that attacks the virus strain is virulent, susceptible plants are attacked, and environmental conditions favor disease development time. Host factors that influence viral infection and disease are age and plant genotype. in systemic infection, plant age affects the spread of the virus in the current crop of elderly host.The more plants infected with the virus, the more limited spread of virus in plants. While the influence of plant genotype corrections to virus. Characteristic resistant crop plants against viruses is controlled by the genes of plants. The reaction of the host against virus infection can be divided into four, as follows.

ü    Resistant, if the plant is only a slight infection or infections are limited.

ü    Hypersensitivity, when the plants show symptoms of necrotic local spots on the site of infection and the virus does not spread to other parts of the plant.

ü    Tolerant, if the virus infects the plant and spread to other parts of plants as well as on the susceptible plants, but the result of the plant was not significantly decreased.

ü    Vulnerable, when the plants showed severe symptoms followed by a decrease in high yield.

             Conditions affecting the environment in which plants grow virus infection. Environmental conditions prior to inoculation, at inoculation, and post-inoculation of the virus will affect the susceptibility of plants to viruses.

      Plant virus infection cycle begins when the virus into the cytoplasm through the help of a vector or mekanis. After injuries in the host cell cytoplasm, the virus releases the viral genome (DNA or RNA nucleic acid) of the virion (uncoating). Furthermore, the viral nucleic acid joins with trap host metabolism to viral protein translation. Expression of viral genes necessary for viral genome replication and viral pathogenesis. Replication of viral genomes directed to the synthesis of new virus (DNA or RNA). Preparation of new virions through viral genome packaging by capsid protein subunits form a new virus virus. After formed, there was transfer of virus to surrounding cells via plasmodesmata. Beside, the long-distance migration occurs through vascular system of the host.

            Virus infection would affect cell metabolism and result in changes in biochemical and cell physiology. Changes in cell metabolism will lead to different plant growth when compared with healthy plants. The changes are there that are external or makroskopi on leaves and other plant organs, which in virology called the outer symptoms or external symptoms. In addition, there are also symptoms that are internal within the plant tissue and can only be observed with the aid of a light microscope or a microscope electron.This symstoms also-called internal symptoms.

            In general, symptoms of primary infection in eksternal causing by the inoculated cells and by a secondary infection caused by a virus spread from the primary site of infection to other parts of the plant inang. Primary symtoms infection in the inoculated leaf called a local phenomenon, which in virology described as the local spots. For example local spot symptoms on leaves of Chenopodium amaranticolor infected PStV.

                      

      Plant viruses are generally transmitted by intermediate vectors (insects, nematodes, and fungi), some viruses can be transmitted in the field through mechanical friction between the leaves of plants are sick and contagious health. Virus in mecanic in the field occurs only for the virus that is stable and has a high concentration in host plants, such as TMV and PVX. Some virus can be transmitted through pollen and seeds from parent plants infected with the virus.

       Transmission of the virus also happened through vegetative propagation (grafting, grafting, grafting, and tissue culture). Insects are the most important vector in transmitting the virus of plants, 94% of the phylum arthropods and 6% of the nematode phylum. Insects are the most dominant virus vector according to Black et al., (1991) are aphids (Myzus persicae), leafhoppers (Circulifer ternellus), trips (Frankliniella occidentalis), trips (Frankliniella occidentalis), and white louse (Bemisia tabaci).

A.        Insects.This group forms the largest and most significant vectors and mainly include:

·             Aphids: transmit viruses from different genera, including Potyvirus, Cucumovirus and Luteovirus picture shows a green tick peach Myzus persicae, a vector of plant viruses, including potato virus Y

(Picture of Nuessly & Webb, .. Insect Management Plant leafy vegetables, Eny- 475, September 2003, University of Florida, Institute of Food and Agricultural Sciences (UF / IFAs)).

·             Whiteflies: sending a virus of the genus but especially in the genus Begomovirus.

Picture shows Bemisia tabaci, the vector viruses, including tomato yellow leaf curl virus and Lettuce infectious yellow virus.

·             Hoppers: sending a virus of the genus, including the family Rhabdoviridae and Reoviridae.

Picture shows Micrutalis malleifera, treehopper vector of Tomato pseudo-curly top virus.

·             Thrips: transmit the virus in the genus Tospovirus.

 Picture shows Frankinella occidentalis, western flower thrips is a major vector Tomato spotted wilt virus .

·             Beetles: transmit the virus of the genus, including Comovirus and Sobemovirus

B.         Nematodes: This is the root-feeding parasites, some of which transmit the virus in the genus and Tobravirus Nepovirus. The picture shows an adult female from Paratrichodorus pachydermus, Tobacco rattle virus vector. 

(Figure from Description 398, owned by the Scottish Crop Research Station).

C.         Plasmodiophorids: This is the root-infecting obligate parasites traditionally regarded as fungi but now known to be closer to protists. They transmit the virus, Bymovirus Benyvirus genera, Pecluvirus Furovirus, and Pomovirus.

Picture shows polymyxa graminis, some cereal virus vector including Barley yellow mosaic virus, grown in cells of barley roots.

D.        Mites: transmit this virus in the genus and Tritimovirus Rymovirus. Picture shows Aceria tosichella, Wheat streak mosaic virus vector.

Virus-vector relationships are of several types:

·   At one extreme, the association occurs in the feeding apparatus of insects, in which the virus can be quickly absorbed and then released into the plant cells are different. Insects eat quickly looses virus when feeding on uninfected plants. Relationships like this are called "non-persistent". The best studied example is the potyvirus transmission by aphids.

·   At the other extreme, was appointed to the virus vector, the vector and circulating in the body is released via the salivary glands. Vectors need to feed on infected plants for much longer and there is an interval (possibly several hours) before it can transmit. After becoming viruliferous, the vector will remain so for several days and the family that succeeded because it called "persistent" or "circulative". The best studied example is the transmission of luteovirus by aphids. In a few instances of this type (eg some hopper and thrips), the virus multiplies in the vector and is called"propagative".
    

            Based on the retention properties of the virus (the virus to survive longer in the vector), the relationship between the virus and the vector can be divided into, namely nirpersistence, semipersistence, and the presence of virus in the body persisten.

            Based on vector, the relationship with the vector virus can be divided into tularstilet (stiletborne) and sirculative. The relationship between the virus and the presence of virus in the vector can be divided into two, namely that covers nirsirculative nirpersistence and semypersistence; and sirkulatif (persistence) which covers sirculative and sirlculative propagatif.

Table 1. Nirpersistence Plant viruse

Plant Viruses	Vector
Peanut stripe virus (PStV)	Aphis craccivora, A. glycine
Peanut mottle virus (PMoV)	Aphis craccivora, A. glycine
Cucumber mosaic virus (CMV)	Aphis gossypii
Potato virus Y (PVY)	Mizus persicae
Soybean mosaic virus (SMV)	Aphis glicyne

Table 2. Semipersistence Plant Viruses

Plant viruses	Vector
bean yellow mosaic virus (BYMV)	Mizus persicae
rice tungro virus (RTV)	Nepotetic virescens
citrus tristesa virus (CTV)	Toxoptera citricidus

Table 3. Persistence Plant viruses

Virus Tumbuhan	Vector
banana bunchy top virus(BBTV)	Pentalonia nigronervora
strawberry crinkle virus(SCV)	Chaetosiphon jacobi
rice drawf virus(RDV)	Nipotetic cinticeps
rice grassy stunt virus(RGStV)	Nilaparpata lugens
african cassava mosaic virus(ACMV)	Bemisia tabaci
tobacco leaf crulf virus(TLCV)	Bemisia tabaci

Some diseases in plants caused by the virus, namely:

1.      Budok

      The disease is caused by a virus or MLO (Mycoplasm Like Organism) are spread by insects vektor.Leaf first transformed into a like crackers with a thickness exceeding normal.Warna leaf bottom leaf surface becomes rough, thick leaves and keriput.deviaion bone will be spread to the shoots and leaves another in one final tree.until depressed plant growth and can not grow, as well as any canopy dimmed .for  prevent attacks, such as spraying insecticides on a regular basis with Sevin 85 S, Basudin or Azodrin 15% interval 2 -6 weeks.

2. Mosaic disease

                  Mosaic disease, which is kind of diseases that attack plants are tobacco mosaic virus (TMV)that attact tobacco . Tungro disease, the types of diseases that attack plants are virus Tungro is the viruses that bout the rice plant . Degeneration in sieve vessel in citrus causing bye a viruse called citrus vein phloem degeneration (CVPD).

2.      Yellow Virus

      One of the pest to watch is the Yellow Virus disease. This disease is a virus that inflict a financial. Diseases in chilli plants yellow or blue viruses are very bothersome .Caused by insects called kebul thicks. Bout of  Besmisia tabaci or yellow virus can result in decreased production of pepper and even a tendency to crop failure.In the visible symptoms of the disease is easily recognizable by Yellow Virus characteristics: There is chlorosis in young leaves of the bones of young leaves and spread into other parts of plants, plants to appear yellow, leaves are curling upwards, thickened with a smaller size. Stunted growth or dwarf. If the traits of  Yellow Virus disease has been known, the next steps forward in IPM control methods, so that plants can be safe but also safe from environmental pollution caused by the use of pesticides that are less wise.

3.      Stripe Virus

      Mottle virus disease in peanuts is an important and widespread disease in the central area of ​​the peanut crop in Indonesia. Suffer from a loss product because of mottle virus disease attack in range from 10-60% depending on the type peanuts as well as season and plant age at frequently infected. Indication symptoms encountered in the field is surrounded by a dark green colored striped areas lighter or yellowish-green. In generally the initial symptom in the young leaves vsible chlorotic spots which then evolved into the dappled circle. in old leaves striped green and yellow with bottle green-striped. Growing of infected plants are become stunted, so the plants become shorter than healthy plants, especially if plants are infected since adult.Deviation of anatomical institute also found in seed plants.

·                     Some examples of images of leaves of plants infected with the virus.
  
Figure 1. bean Leaf mottle virus                     Figure 2.Soybean mosaic Virus

                     

            Figure 3.Potato virus Y                                   Figure4.Tobacco Mozaic Viruse

Figure5. Yellow leaf spot disease of tobacco        

      Nature of the virus on which the identification of a virus is a symptom of disease, host range, and the peculiarities vector.Beside microscop electrons can also be used to determine the genus and family of viruses based on shape and size based on the traces of nucleotides virion.Deteksi virus genome is a very typical because traces of nucleotides of the viral genome is different for each type of virus virus. Detection based on traces of nucleotides can be done by using RT-PCR and DNA tracer (probe). Effective control of viral diseases need proper identification of the virus as well as knowledge of the ecology and epidemiology of viral diseases memadai.some virus disease control can generally be grouped into

·                     removal of the source of inoculum,

·                     avoidance of sources of infection,

·                     vector control virus, and

·                     protection of plants with a weak strain (cross protection).

VIRUSES IN ANIMALS

            The study of animal viruses is important from a veterinary viewpoint and many of these viruses cause diseases that are economically devastating. Many animal viruses are also important from a human medical perspective. The emergence of the SARS virus in the human population, coming from an animal source, highlights the importance of animals in bearing infectious agents; avian influenza viruses can directly infect humans. In addition research into animal viruses has made an important contribution to our understanding of viruses in general, their replication, molecular biology, evolution and interaction with the host.

            The primary criteria for taxonomic classification of animal viruses are based on morphology (size, shape, etc.), type of nucleic acid (DNA,  RNA, single-stranded, double-stranded, linear, circular, segmented, etc.), and occurrence of envelopes.  ssRNA viruses possess either (+)RNA (if it serves as messenger RNA) or (-)RNA (if it serves as a template for messenger RNA).  Host range is not a particularly reliable criterion for classification. Although some animal viruses exhibit a very narrow or specific host range, such as HIV in humans or canine distemper virus (CDV) in dogs. But for classification purposes, host range cannot be a criterion because each animal species is subject to infection by a wide variety of viral agents, and numerous viruses infect several different animal species. For example, West Nile virus has a primary host of birds, but it infects and causes disease in horses and humans. Some viruses, such as the influenza virus, are able to change their structure in such a way that they can shift from one primary host to another, for example birds to humans.

            Morphologic similarity among animal viruses correlates closely with similarity of viral components, particularly with the type and size of the viral nucleic acid (genome). For example, all viruses with the morphology of adenoviruses contain dsDNA genomes with a molecular weight of about 23 million daltons; all reoviruses contain segmented dsRNA genomes. In fact, a system of virus classification based on structure and size of viral genomes yields that same grouping as one based on morphology. This information is organized in two ways.

            According to the Baltimore method of classification, animal viruses are be separated into several classes, grouped by type of nucleic acid. Class I. dsDNA viruses; Class II. ssDNA viruses; Class III. dsRNA viruses; Class IV. (+)RNA viruses; Class V. (-)RNA viruses: Class VI.  RNA reverse transcribing viruses. The Baltimore method of classification is illustrated in the table below.

 

source: http://textbookofbacteriology.net/themicrobialworld/AnimalViruses.html

                On the basis of morphology alone, animal viruses are organized into a hierarchical scheme consisting of virus families and constitutive genera based on size, shape, type of nucleic acid and the presence or absence of an envelope. Some families of viruses generated in this scheme are described and illustrated below:

            Animal viruses have many shapes ranging from cubical, bullet-shaped, polygonal, spherical, filamentous or helical, to a complex layered morphology. One of the most common morphologies of the viral capsid is the icosahedron, which consists of 20 triangular faces (capsomeres) that coalesce to form a roughly spherical structure enclosing the viral nucleic acid. The herpes virus illustrated above has the icosahedral shape.

Common morphologies seen in animal viruses. Left to Right. A naked icosahedral virus (e.g. poliovirus), an enveloped icosahedral virus (e.g. herpes virus), a naked helical virus,  and an enveloped helical virus (e.g. influenza virus). Individual capsomeres are arranged to form a capsid which encloses the nucleic acid (DNA or RNA) of the virus.

Replication of Animal Viruses

Outside its host cell a virus is an inert particle. However, when it encounters a host cell it becomes a highly efficient replicating machine. After attachment and gaining entry into its host cell, the virus subverts the biosynthetic and protein synthesizing abilities of the cell in order to replicate the viral nucleic acid, make viral proteins and arrange its escape from the cell. The process occurs in several stages and differs in its details among DNA-containing and RNA-containing viruses.

The Stages of Replication

1. The first stage in viral replication is called the attachment (adsorption) stage. Like bacteriophages, animal viruses attach to host cells by means of a complementary association between attachment sites on the surface of the virus and receptor sites on the host cell surface. This accounts for specificity of viruses for their host cells. Attachment sites on the viruses (usually called virus receptors) are distributed over the surface of the virus coat (capsid) or envelope, and are usually in the form of glycoproteins or proteins.  Receptors on the host cell (called the host cell receptors) are generally glycoproteins imbedded into the cell membrane. Cells lacking receptors for a certain virus are resistant to it and cannot be infected. Attachment can be blocked by antibody molecules that bind to viral attachment sites or to host cell receptors. Since antibodies block the initial attachment of viruses to their host cells, the presence of these antibodies in the host organism are the most important basis for immunization against viral infections.

2. The penetration stage follows attachment. Penetration of the virus occurs either by engulfment of the whole virus, or by fusion of the viral envelope with the cell membrane allowing only the nucleocapsid of the virus to enter the cell. Animal viruses generally do not "inject" their nucleic acid into host cells as do bacteriophages, although occasionally non enveloped viruses leave their capsid outside the cell while the genome passes into the cell.

3. Once the nucleocapsid gains entry into the host cell cytoplasm, the process of uncoating occurs. The viral nucleic acid is released from its coat. Uncoating processes are apparently quite variable and only poorly understood. Most viruses enter the host cell in an engulfment process called receptor mediated endocytosis and actually penetrate the cell contained in a membranous structure called an endosome. Acidification of the endosome is known to cause rearrangements in the virus coat proteins which probably allows extrusion of the viral core into the cytoplasm. Some antiviral drugs such as amantadine exert their antiviral effect my preventing uncoating of the viral nucleic acid.

4. Immediately following uncoating, the viral synthesis stage begins. Exactly how these events will unfold depends upon whether the infecting nucleic acid is DNA or RNA.

In DNA viruses, such as Herpes, the viral DNA is released into the nucleus of the host cell where it is transcribed into early mRNA for transport into the cytoplasm where it is translated into early viral proteins. The early viral proteins are concerned with replication od the viral DNA, so they are transported back into the nucleus where they become involved in the synthesis of  multiple copies of viral DNA. These copies of the viral genome are then templates for transcription into late mRNAs which are also transported back into the cytoplasm for translation into late viral proteins. The late proteins are structural proteins (e.g. coat, envelope proteins) or core proteins (certain enzymes) which are then transported back into the nucleus for the next stage of the replication cycle.

In the case of some RNA viruses (e.g. picornaviruses), the viral genome (RNA) stays in the cytoplasm where it mediates its own replication and translation into viral proteins. In other cases (e.g. orthomyxoviruses), the infectious viral RNA enters into the nucleus where it is replicated before transport back to the cytoplasm for translation into viral proteins.

5. Once the synthesis of the various viral components is complete, the assembly stage begins. The capsomere proteins enclose the nucleic acid to form the viral nucleocapsid. The process is called encapsidation. If the virus contains an envelope it will acquire that envelope and asssociated viral proteins in the next step.

6. The release stage is the final event in viral replication, and it results in the exit of the mature virions from their host cell. Virus maturation and release occurs over a considerable period of time. Some viruses are released from the cell without cell death, by egestion, whereas others are released when the cell dies and disintegrates. In the case of enveloped viruses, the nucleocapsid acquires its final envelope from the nuclear or cell membrane by a budding off process (envelopment) before egress (exit) out of the host cell. Whenever a virus acquires a membrane envelope, it always inserts specific viral proteins into the that envelope which become unique viral antigens and which will be used by the virus to gain entry into a new host cell.

The Stages of Viral Infections

1.         Entry into the Host

The first stage in any virus infection, irrespective of whether the virus is pathogenic or not. In the case of pathogenic infections, the site of entry can influence the disease symptoms produced. Infection can occur via several portals of entry.

Skin - Most viruses which infect via the skin require a breach in the physical integrity of this effective barrier, e.g. cuts or abrasions. Some viruses employ vectors, e.g. ticks, mosquitos, etc. to breach the skin.

Respiratory tract - The respiratory tract and all other mucosal surfaces possess sophisticated immune defense mechanisms, as well as non-specific inhibitory mechanisms (ciliated epithelium, mucus secretion, lower temperature, etc.) which viruses must overcome. Nonetheless, this is the most common point of entry for most viral pathogens.
Gastrointestinal tract - a fairly protected mucosal surface, but some viruses (e.g. enteroviruses, including polioviruses) enter at this site.

Genitourinary tract - less protected than the GI tract, but less frequently exposed to extraneous viruses.

Conjunctiva - an exposed site and relatively unprotected.

2.         Primary Replication

                Having gained entry to a potential host, the virus must initiate an infection by entering a susceptible cell. Some viruses remain localized after primary infection, but others replicate at a primary site before dissemination and spread to a secondary site.

3.         Dissemination Stage

                There are two main mechanisms for viral spread throughout the host: via the bloodstream and via the nervous system.

                The virus may get into the bloodstream by direct inoculation - e.g. arthropod vectors, blood transfusion or I.V. drug abuse. The virus may travel free in the plasma (Togaviruses, Enteroviruses), or in association with red cells (Orbiviruses), platelets (HSV), lymphocytes (EBV, CMV) or monocytes (Lentiviruses). the presence of viruses in the bloodstream is referred to as a viremia. Primary viremia may be followed by more generalized secondary viremia as the virus reaches other target tissues or replicates directly in blood cells.

                In some cases, spread to nervous system is preceded by primary viremia, as above. In other cases, spread occurs directly by contact with neurons at the primary site of infection. Once in peripheral nerves, the virus can spread to the CNS by axonal transport along neurons (e.g. HSV). Viruses can cross synaptic junctions since these frequently contain virus receptors, allowing the virus to jump from one cell to another.

4. Tissue/Cell tropism

Tropism is the ability of a virus to replicate in particular cells or tissues. It is influenced partly by the route of infection but largely by the interaction of a virus attachment sites (virus receptors) with specific receptors on the surface of a cell. The interaction of the virus receptors with the host cell receptors may have a considerable effect on pathogenesis.

5. Host Immune Responses

There are several ways that the host immune responses may contribute to viral pathology. The mechanisms of cell mediated immunity are designed to kill cells which are infected with viruses. If the mechanisms of antibody mediated immunity result in the production of antibodies that cross-react with tissues, an autoimmune pathology may result.

6. Secondary Replication

This occurs in systemic infections when a virus reaches other tissues in which it is capable of replication. For example, polioviruses initiate infection in the GI where the produce an asymptomatic infection. However, when disseminated to neurons in the brain and spinal cord, where the virus replicates secondarily, the serious paralytic complication of poliomyelitis occurs.  If a virus can be prevented from reaching tissues where secondary replication can occur, generally no disease results.

7. Direct Cell and Tissue Damage

                Viruses may replicate widely throughout the body without any disease symptoms if they do not cause significant cell damage or death. Although retroviruses (e.g. HIV) do not generally cause cell death, being released from the cell by budding rather than by cell lysis, they cause persistent infections and may be passed vertically to offspring if they infect the germ line.  Conversely, most other viruses, referred to as virulent viruses, ultimately damage or kill their host cell by several mechanisms, including inhibition of synthesis of host cell macromolecules, damage to cell lysosomes, alterations of the cell membrane, development of inclusion bodies, and induction of chromosomal aberrations.

8. Persistence versus Clearance

The eventual outcome of any virus infection depends on a balance between the ability of the virus to persist or remain latent (persistence) and the forces of the host to completely eliminate the virus (clearance).

            The kinds of viruses that can be found in animals are:

1.                  Foot-and-Mouth Disease Virus

            Foot and Mouth Disease (FMD) is a highly contagious viral disease that attacks even ungulate (pig, she.ep, deer, goats and cows). The disease causes fever and lameness in animals, with blisters on the mouth or on foot. Not usually fatal in adult animals and may recover naturally within 2-3 weeks. FMD is not a direct threat to human health. This disease can be recognized by gejal vesicles (blisters) in the mouth, the tongue and lips, the nipple, or between your toes as well as excessive salivation or lameness. The blisters can not be observed until they have been broken. Other signs, including fever, reduced feed intake, and abortion, may also appear on an infected animal. Even before clinical symptoms appear, the virus can be shed through exhaled air, lesions, milk, semen, and blood, making it difficult to control transmission. It is a highly variable and transmissible virus. The viral genome consists of a single stranded positive RNA.

            Foot-and-mouth disease virus (FMDV) is the prototypic member of the Aphthovirus genus in the Picornaviridae family. This picornavirus is the etiological agent of an acute systemic vesicular disease that affects cattle worldwide, foot-and-mouth disease. It enters the body through inhalation. Soon after infection, the single stranded positive RNA that constitutes the viral genome is efficiently translated using a cap-independent mechanism driven by the internal ribosome entry site element (IRES). This process occurs concomitantly with the inhibition of cellular protein synthesis, caused by the expression of viral proteases. Processing of the viral polyprotein is achieved cotranslationally by viral encoded proteases, giving rise to the different mature viral proteins. Viral RNA as well as viral proteins interact with different components of the host cell, acting as key determinants of viral pathogenesis. In depth knowledge of the molecular basis of the viral cycle is needed to control viral pathogenesis and disease spreading.