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) .
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
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
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 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.
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.
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
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.
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
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.
