How Does The Spread Of Viruses Differ Between Plants And Animals?

102 Virus Infections and Hosts

By the cease of this section, you will be able to exercise the following:

• List the steps of replication and explain what occurs at each step
• Describe the lytic and lysogenic cycles of virus replication
• Explain the transmission of plant and animal viruses
• Discuss some of the diseases caused past plant and animal viruses
• Talk over the economic touch on of plant and creature viruses

Viruses are obligate, intracellular parasites. A virus must kickoff recognize and attach to a specific living cell prior to inbound it. After penetration, the invading virus must re-create its genome and manufacture its own proteins. Finally, the progeny virions must escape the host cell so that they can infect other cells. Viruses can infect only certain species of hosts and only sure cells within that host. Specific host cells that a virus must occupy and use to replicate are chosen permissive. In most cases, the molecular basis for this specificity is due to a particular surface molecule known as the viral receptor on the host cell surface. A specific viral receptor is required for the virus to attach. In add-on, differences in metabolism and host-cell immune responses (based on differential factor expression) are a likely factor in determining which cells a virus may target for replication.

Steps of Virus Infections

A virus must employ its host-cell processes to replicate. The viral replication bicycle tin produce dramatic biochemical and structural changes in the host cell, which may cause cell damage. These changes, chosen cytopathic furnishings, tin change cell functions or even destroy the cell. Some infected cells, such as those infected by the cold virus known as rhinovirus, die through lysis (bursting) or apoptosis (programmed cell death or "prison cell suicide"), releasing all progeny virions at one time. The symptoms of viral diseases result both from such cell harm caused by the virus and from the immune response to the virus, which attempts to control and eliminate the virus from the body.

Many beast viruses, such as HIV (human immunodeficiency virus), exit the infected cells of the immune organisation by a procedure known equally budding , where virions leave the prison cell individually. During the budding procedure, the cell does not undergo lysis and is non immediately killed. Nonetheless, the damage to the cells that the virus infects may make information technology impossible for the cells to function unremarkably, fifty-fifty though the cells remain alive for a period of time. Most productive viral infections follow similar steps in the virus replication cycle: attachment, penetration, uncoating, replication, assembly, and release (Figure ane).

Attachment

A virus attaches to a specific receptor site on the host jail cell membrane through zipper proteins in the capsid or via glycoproteins embedded in the viral envelope. The specificity of this interaction determines the host—and the cells inside the host—that can be infected by a particular virus. This can be illustrated by thinking of several keys and several locks, where each key will fit only ane specific lock.

Entry

Viruses may enter a host cell either with or without the viral capsid. The nucleic acid of bacteriophages enters the host cell "naked," leaving the capsid outside the cell. Plant and beast viruses can enter through endocytosis (as y'all may recollect, the cell membrane surrounds and engulfs the entire virus). Some enveloped viruses enter the prison cell when the viral envelope fuses straight with the jail cell membrane. Once inside the cell, the viral capsid degrades, so the viral nucleic acid is released and becomes bachelor for replication and transcription.

Replication and Associates

The replication mechanism depends on the viral genome. DNA viruses usually utilise host-cell proteins and enzymes to replicate the viral Dna and to transcribe viral mRNA, which is and then used to directly viral protein synthesis. RNA viruses usually use the RNA core as a template for synthesis of viral genomic RNA and mRNA. The viral mRNA directs the host cell to synthesize viral enzymes and capsid proteins, and assemble new virions.

Of class, there are exceptions to this design. If a host cell does not provide the enzymes necessary for viral replication, viral genes supply the data to direct synthesis of the missing proteins. Retroviruses, such as HIV (group Six of the Baltimore classification scheme), have an RNA genome that must exist reverse transcribed into DNA, which then is incorporated into the host cell genome. To convert RNA into DNA, retroviruses must contain genes that encode the virus-specific enzyme contrary transcriptase that transcribes an RNA template to Deoxyribonucleic acid. Reverse transcription never occurs in uninfected host cells—the enzyme reverse transcriptase is only derived from the expression of viral genes inside the infected host cells. The fact that HIV produces some of its ain enzymes non plant in the host has immune researchers to develop drugs that inhibit these enzymes without affecting the host's metabolism.

This approach has led to the development of a variety of drugs used to treat HIV and has been effective at reducing the number of infectious virions (copies of viral RNA) in the claret to non-detectable levels in many HIV-infected individuals.

Egress

The last stage of viral replication is the release of the new virions produced in the host organism, where they are able to infect adjacent cells and repeat the replication cycle. As yous've learned, some viruses are released when the host cell dies, and other viruses can leave infected cells past budding through the membrane without directly killing the cell.

VISUAL CONNECTION

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Figure 1: The influenza reproductive cycle. In influenza virus infection, glycoproteins on the capsid adhere to a host epithelial cell. Following this, the virus is engulfed. RNA and proteins are and so made and assembled into new virions.

Flu virus is packaged in a viral envelope that fuses with the plasma membrane. This fashion, the virus tin can exit the host cell without killing it. What advantage does the virus gain by keeping the host cell alive?

Respond:
The host prison cell can continue to make new virus particles.

Different Hosts and Their Viruses

Equally you've learned, viruses often infect very specific hosts, as well equally specific cells within the host. This feature of a virus makes it specific to one or a few species of life on World. On the other hand, so many different types of viruses exist on Globe that virtually every living organism has its own set of viruses trying to infect its cells. Fifty-fifty prokaryotes, the smallest and simplest of cells, may be attacked past specific types of viruses. In the following section, we will look at some of the features of viral infection of prokaryotic cells. Every bit nosotros have learned, viruses that infect bacteria are called bacteriophages (Figure 2). Archaea have their own similar viruses.

Bacteriophages

Effigy 2: Bacteriophages attached to a host cell (transmission electron micrograph). In bacteriophage with tails, like the one shown here, the tails serve as a passageway for transmission of the phage genome. (credit: modification of work by Dr. Graham Beards; calibration-bar data from Matt Russell)

Near bacteriophages are dsDNA viruses, which utilise host enzymes for DNA replication and RNA transcription. Phage particles must bind to specific surface receptors and actively insert the genome into the host jail cell. (The complex tail structures seen in many bacteriophages are actively involved in getting the viral genome across the prokaryotic cell wall.) When infection of a cell by a bacteriophage results in the product of new virions, the infection is said to be productive . If the virions are released by bursting the cell, the virus replicates past means of a lytic cycle (Figure 3). An example of a lytic bacteriophage is T4, which infects Escherichia coli institute in the man intestinal tract. Sometimes, even so, a virus can remain within the cell without being released. For example, when a temperate bacteriophage infects a bacterial jail cell, it replicates by means of a lysogenic cycle (Figure 3), and the viral genome is incorporated into the genome of the host jail cell. When the phage Deoxyribonucleic acid is incorporated into the host-prison cell genome, it is called a prophage. An example of a lysogenic bacteriophage is the λ (lambda) virus, which also infects the E. coli bacterium. Viruses that infect plant or animal cells may sometimes undergo infections where they are non producing virions for long periods. An instance is the beast herpesviruses, including herpes simplex viruses, the cause of oral and genital herpes in humans. In a procedure called latency, these viruses can exist in nervous tissue for long periods of time without producing new virions, only to leave latency periodically and cause lesions in the peel where the virus replicates. Even though there are similarities between lysogeny and latency, the term lysogenic cycle is usually reserved to describe bacteriophages. Latency will be described in more particular in the next section.

VISUAL CONNECTION

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Effigy 3: A temperate bacteriophage has both lytic and lysogenic cycles. In the lytic bicycle, the phage replicates and lyses the host cell. In the lysogenic bike, phage Dna is incorporated into the host genome, where it is passed on to subsequent generations. Ecology stressors such as starvation or exposure to toxic chemicals may cause the prophage to excise and enter the lytic bike.

Which of the following statements is false?

1. In the lytic bicycle, new phages are produced and released into the surroundings.
2. In the lysogenic cycle, phage Dna is incorporated into the host genome.
3. An environmental stressor can cause the phage to initiate the lysogenic bike.
4. Cell lysis just occurs in the lytic cycle.

Answer:
Statement c is false.

Institute Viruses

Almost plant viruses, similar the tobacco mosaic virus, have single-stranded (+) RNA genomes. Withal, there are as well constitute viruses in about other virus categories. Dissimilar bacteriophages, establish viruses do not have active mechanisms for delivering the viral genome across the protective cell wall. For a establish virus to enter a new host plant, some type of mechanical damage must occur. This damage is oftentimes caused by conditions, insects, animals, fire, or human activities similar farming or landscaping. Motility from cell to cell within a plant tin be facilitated past viral modification of plasmodesmata (cytoplasmic threads that pass from 1 plant cell to the next). Additionally, institute offspring may inherit viral diseases from parent plants. Plant viruses can be transmitted by a variety of vectors, through contact with an infected plant's sap, by living organisms such every bit insects and nematodes, and through pollen. The transfer of a virus from one establish to some other is known as horizontal manual, whereas the inheritance of a virus from a parent is chosen vertical transmission.

Symptoms of viral diseases vary according to the virus and its host (Table one). Ane common symptom is hyperplasia , the abnormal proliferation of cells that causes the appearance of constitute tumors known as galls. Other viruses induce hypoplasia , or decreased prison cell growth, in the leaves of plants, causing thin, yellowish areas to appear. Still other viruses affect the found by directly killing institute cells, a procedure known as cell necrosis . Other symptoms of plant viruses include malformed leaves; black streaks on the stems of the plants; altered growth of stems, leaves, or fruits; and band spots, which are round or linear areas of discoloration found in a leaf.

Tabular array 1: Some Common Symptoms of Plant Viral Diseases

Symptom	Appears as
Hyperplasia	Galls (tumors)
Hypoplasia	Thinned, yellow splotches on leaves
Cell necrosis	Dead, blackened stems, leaves, or fruit
Aberrant growth patterns	Malformed stems, leaves, or fruit
Discoloration	Yellow, red, or black lines, or rings in stems, leaves, or fruit

Found viruses tin can seriously disrupt ingather growth and evolution, significantly affecting our nutrient supply. They are responsible for poor crop quality and quantity globally, and tin can bring virtually huge economic losses annually. Others viruses may damage plants used in landscaping. Some viruses that infect agricultural food plants include the name of the plant they infect, such as tomato spotted wilt virus, bean common mosaic virus, and cucumber mosaic virus. In plants used for landscaping, two of the well-nigh common viruses are peony ring spot and rose mosaic virus. At that place are far too many plant viruses to discuss each in detail, only symptoms of edible bean common mosaic virus outcome in lowered bean production and stunted, unproductive plants. In the ornamental rose, the rose mosaic disease causes wavy xanthous lines and colored splotches on the leaves of the establish.

Animal Viruses

Animal viruses, different the viruses of plants and bacteria, practice not take to penetrate a prison cell wall to proceeds access to the host prison cell. The virus may even induce the host prison cell to cooperate in the infection process. Non-enveloped or "naked" animal viruses may enter cells in 2 different ways. As a poly peptide in the viral capsid binds to its receptor on the host cell, the virus may be taken inside the cell via a vesicle during the normal cell process of receptor-mediated endocytosis. An alternative method of cell penetration used by non-enveloped viruses is for capsid proteins to undergo shape changes later on binding to the receptor, creating channels in the host jail cell membrane. The viral genome is so "injected" into the host cell through these channels in a fashion analogous to that used by many bacteriophages.

Enveloped viruses also have two ways of entering cells later binding to their receptors: receptor-mediated endocytosis, or fusion. Many enveloped viruses enter the jail cell by receptor-mediated endocytosis in a fashion similar to that seen in some non-enveloped viruses. On the other hand, fusion just occurs with enveloped virions. These viruses, which include HIV among others, use special fusion proteins in their envelopes to cause the envelope to fuse with the plasma membrane of the cell, thus releasing the genome and capsid of the virus into the jail cell cytoplasm.

After making their proteins and copying their genomes, brute viruses consummate the assembly of new virions and get out the cell. Every bit we take already discussed using the example the influenza virus, enveloped animal viruses may bud from the cell membrane equally they get together themselves, taking a piece of the cell's plasma membrane in the process. On the other manus, non-enveloped viral progeny, such as rhinoviruses, accumulate in infected cells until there is a indicate for lysis or apoptosis, and all virions are released together.

Equally you lot will larn in the next module, animal viruses are associated with a variety of human diseases. Some of them follow the archetype pattern of acute disease, where symptoms get increasingly worse for a short menstruum followed by the elimination of the virus from the body past the immune organization and eventual recovery from the infection. Examples of astute viral diseases are the mutual cold and influenza. Other viruses cause long-term chronic infections, such as the virus causing hepatitis C, whereas others, like herpes simplex virus, merely cause intermittent symptoms. Still other viruses, such as homo herpesviruses 6 and vii, which in some cases can crusade the small childhood disease roseola, often successfully crusade productive infections without causing any symptoms at all in the host, and thus nosotros say these patients have an asymptomatic infection.

In hepatitis C infections, the virus grows and reproduces in liver cells, causing low levels of liver damage. The damage is so low that infected individuals are often unaware that they are infected, and many infections are detected simply past routine blood piece of work on patients with risk factors such as intravenous drug utilise. On the other mitt, since many of the symptoms of viral diseases are acquired by immune responses, a lack of symptoms is an indication of a weak allowed response to the virus. This allows the virus to escape emptying by the immune system and persist in individuals for years, all the while producing low levels of progeny virions in what is known every bit a chronic viral affliction. Chronic infection of the liver by this virus leads to a much greater chance of developing liver cancer, sometimes every bit much as xxx years after the initial infection.

Every bit already discussed, herpes simplex virus can remain in a state of latency in nervous tissue for months, even years. Every bit the virus "hides" in the tissue and makes few if any viral proteins, there is goose egg for the immune response to act against, and immunity to the virus slowly declines. Nether certain conditions, including various types of physical and psychological stress, the latent canker simplex virus may exist reactivated and undergo a lytic replication cycle in the skin, causing the lesions associated with the affliction. One time virions are produced in the skin and viral proteins are synthesized, the immune response is once more stimulated and resolves the skin lesions in a few days or weeks by destroying viruses in the skin. Every bit a result of this type of replicative cycle, appearances of common cold sores and genital herpes outbreaks just occur intermittently, fifty-fifty though the viruses remain in the nervous tissue for life. Latent infections are common with other herpesviruses likewise, including the varicella-zoster virus that causes chickenpox. Afterwards having a chickenpox infection in childhood, the varicella-zoster virus tin remain latent for many years and reactivate in adults to cause the painful condition known as "shingles" (Figure 4).

Figure 4: A latent virus infection. (a) Varicella-zoster, the virus that causes chickenpox, has an enveloped icosahedral capsid visible in this transmission electron micrograph. Its double-stranded DNA genome becomes incorporated in the host Deoxyribonucleic acid and can reactivate afterwards latency in the grade of (b) shingles, often exhibiting a rash. (credit a: modification of work past Dr. Erskine Palmer, B. G. Martin, CDC; credit b: modification of work by "rosmary"/Flickr; scale-bar information from Matt Russell)

Some animal-infecting viruses, including the hepatitis C virus discussed higher up, are known as oncogenic viruses: They have the ability to crusade cancer. These viruses interfere with the normal regulation of the host cell cycle either by introducing genes that stimulate unregulated cell growth (oncogenes) or by interfering with the expression of genes that inhibit cell growth. Oncogenic viruses can exist either DNA or RNA viruses. Cancers known to be associated with viral infections include cervical cancer, caused past human papillomavirus (HPV) (Figure 5), liver cancer caused past hepatitis B virus, T-cell leukemia, and several types of lymphoma.

Effigy five: HPV, or human papillomavirus, has a naked icosahedral capsid visible in this manual electron micrograph and a double-stranded Dna genome that is incorporated into the host DNA. The virus, which is sexually transmitted, is oncogenic and can lead to cervical cancer. (credit: modification of work by NCI, NIH; calibration-bar data from Matt Russell)

LINK TO LEARNING

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View this video to learn the various stages of the replicative cycles of animal viruses and click on the flash animation links.

acute disease

disease where the symptoms rise and fall within a curt menstruation of time

asymptomatic disease

disease where at that place are no symptoms and the individual is unaware of being infected unless lab tests are performed

AZT

anti-HIV drug that inhibits the viral enzyme opposite transcriptase

bacteriophage

virus that infects bacteria

budding

method of get out from the cell used in certain animate being viruses, where virions exit the cell individually past capturing a slice of the host plasma membrane

cell necrosis

cell death

chronic infection

describes when the virus persists in the torso for a long catamenia of time

cytopathic

causing cell damage

fusion

method of entry by some enveloped viruses, where the viral envelope fuses with the plasma membrane of the host prison cell

gall

advent of a plant tumor

horizontal transmission

manual of a affliction between unrelated individuals

hyperplasia

abnormally high jail cell growth and sectionalisation

hypoplasia

abnormally low cell growth and division

intermittent symptom

symptom that occurs periodically

latency

virus that remains in the body for a long flow of time simply only causes intermittent symptoms

lysis

bursting of a prison cell

lytic cycle

blazon of virus replication in which virions are released through lysis, or bursting, of the cell

lysogenic cycle

type of virus replication in which the viral genome is incorporated into the genome of the host cell

oncogenic virus

virus that has the power to cause cancer

permissive

cell blazon that is able to support productive replication of a virus

productive

viral infection that leads to the product of new virions

prophage

phage Dna that is incorporated into the host cell genome

vertical transmission

transmission of disease from parent to offspring

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Access for free at https://openstax.org/books/biology-2e/pages/1-introduction

Source: https://pressbooks.umn.edu/introbio/chapter/virusesinfections/

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