Watch this video on viruses, identifying structures, modes of transmission, replication, and more. This feature of a virus makes it specific to one or a few species of life on Earth.
On the other hand, so many different types of viruses exist on Earth that nearly every living organism has its own set of viruses trying to infect its cells. Even prokaryotes, the smallest and simplest of cells, may be attacked by specific types of viruses. In the following section, we will look at some of the features of viral infection of prokaryotic cells.
As we have learned, viruses that infect bacteria are called bacteriophages Figure 2. Archaea have their own similar viruses. Phage particles must bind to specific surface receptors and actively insert the genome into the host 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 production of new virions, the infection is said to be productive. If the virions are released by bursting the cell, the virus replicates by means of a lytic cycle Figure 3. An example of a lytic bacteriophage is T4, which infects Escherichia coli found in the human intestinal tract.
Sometimes, however, a virus can remain within the cell without being released. For example, when a temperate bacteriophage infects a bacterial cell, it replicates by means of a lysogenic cycle Figure 3 , and the viral genome is incorporated into the genome of the host cell. When the phage DNA is incorporated into the host-cell genome, it is called a prophage. Viruses that infect plant or animal cells may sometimes undergo infections where they are not producing virions for long periods.
An example is the animal herpesviruses , including herpes simplex viruses, the cause of oral and genital herpes in humans. In a process 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 skin 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 detail in the next section. However, there are also plant viruses in most other virus categories. Unlike bacteriophages, plant viruses do not have active mechanisms for delivering the viral genome across the protective cell wall.
For a plant virus to enter a new host plant, some type of mechanical damage must occur. This damage is often caused by weather, insects, animals, fire, or human activities like farming or landscaping. Movement from cell to cell within a plant can be facilitated by viral modification of plasmodesmata cytoplasmic threads that pass from one plant cell to the next. Additionally, plant offspring may inherit viral diseases from parent plants. The transfer of a virus from one plant to another is known as horizontal transmission , whereas the inheritance of a virus from a parent is called vertical transmission.
Symptoms of viral diseases vary according to the virus and its host Table 1. One common symptom is hyperplasia , the abnormal proliferation of cells that causes the appearance of plant tumors known as galls. Other viruses induce hypoplasia , or decreased cell growth, in the leaves of plants, causing thin, yellow areas to appear. Still other viruses affect the plant by directly killing plant cells, a process 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 ring spots, which are circular or linear areas of discoloration found in a leaf. Plant viruses can seriously disrupt crop growth and development, significantly affecting our food supply. They are responsible for poor crop quality and quantity globally, and can bring about 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 most common viruses are peony ring spot and rose mosaic virus. There are far too many plant viruses to discuss each in detail, but symptoms of bean common mosaic virus result in lowered bean production and stunted, unproductive plants.
In the ornamental rose, the rose mosaic disease causes wavy yellow lines and colored splotches on the leaves of the plant. Animal viruses, unlike the viruses of plants and bacteria, do not have to penetrate a cell wall to gain access to the host cell. The virus may even induce the host cell to cooperate in the infection process. As a protein 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 after binding to the receptor, creating channels in the host cell membrane. Enveloped viruses also have two ways of entering cells after binding to their receptors: receptor-mediated endocytosis, or fusion. Occasionally, mild fever and malaise occur during viremia, but they often are transient and have little diagnostic value.
The incubation period tends to be brief 1 to 3 days in infections in which virus travels only a short distance to reach the target organ i. Conversely, incubation periods in generalized infections are longer because of the stepwise fashion by which the virus moves through the body before reaching the target organs. Other factors also may influence the incubation period. Generalized infections produced by togaviruses may have an unexpectedly short incubation period because of direct intravascular injection insect bite of a rapidly multiplying virus.
The mechanisms governing the long incubation period months to years of persistent infections are poorly understood. The persistently infected cell is often not lysed, or lysis is delayed. In addition, disease may result from a late immune reaction to viral antigen e. Virus replication in the target organ resembles replication at other body sites except that 1 the target organ in systemic infections is usually reached late during the stepwise progression of virus through the body, and 2 clinical disease originates there.
At each step of virus progression through the body, the local recovery mechanisms local body defenses, including interferon, local inflammation, and local immunity are activated. Thus, when the target organ is infected, the previously infected sites may have reached various stages of recovery. Figure illustrates this staging of infection and recovery in different tissues during a spreading surface infection.
Circulating interferon and immune responses probably account for the termination of viremia, but these responses may be too late to prevent seeding of virus into the target organ and into sites of shedding. Nevertheless, these systemic defenses can diffuse in various degrees into target organs and thereby help retard virus replication and disease.
Depending on the balance between virus and host defenses see Chs. Additional constitutional disease such as fever and malaise may result from diffusion of toxic products of virus replication and cell necrosis, as well as from release of lymphokines and other inflammatory mediators. Release of leukotriene C4 during respiratory infection may cause bronchospasm.
Viral antigens also may participate in immune reactions, leading to disease manifestations. In addition, impairment of leukocytes and immunosuppression by some viruses may cause secondary bacterial infection. Because of the diversity of viruses, virtually every possible site of shedding is utilized Table ; however, the most frequent sites are the respiratory and alimentary tracts.
Blood and lymph are sites of shedding for the arboviruses, since biting insects become infected by this route. HIV is shed in blood and semen. Milk is a site of shedding for viruses such as some RNA tumor viruses retroviruses and cytomegalovirus a herpesvirus.
Several viruses e. The genital tract is a common site of shedding for herpesvirus type 2 and may be the route through which the virus is transmitted to sexual partners or the fetus. Saliva is the primary source of shedding for rabies virus. Cytomegalovirus is also shed from these last two sites. Finally, viruses such as tumor viruses that are integrated into the DNA of host cells can be shed through germ cells.
Infection of the fetus is a special case of infection in a target organ. The factors that determine whether a target organ is infected also apply to the fetus, but the fetus presents additional variables. The immune and interferon systems of the very young fetus are immature. This immaturity, coupled with the partial placental barrier to transfer of maternal immunity and interferon, deprive the very young fetus of important defense mechanisms. Another variable is the high vulnerability to disruption of the rapidly developing fetal organs, especially during the first trimester of pregnancy.
Furthermore, susceptibility to virus replication may be modulated by the undifferentiated state of the fetal cells and by hormonal changes during pregnancy.
Although virus multiplication in the fetus may lead to congenital anomalies or fetal death, the mother may have only a mild or inapparent infection. To cause congenital anomalies, virus must reach the fetus and multiply in it, thereby causing maldeveloped organs. Generally, virus reaches the fetus during maternal viremia by infecting or passing through the placenta to the fetal circulation and then to fetal target organs. Sufficient virus multiplication may disrupt development of fetal organs, especially during their rapid development the first trimester of pregnancy.
Although many viruses occasionally cause congenital anomalies, cytomegalovirus and rubella virus are the most common offenders. Virus shedding by the congenitally infected newborn infant may occur as a result of persistence of the virus infection at sites of shedding. Turn recording back on. National Center for Biotechnology Information , U. Show details Baron S, editor. Search term. General Concepts Pathogenesis Pathogenesis is the process by which an infection leads to disease. Cellular Pathogenesis Direct cell damage and death from viral infection may result from 1 diversion of the cell's energy, 2 shutoff of cell macromolecular synthesis, 3 competition of viral mRNA for cellular ribosomes, 4 competition of viral promoters and transcriptional enhancers for cellular transcriptional factors such as RNA polymerases, and inhibition of the interferon defense mechanisms.
Tissue Tropism Viral affinity for specific body tissues tropism is determined by 1 cell receptors for virus, 2 cell transcription factors that recognize viral promoters and enhancer sequences, 3 ability of the cell to support virus replication, 4 physical barriers, 5 local temperature, pH, and oxygen tension enzymes and non-specific factors in body secretions, and 6 digestive enzymes and bile in the gastrointestinal tract that may inactivate some viruses.
Implantation at the Portal of Entry Virions implant onto living cells mainly via the respiratory, gastrointestinal, skin-penetrating, and genital routes although other routes can be used. Local Replication and Local Spread Most virus types spread among cells extracellularly, but some may also spread intracellularly.
Dissemination from the Portal of Entry Viremic : The most common route of systemic spread from the portal of entry is the circulation, which the virus reaches via the lymphatics.
Incubation Period The incubation period is the time between exposure to virus and onset of disease. Multiplication in Target Organs Depending on the balance between virus and host defenses, virus multiplication in the target organ may be sufficient to cause disease and death. Shedding of Virus Although the respiratory tract, alimentary tract, urogenital tract and blood are the most frequent sites of shedding, diverse viruses may be shed at virtually every site.
Introduction Pathogenesis is the process by which virus infection leads to disease. Cellular Pathogenesis Direct cell damage and death may result from disruption of cellular macromolecular synthesis by the infecting virus. Tissue Tropism Most viruses have an affinity for specific tissues; that is, they display tissue specificity or tropism. Sequence of Virus Spread in the Host Implantation at Portal of Entry Viruses are carried to the body by all possible routes air, food, bites, and any contaminated object.
Local Replication and Local Spread Successful implantation may be followed by local replication and local spread of virus Fig. Figure Virus spread during localized infection. Figure Spread of picornavirus over body surfaces from eye to pharynx and intestine during natural infection. Dissemination from the Portal of Entry Dissemination in the Bloodstream At the portal of entry, multiplying virus contacts pathways to the blood and peripheral nerves, the principal routes of widespread dissemination through the body.
Figure Virus spread through bloodstream during a generalized infection. Dissemination in Nerves Dissemination through the nerves is less common than bloodstream dissemination, but is the means of spread in a number of important diseases Fig.
Figure Virus spread through nerves during a generalized infection. Incubation Period During most virus infections, no signs or symptoms of disease occur through the stage of virus dissemination.
Multiplication in Target Organs Virus replication in the target organ resembles replication at other body sites except that 1 the target organ in systemic infections is usually reached late during the stepwise progression of virus through the body, and 2 clinical disease originates there. Shedding of Virus Because of the diversity of viruses, virtually every possible site of shedding is utilized Table ; however, the most frequent sites are the respiratory and alimentary tracts.
Congenital Infections Infection of the fetus is a special case of infection in a target organ. Cell activation signals and the pathogenesis of human cytomegalovirus. Coen DM. Acyclovir-resistant, pathogenic herpesviruses. Trends Microbiol. Fields BN. How do viruses cause different diseases? J Am Med Assoc.
For example, when a temperate bacteriophage infects a bacterial cell, it replicates by means of a lysogenic cycle Figure When the phage DNA is incorporated into the host cell genome, it is called a prophage.
Viruses that infect plant or animal cells may also undergo infections where they are not producing virions for long periods. An example is the animal herpesviruses, including herpes simplex viruses, the cause of herpes in humans. In a process 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 skin 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 detail below. Animal viruses, unlike the viruses of plants and bacteria, do not have to penetrate a cell wall to gain access to the host cell. As a protein 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 after binding to the receptor, creating channels in the host cell membrane. Enveloped viruses also have two ways of entering cells after binding to their receptors: receptor-mediated endocytosis, or fusion.
Many enveloped viruses enter the cell by receptor-mediated endocytosis in a fashion similar to some non-enveloped viruses. On the other hand, fusion only 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 cell cytoplasm. On the other hand, non-enveloped viral progeny, such as rhinoviruses, accumulate in infected cells until there is a signal for lysis or apoptosis, and all virions are released together.
As you will learn in the next module, animal viruses are associated with a variety of human diseases. Some of them follow the classic pattern of acute disease , where symptoms get increasingly worse for a short period followed by the elimination of the virus from the body by the immune system and eventual recovery from the infection. Examples of acute viral diseases are the common cold and influenza. Other viruses cause long-term chronic infections , such as the virus causing hepatitis C, whereas others, like herpes simplex virus, only cause intermittent symptoms.
Still other viruses, such as human herpesviruses 6 and 7, which in some cases can cause the minor childhood disease roseola, often successfully cause productive infections without causing any symptoms at all in the host, and thus we 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 only by routine blood work on patients with risk factors. On the other hand, since many of the symptoms of viral diseases are caused by immune responses, a lack of symptoms is an indication of a weak immune response to the virus.
This allows for the virus to escape elimination by the immune system and persist in individuals for years, all the while producing low levels of progeny virions in what is known as a chronic viral disease. As already discussed, herpes simplex virus can remain in a state of latency in nervous tissue for months, even years. Under certain conditions, including various types of physical and psychological stress, the latent herpes simplex virus may be reactivated and undergo a lytic replication cycle in the skin, causing the lesions associated with the disease.
Once virions are produced in the skin and viral proteins are synthesized, the immune response is again stimulated and resolves the skin lesions in a few days by destroying viruses in the skin. As a result of this type of replicative cycle, appearances of cold sores outbreaks only occur intermittently, even though the viruses remain in the nervous tissue for life.
Latent infections are common with other herpesviruses as well, including the varicella-zoster virus that causes chickenpox. Some animal-infecting viruses, including the hepatitis C virus discussed above, are known as oncogenic viruses : They have the ability to cause cancer.
These viruses interfere with the normal regulation of the host cell cycle either by either introducing genes that stimulate unregulated cell growth oncogenes or by interfering with the expression of genes that inhibit cell growth. Cancers known to be associated with viral infections include cervical cancer caused by human papillomavirus HPV Figure Visit the interactive animations showing the various stages of the replicative cycles of animal viruses and click on the flash animation links.
You have already learned about one of these, the tobacco mosaic virus. As plant cells have a cell wall to protect their cells, these viruses do not use receptor-mediated endocytosis to enter host cells as is seen with animal viruses. This damage is often caused by weather, insects, animals, fire, or human activities like farming or landscaping. Additionally, plant offspring may inherit viral diseases from parent plants.
When plants viruses are transferred between different plants, this is known as horizontal transmission , and when they are inherited from a parent, this is called vertical transmission.
Symptoms of viral diseases vary according to the virus and its host Table One common symptom is hyperplasia , the abnormal proliferation of cells that causes the appearance of plant tumors known as galls. Other viruses induce hypoplasia , or decreased cell growth, in the leaves of plants, causing thin, yellow areas to appear.
Still other viruses affect the plant by directly killing plant cells, a process 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 ring spots, which are circular or linear areas of discoloration found in a leaf. Plant viruses can seriously disrupt crop growth and development, significantly affecting our food supply. They are responsible for poor crop quality and quantity globally, and can bring about 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 most common viruses are peony ring spot and rose mosaic virus. There are far too many plant viruses to discuss each in detail, but symptoms of bean common mosaic virus result in lowered bean production and stunted, unproductive plants.
In the ornamental rose, the rose mosaic disease causes wavy yellow lines and colored splotches on the leaves of the plant. Plant viruses can be spread through sap, insects, organisms living in the soil, seeds, and pollen.
They cause damage to fruit, leaves, and stems, which has a large economic impact.
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