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Describe a viral infection and explain what impact an infection has on its host
Viruses can be seen as obligate, intracellular parasites. The permissive cell must make the substances that the virus needs or the virus will not be able to replicate there.
What You’ll Learn to Do
- List the steps of replication and explain what occurs at each step
- Explain the transmission and diseases of viruses that infect animals
- Explain the transmission and diseases of viruses that infect plants
The learning activities for this section include the following:
- Steps of Virus Infections
- Different Hosts and Their Viruses
- Self Check: Virus Infections and Hosts
Introduction to the Biology of Infectious Diseases
A healthy person lives in harmony with the microbial flora that helps protect its host from invasion by pathogens, usually defined as microorganisms that have the capacity to cause disease. The microbial flora is mostly bacteria and fungi and includes normal resident flora, which is present consistently and which promptly reestablishes itself if disturbed, and transient flora, which may colonize the host for hours to weeks but does not permanently establish itself. Organisms that are normal flora can occasionally cause disease, especially when defenses are disrupted.
Tropisms (attractions to certain tissues) determine which body sites microorganisms colonize. Normal flora is influenced by tropisms and many other factors (eg, diet, hygiene, sanitary conditions, air pollution). For example, lactobacilli are common in the intestines of people with a high intake of dairy products Haemophilus influenzae colonizes the tracheobronchial tree in patients with COPD (chronic obstructive pulmonary disease). As a result, different body habitats contain microbial communities, forming microbiomes that differ by microbial composition and function.
The adenoviruses are common pathogens of humans and animals. Moreover, several strains have been the subject of intensive research and are used as tools in mammalian molecular biology. More than 100 serologically distinct types of adenovirus have been identified, including 49 types that infect humans. The family Adenoviridae is divided into two Genera, the mammalian adenoviruses (mastadenoviruses) and the avian adenoviruses (aviadenoviruses). The adenoviruses are named after the human adenoids, from which they were first isolated.
Several adenoviruses can cause respiratory and conjunctival diseases. In addition, a few types of human adenoviruses induce undifferentiated sarcomas in newborn hamsters and other rodents and can transform certain rodent and human cell cultures. There is currently no evidence that adenoviruses are oncogenic in humans, but the possibility remains of interest.
Begin by asking how many of the students have gotten sick this pass year and what kind of diseases they had.
Then ask how many were prescribed medication to treat their illnesses.
After asking the last question, introduce today’s topic as “Intro to Viruses”.
How many of you have gotten sick this past year?
And how many have taken medicine/antibiotics to get better/treat your illnesses?
Can you think of reasons how you got sick and what caused your illnesses?
Most everyone will raise their hands.
Most everyone will raise their hands.
Various responses: (I got sick from others it was really cold outside from viruses from bacteria etc.)
Checking for Understanding
(Decision Point Assessment):
Can you think of reasons why and how you got sick?
Various responses: I got sick from others it was really cold outside from viruses from bacteria etc. (Once students bring up reasons such as germs, viruses, and bacteria, I will move onto the next section.)
The cycle of infection
Viruses can reproduce only within a host cell. The parental virus (virion) gives rise to numerous progeny, usually genetically and structurally identical to the parent virus. The actions of the virus depend both on its destructive tendencies toward a specific host cell and on environmental conditions. In the vegetative cycle of viral infection, multiplication of progeny viruses can be rapid. This cycle of infection often results in the death of the cell and the release of many virus progeny. Certain viruses, particularly bacteriophages, are called temperate (or latent) because the infection does not immediately result in cell death. The viral genetic material remains dormant or is actually integrated into the genome of the host cell. Cells infected with temperate viruses are called lysogenic because the cells tend to be broken down when they encounter some chemical or physical factor, such as ultraviolet light. In addition, many animal and plant viruses, the genetic information of which is not integrated into the host DNA, may lie dormant in tissues for long periods of time without causing much, if any, tissue damage. Viral infection does not always result in cell death or tissue injury in fact, most viruses lie dormant in tissue without ever causing pathological effects, or they do so only under other, often environmental, provocations.
Although the reproductive pathways of different viruses vary considerably, there are certain basic principles and a particular series of events in the cycle of infection for most, if not all, viruses. The first step in the cycle of infection is that the invading parental virus (virion) must attach to the surface of the host cell ( adsorption). In the second step, the intact virion either penetrates the outer membrane and enters the cell’s interior (cytoplasm) or injects the genetic material of the virus into the interior of the cell while the protein capsid (and envelope, if present) remains at the cell surface. In the case of whole-virion penetration, a subsequent process (uncoating) liberates the genetic material from the capsid and envelope, if present. In either case, the viral genetic material cannot begin to synthesize protein until it has emerged from the capsid or envelope.
Certain bacterial viruses, such as the T4 bacteriophage, have evolved an elaborate process of infection: following adsorption and firm attachment of the virus’s tail to the bacterium surface by means of proteinaceous “pins,” the musclelike tail contracts, and the tail plug penetrates the cell wall and underlying membrane and injects virus (phage) DNA into the cell. Other bacteriophages penetrate the cell membrane by different means, such as injecting the nucleic acid through the male (sex) pili of the bacterium. In all bacterial viruses, penetration transmits the viral nucleic acid through a rigid bacterial cell wall.
Plant cells also have rigid cell walls, which plant viruses cannot ordinarily penetrate. Plant viruses, however, have not evolved their own systems for injecting nucleic acids into host cells, and so they are transmitted by the proboscis of insects that feed on plants. In the laboratory, plant viruses penetrate plant cells if the cell walls have been abraded with sandpaper or if cell protoplasts (plasma membrane, cytoplasm, and nucleus) are devoid of walls.
Penetration of animal cells by viruses involves different processes, because animal cells are enclosed not by walls but by a flexible lipoprotein bilayer membrane. Most animal viruses, whether or not they are encased in lipid envelopes, penetrate cells in an intact form by a process called endocytosis. The membrane invaginates and engulfs a virus particle adsorbed to a cell, usually in an area of the membrane called a coated pit, which is lined by a special protein known as clathrin. As the coated pit invaginates, it is pinched off in the cytoplasm to form a coated vesicle. The coated vesicle fuses with cytoplasmic endosomes (membrane-enclosed vesicles) and then with cell organelles called lysosomes, which are membrane-enclosed vesicles containing enzymes. In an acidic environment, the membrane of an enveloped virus fuses with the endosome membrane, and the viral nucleocapsid is released into the cytoplasm. Nonenveloped viruses presumably undergo a similar process, by which the protein capsid is degraded, releasing the naked viral nucleic acid into the cytoplasm.
The order of the stages of viral replication that follow the uncoating of the genome varies for different virus classes. For many virus families the third step in the cycle of infection is transcription of the genome of the virus to produce viral mRNA, followed by the fourth step, translation of viral mRNA into proteins. For those viruses in which the genomic nucleic acid is an RNA that can serve as a messenger (i.e., positive-strand RNA viruses), the third step is the translation of the RNA to form viral proteins some of these newly synthesized viral proteins are enzymes that synthesize nucleic acids (polymerases), which carry out a fourth step, the transcription of more mRNA from the viral genome. For the more complicated DNA viruses, such as adenoviruses and herpesviruses, some regions of the genome synthesize “early” mRNAs, which are translated into polymerases that initiate the transcription of “late” regions of the DNA into mRNAs, which are then translated into structural proteins.
Regardless of how the third and fourth steps proceed, the fifth step in the cycle of infection is replication (reproduction of the parental genome to make progeny genomes). The sixth step is the assembly of the newly replicated progeny genomes with structural proteins to make fully formed progeny virions. The seventh and last step is the release of progeny virions by lysis of the host cell through the process of either extrusion or budding, depending on the nature of the virus. In a host animal or cell culture, this seven-step process may be repeated many times the progeny virions released from the original site of infection are then transmitted to other sites or to other individuals.
For most animal and plant RNA viruses, all replicative events take place in the cytoplasm in fact, many of these RNA viruses can grow in host cells in which the nucleus has been removed. Replication of most animal and plant DNA viruses, as well as the RNA influenza virus, takes place in the nucleus. In these viruses, transcription takes place in the nucleus, the mRNA migrates to the cytoplasm, where it is translated, and these viral proteins migrate back to the nucleus, where they assemble with newly replicated progeny genomes. Migration of newly translated viral proteins from the cytoplasm to the nucleus is generally a function of specific amino acid sequences called “signals,” which translocate the protein through pores in the nucleus membrane.
Historically they have been named for a variety of factors, including
- the associated diseases (poliovirus, rabies) the type of disease caused (murine leukemia virus)
- the sites in the body affected or from which the virus was first isolated (rhinovirus, adenovirus)
- where they were first isolated (Ebola virus, Hantavirus)
- the animal that carries the virus (bird flu, swine flu)
- for the way people imagined they were contracted (dengue = &lsquoevil spirit&rsquo influenza = &lsquoinfluence&rsquo of bad air).
Example of an Influenza Virus Naming
Focus on Human Immunodeficiency Virus
- Causes the disease AIDS (Acquired Immune Deficiency Syndrome)
HIV Infection Cycle (animation) | HIV Life Cycle - drugs target specific viral processes
HIV Coloring Assignment *Make sure you understand the steps involved in infection and how drugs treat the disease.
Related to Viruses
Viroids - even smaller than viruses, consist of RNA strands that lack a protein coat
Prions - "rogue protein", believed to be the cause of Mad Cow Disease, also may cause Kuru in cannibal tribes
Treatment of Viruses
Visual Connection Questions
Figure 5.12 A doctor injects a patient with what the doctor thinks is an isotonic saline solution. The patient dies, and an autopsy reveals that many red blood cells have been destroyed. Do you think the solution the doctor injected was really isotonic?
Figure 5.16 Injecting a potassium solution into a person’s blood is lethal. Capital punishment and euthanasia utilize this method in their subjects. Why do you think a potassium solution injection is lethal?
Figure 5.19 If the pH outside the cell decreases, would you expect the amount of amino acids transported into the cell to increase or decrease?
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Viruses are tiny infectious agents that invade host cells and cause disease. Although they are harmful, viruses also have interesting technological potential.
Viruses are microscopic biological agents that invade living hosts and infect their bodies by reproducing within their cell tissue.
Photograph by Maryna Olyak
Viruses are tiny infectious agents that rely on living cells to multiply. They may use an animal, plant, or bacteria host to survive and reproduce. As such, there is some debate as to whether or not viruses should be considered living organisms. A virus that is outside of a host cell is known as a virion.
Not only are viruses microscopic, they are smaller than many other microbes, such as bacteria. Most viruses are only 20&ndash400 nanometers in diameter, whereas human egg cells, for example, are about 120 micrometers in diameter, and the E. coli bacteria has a diameter of around 1 micrometer. Viruses are so small that they are best viewed using an electron microscope, which is how they were first visualized in the 1940s.
Viruses generally come in two forms: rods or spheres. However, bacteriophages (viruses that infect bacteria) have a unique shape, with a geometric head and filamentous tail fibers. No matter the shape, all viruses consist of genetic material (DNA or RNA) and have an outer protein shell, known as a capsid.
There are two processes used by viruses to replicate: the lytic cycle and lysogenic cycle. Some viruses reproduce using both methods, while others only use the lytic cycle. In the lytic cycle, the virus attaches to the host cell and injects its DNA. Using the host&rsquos cellular metabolism, the viral DNA begins to replicate and form proteins. Then fully formed viruses assemble. These viruses break, or lyse, the cell and spread to other cells to continue the cycle.
Like the lytic cycle, in the lysogenic cycle the virus attaches to the host cell and injects its DNA. From there, the viral DNA gets incorporated into the host&rsquos DNA and the host&rsquos cells. Each time the host&rsquos cells go through replication, the virus&rsquos DNA gets replicated as well, spreading its genetic information throughout the host without having to lyse the infected cells.
In humans, viruses can cause many diseases. For example, the flu is caused by the influenza virus. Typically, viruses cause an immune response in the host, and this kills the virus. However, some viruses are not successfully treated by the immune system, such as human immunodeficiency virus, or HIV. This leads to a more chronic infection that is difficult or impossible to cure often only the symptoms can be treated.
Unlike bacterial infections, antibiotics are ineffective at treating viral infections. Viral infections are best prevented by vaccines, though antiviral drugs can treat some viral infections. Most antiviral drugs work by interfering with viral replication. Some of these drugs stop DNA synthesis, preventing the virus from replicating
Although viruses can have devastating health consequences, they also have important technological applications. Viruses are particularly vital to gene therapy. Because some viruses incorporate their DNA into host DNA, they can be genetically modified to carry genes that would benefit the host. Some viruses can even be engineered to reproduce in cancer cells and trigger the immune system to kill those harmful cells. Although this is still an emerging field of research, it gives viruses the potential to one day do more good than harm.
Viruses are microscopic biological agents that invade living hosts and infect their bodies by reproducing within their cell tissue.
Nonspecific Immune Responses (Innate Immune Responses)
Cytokines (including interleukins 1 and 6, tumor necrosis factor-alpha, and interferon-gamma) are produced principally by macrophages and activated lymphocytes and mediate an acute-phase response that develops regardless of the inciting microorganism. The response involves fever and increased production of neutrophils by the bone marrow. Endothelial cells also produce large amounts of interleukin-8, which attracts neutrophils.
The inflammatory response directs immune system components to injury or infection sites and is manifested by increased blood supply and vascular permeability, which allows chemotactic peptides, neutrophils, and mononuclear cells to leave the intravascular compartment.
Microbial spread is limited by engulfment of microorganisms by phagocytes (eg, neutrophils, macrophages). Phagocytes are drawn to microbes via chemotaxis and engulf them, releasing phagocytic lysosomal contents that help destroy microbes. Oxidative products such as hydrogen peroxide are generated by the phagocytes and kill ingested microbes. When quantitative or qualitative defects in neutrophils result in infection (eg, chronic granulomatous disease), the infection is usually prolonged and recurrent and responds slowly to antimicrobial drugs. Staphylococci, gram-negative organisms, and fungi are the pathogens usually responsible.
Symptoms of Virus Infection in Plants
These are the initial symptoms and are the result of local reaction at the spot of inoculation. These symptoms appear in the form of local lesions and clearing of veins. The local lesions appear as a result of death of the cells of small area at the inoculation point. In vein clearing, the veins of the young leave become conspicuous due to clearing or chlorosis of tissue in or adjacent to it.
(b) Systemic Symptoms:
In this most parts or whole of the plant is involved.
The chief systemic symptoms are:
It is characterized by the uneven distribution of chlorophyll in yellow and green patches on the leaf. These patches are irregularly distributed among normal green tissues and make a mosaic pattern. This is the most common symptom and is produced by various viruses e.g., mosaic of cucurbits, mosaic of potato, mosaic of sugarcane and Tobacco mosaic (Fig. 1) etc.
In this symptom uniform chlorosis of the leaves take place e.g., Rice yellows.
(iii) Necrosis (death of cells):
In this type of symptom, the infected part of the plant, group of cells collapse, become brown and die. It appears in various forms. Some viruses affect the tissue at point of inoculation by causing a localized breakdown, it is known as local necrosis. Some-times necrosis involves parenchyma and veins of leaves and is called as streak. A rapid killing of bud or branch of entire top of the plants is known as top necrosis e.g., Tobacco necrosis, Tomato streak etc.
On infected leaves, this symptom appears in localized spots. These spots consist of various types of chlorosis and necrosis. The spots may be circular chlorotic areas and are called chlorotic ring spots. In other cases, the necrosis may appear in rings alternating with normal green areas. Such spots are called necrotic ring spot, for example, Tobacco ring spot disease.
It is a common symptom of virus diseases. This symptom is characterized by the alteration in the symmetry of leaf arrangement, crinkling of edges of the leaf, leaf rolling and leaf resetting, e.g., leaf roll of potato, leaf curl of papaya, leaf curl of tomato etc. Sometimes the leaves become reduced in size, at the internodes and there is production of a cluster of distorted shoots. It is called witches broom.
This symptom is characterized by the reduction of the size of the leaves, fruits, petioles and internodes e.g., Bean yellow mosaic, Bunchy top of banana etc.
(vii) Breaking and Greening of Blossoms:
This symptom is characterized by the attractive variegation in flower colour. This is called breaking of flower colour e.g., Tulip, Abutilon etc. Sometimes petals become green due to virus infection and it is called virescence.
Hair-like out-growth appears on the leaves and stems etc. These out-growths are known as entations for example, Dolichos entation mosaic.
(ix) Production of Outgrowths:
Various types of abnormal growths like tumors, swelling and hills appear on infected parts for example, Fiji disease of sugarcane, Tobacco leaf curl disease, etc.
Infected plants show the drying of lateral roots, over production of tumors and galls in roots e.g., wound tumor disease of Pea.
Internal Symptoms of Virus Infection:
These are of two types:
(a) Histological Symptoms:
Infected plants show reduced growth and differentiation.
Infected plants show excessive growth and abnormal development of tissues due to an increase in the number of cells.
Death of the cells or tissues takes place and some other histological changes can also be seen. Phloem cells degenerate or die, callose deposition occurs on the phloem sieve plates. Tyloses are formed in the xylem elements. The xylem elements develop characteristic signified strands which are known as endo-cellular cordons.
(b) Cytological Symptoms:
The main cytological symptom of virus infection is the development of intracellular inclusion bodies, which are of two main types (a) crystalline and (b) amoeba like amorphous bodies. The latter are also known as X bodies. The exact nature of these bodies is not known.
These bodies are common in the epidermal cells of leaves and stems. They are also present in roots, flowers and in most tissues, except the phloem sieve element. The bodies have been reported in plants infected with TMV, Tobacco-ring spot, Turnip yellow mosaic, Potato virus and Hyosyamus mosaic virus etc.
In many cases symptoms shown by the infected plants are due to synergistic or combined action of two or more viruses. For example, Rugose mosaic of potato is due to infection by two viruses namely potato virus X and potato virus Y.