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Please, checkout the uploaded file below, where you will find information and instructions. Ill upload the video in a moment. Thank you. biod_171___module_6_questions..docx Unformatted Attachment Preview BIOD 171 - module 6 questions. Page 1 Viruses Please watch this 1st video below as you study the material in this module. Virus Composition: Size and Shape Viruses, although they are considered neither prokaryotic nor eukaryotic, do play a large role in microbiology. Viruses are small, non-cellular particles that cannot replicate unless inside a living host cell. As they cannot replicate on their own, viruses are therefore, by definition, considered obligate intracellular parasites. With regards to composition, all viruses have two basic components: (1) Genomic material comprised of either DNA or RNA and (2) a capsid, a membrane-like protective structure that contains the genetic material, similar to the nucleus of a eukaryotic cell. Unlike prokaryotic and eukaryotic genomes, which contain a double-stranded DNA genome, the viral genome is quite diverse. Viral genomes can be either double or single stranded, and may be found in circular or linear arrangements. The size of viral genomes can also vary from just a few thousand nucleotide base pairs (~3,200 bp for Poliovirus) to roughly 2.5 million nucleotides from the Pandoravirus, which houses the largest known viral genome. Note: Compared to the bacterial genome of E coli (~4.6 million nucleotides) or to the human genome (~3 billion nucleotides) the viral genome is surprisingly small. While the Pandoravirus (~2.5 million), Megavirus (~1.25 million) and Mimivirus (~1.2 million) are large, they are the exception and do not conform to conventional definitions as the vast majority of viral genomes are much smaller. For many viruses an additional membrane called the envelope surrounds the capsid. The envelope is derived from the host cell membrane and serves as an additional barrier to the external environment. In contrast, a virus simply surrounded by the protein capsid is referred to as a naked or non-enveloped virus. As an important distinction, the overwhelming majority of animal viruses are enveloped whereas the majority of plant or bacteria-infecting viruses are not. It is important to note that not all viruses appear the same. The differences in virion composition can also significantly influence the shape and appearance of the virus. For instance, the smallpox virus (variola virus) is an enveloped, ~ 200 nm long and has a distinct dumbbell shaped viral capsid (Figure 6.1A). In contrast, the poliovirus is non-enveloped and only ~30 nm in diameter (Figure 6.1B). These differences can be observed by using an electron microscope. Although EM images are capable of resolving the differences in the shape of the virus, looks can be deceiving. Paramyxoviruses and orthomyxoviruses are both enveloped, spherical and ~100-150 nm in diameter but vary drastically in composition and function (Figure 6.1C and D). Paramyxoviruses, the causative agent of measles and mumps, contain a single-stranded linear genome and fuses with the host cell membrane to initiate entry and viral replication. In contrast, orthomyxoviruses, the causative agent of the flu, contain eight segments of RNA and enters the host cell via endocytosis. Figure 6.1 Virion shape via electron microscope. (A) EM image of the smallpox virus and its trademark dumbbell shaped capsid. (B) Compared to the ~200 nanometer length of smallpox, the ~30 nanometer non-enveloped poliovirus is significantly smaller. (C) Paramyxovirus, the causative agent of measles/mumps contains a single-stranded, linear (albeit twisted and ‘clumped’) genome compared to the eight RNA segments of the orthomyxovirus (flu) show in (D). Page 2 Replication Viruses also require host cell enzymes in order to successfully replicate. Outside of a host cell viruses have no metabolism and are essentially dormant—the virus takes up neither energy nor nutrients. Because of this dependence all viruses must possess a means for entering the cell and then exiting the cell. The basics of how a virus enters a cell to initiate replicating its genome are described below. The viral envelope is often required to interact with and promote successful entry into the host cell. As such, any proteins required for this interaction must be present on the outer surface of the viral envelope. As the envelope is derived from the host cell membrane, this camouflages the virus and lowers the likelihood of immune detection by making it appear similar to the normal biological host cell. Once viral proteins interact with complementary proteins found on the surface of the host cell, the virus attaches and the envelope fuses with the membrane and opens, effectively releasing the capsid into the cytoplasm (Figure 6.2). Once the nucleocapsid enters the cytoplasm it uncoats (unravels) and releases the viral genome into the cell. For non-enveloped viruses, entry often entails the entire virion being encapsulated and endocytosed (internalized) into the host cell. Once in the cytoplasm the capsid disassembles (uncoating) to release the genome. For all viruses, the genome is replicated following attachment and entry, never before. New viral proteins are produced using the host cellular machinery (proteins, enzymes, etc) and are appropriately assembled to become new viral particles—approximately 10,000 new viral particles can be produced from a singly infected cell! The newly released viruses then exit the cell, and may infect additional host cells within the same environment or even leave the organism and enter a new environment. For example, the influenza virus (flu) can be spread when an infected host sneezes and releases viral particles into the air. Once the viral particle infects a new host, the process of attachment, entry, replication and egress repeats. Figure 6.2 Generalized Viral Life Cycle. The virus must first attach to the host cell (1) and quickly penetrate and enter the cell (2). The capsid disintegrates (uncoating), as it enters the cytoplasmic space (3). The viral genome then undergoes transcription/translation to produce new viral proteins (4) as well as duplicates its entire genome (5). New viruses are then assembled (6) and released (7). Page 3 Bacteriophages Please watch this 2nd video below as you study the material in this module. As mentioned above, viruses most likely infect every type of living organism ranging from animals to plants to bacteria. Interestingly, the type of virus that infects bacteria, called a bacteriophage (or just phage) has a unique structure. As shown in Figure 6.3A these viruses possess an icosahedral (20-sided polygon) capsid head group containing the viral genome, and a helical tail. Attached to the tail are tail fibers—fibrous extensions or ‘legs’ that aid in binding host cells. Most distinctively, this particular structural arrangement has not been observed among viruses that infect either animals or plants. Unlike the viruses described above, the phage virus does not pass its capsid into the host cell. Instead, once the tail fibers have mediated binding, the helical tail penetrates the host cell wall and the viral genome is effectively ‘injected’ through the hollow helical tail and into the cytoplasm as shown in Figure 6.3B. Figure 6.3 Bacteriophage. (A) The structural elements of a bacteriophage are shown. An icosahedral head group is separated from the tail region by the collar, while the base plate (fixed at the end of the tail) and tail fibers are located at the conclusion of the helical sheath. (B) Viral DNA is injected into the host cell. As viruses can only replicate within a host cell, researchers must co-culture a virus with appropriate live cells. Once infected, the virus replicates and new progeny viruses can be harvested. Relative to bacteriophages, there are two forms of replication: lytic and lysogenic (Figure 6.4). Lytic bacteriophages replicate within the host bacteria until it lyses, or ruptures, effectively destroying the host bacterial cell. The quantitative amount of virus present in the culture is referred to as the viral titer. Knowing the viral titer is what allows researchers to carefully and effectively plan infectious experiments—too much virus and it will immediately overwhelm and kill the host cells while too little virus will take too long to generate detectable levels of newly produced virus. Alternatively, lysogenic (or temperate) bacteriophages can exist in a non-replicative state such that its viral genome is integrated into the host genome. Upon integration into the host genome the phage is referred to as a prophage. As the host cell replicates its DNA it also replicates the viral DNA. However, the production of viral proteins via transcription and translation is suppressed. Thus, the host cell may carry the phage DNA without risk of lysis. However, under certain stress conditions, the prophage can reactivate, begin full replication of viral proteins and re-enter a lytic replication cycle. Note: Lytic cycle replication is easily detected in lab cultures. During the initial inoculation of virus and bacteria, the media has a high degree of turbidity (cloudiness). However, as the lytic cycle progresses and more and more bacterial cells are destroyed, the culture media turns from turbid to clear, as turbidity is a function of the number of intact bacterial cells present in the media. Thus, as bacterial cell numbers decrease due to lysis, the media becomes clearer. Figure 6.4 Lytic and Lysogenic. The lytic life cycle begins with viral entry and upon successful replication causes severe strain on the host cell to the point of rupture. However, if the viral genome is integrated into the host genome without actively replicating (dormancy) it is considered temperate. However, certain external stresses may cause reactivation of the viral and the lysogenic cycle then becomes lytic. Page 4 Viruses in Microbiology As we have discussed above, viruses are diverse in both structure and function. How certain viruses impact humans to promote illnesses and other maladies has been a constant focus for medical researchers. In fact, there’s a good chance you have already been exposed to or vaccinated against some of the viruses discussed below. Please watch this 3rd video below as you study the material in this module. Rubella (also known as German measles) is a linear, single-stranded, enveloped RNA virus ~10,000-12,000 nucleotides long. The Rubella virus belongs to a family of viruses called Togaviridae. The virus is transmitted via air-borne particles, most commonly derived from the coughs of infected persons. A patient is infectious one week before and after the appearance of the rash (Figure 6.5). The virus multiplies in the upper respiratory tract and in the conjuctiva of the eye early in the course of infection. From the eye it travels to the intestinal tract, urinary tract, skin and central nervous system. Patients may experience a combination of symptoms such as fever, flu-like symptoms, cough, conjuctivitis, and a red blotchy skin rash—starting first on the trunk and then spreading to other areas of the body. In pregnant women, the virus can be transmitted across the placenta to the developing embryo or fetus and cause damage to the eyes, ears, and heart of the newborn infant. Rubella is entirely preventable as children around the age of one year can be inoculated with the MMR (Measles/Mumps/Rubella) vaccine to provide immunity against these three diseases. Figure 6.5 Rubella. The trademark red spot (or rash) has spread and is now localized along the trunk (midsection) of this patient. Measles (Rubeola) is a linear, single-stranded, enveloped RNA virus ~15,000 nucleotides long. The Rubeola virus belongs to a family of viruses called Paramyxovirus. The disease is transmitted via air-borne particles formed during the coughing stage of the disease. Red (Koplik) spots with white centers develop first on the forehead, then on the upper extremities, trunk, and lower extremities. As it was with Rubella, immunity to measles is provided by inoculation with the MMR (Measles/Mumps/Rubella) vaccine. Mumps (also known as epidemic paratitis) is a linear, single-stranded, enveloped RNA virus ~15,000 nucleotides long. The mumps virus also belongs to a family of viruses called Paramyxovirus. Mumps is highly contagious and can spread rapidly among those living in confined areas. Transmission of the virus is through both air-borne droplets (sneezing/coughs) or via direct contact with an infected individual. An infected individual is contagious approximately seven days prior and eight days after the initial symptoms are displayed. Initial symptoms resemble a cold: headache, fever and muscle ache. However, the disease is best characterized by painful swelling of the salivary (parotid) glands located in the neck (Figure 6.6). While the salivary glands are the primary site of inflammation, swelling may also occur in the testes/ovaries, and the pancreas. As it was with Rubella and Measles, immunity to mumps is provided by inoculation with the MMR (Measles/Mumps/Rubella) vaccine. Figure 6.6 Mumps. Infection by the paramyxovirus may cause painful swelling of the salivary (parotid) glands located in the neck. Those affected remain infectious for ~ 8 days after in the initial symptoms appear. Chickenpox (also known as varicella virus or zoster virus) is a linear, single-stranded, enveloped, DNA virus ~125,000 nucleotides long. The chickenpox virus belongs to a family of herpesviruses, and is also referred to as VZV (varicella-zoster virus). The trademark phenotype of chickenpox is the small, itchy, fluid-filled blisters that can form anywhere on the body. Chickenpox is highly contagious and can be transmitted through both air-borne droplets (sneezing/coughs) or via direct contact with the blisters of an infected individual. Individuals are contagious only 1-2 days before the rash appears and are considered non-contagious upon the formation of scabs over the blisters. Although a patient will recover and the blisters will heal, the zoster virus also permanently remains in the body in a dormant (inactive) state. Most commonly around 60 years of age, the zoster virus can reactive, causing a new disease called shingles (Figure 6.7). Prevention is possible with injections of inactivated VZ virus in the chickenpox vaccine. Figure 6.7 Chickpox. Caused by infection with the varicella-zoster virus, the trademark phenotype of chickenpox is the small, itchy, fluid-filled blisters that can form anywhere on the body. Shingles (also known as Herpes zoster) is due to the reactivation of the varicella-zoster virus (VZV) as described above. Because VZV lies dormant in inactive nerve cells, its reactivation typically results in painful blisters (Figure 6.8). However, unlike the initial chickenpox rash, the blisters are localized and limited to small areas. The first symptom is usually severe pain, tingling, or burning localized where the rash will later present. Once the red patches form into small blisters, it is possible for the individual to infect someone who has not been previously exposed to VZV. Thus, someone who has neither (1) previously had chickenpox, nor (2) been administered the VZV vaccine is susceptible to be exposed to and developing chickenpox (not shingles) from a person during the contagious stage of their shingles outbreak. Patients with mild symptoms can be treated with overthe-counter pain medications, while those with increasingly painful blister can be treated with the anti-viral drug, Acyclovir. Figure 6.8 Shingles. Reactivation of the varicella-zoster virus may result in painfully localized blisters limited to small areas. Smallpox (also known as Variola virus) was a linear, double-stranded, enveloped DNA virus ~ 186,000 nucleotides long. There are two variants to the smallpox virus: variola major and variola minor. Variola major was classified as the more severe and most common manifestation of the disease. Smallpox was highly contagious—it was easily transmitted through the air as well as through contact with an infected individual. In both cases, the infection was characterized by an initial high fever followed by a rash in the mouth or throat, as this was often the point of entry. The rash would then appear externally on the face and then begin spreading downwards to the arms and legs and eventually to the hands and feet. The rash became raised bumps filled with a thick, opaque fluid that would eventually form scabs (Figure 6.9). Once the scabs fell off, it often left marks on the skin resembling pitted scars. Most notably, the above description of smallpox uses only the past tense, as the virus has been globally eradicated. Although once a major cause of death in the world, a smallpox vaccine was developed in 1796 by Edward Jenner. Global vaccination efforts have prevented smallpox from appearing in humans since October 26, 1977, making smallpox the first infectious disease ever to be eradicated. Figure 6.9 Smallpox. Caused by the variola major virus, the raised bumps filled with a thick, opaque fluid that would eventually form scabs as shown on a child’s arm and shoulder. Please watch this 4th video below as you study the material in this module. Polio (also known as poliomyelitis) is a single-stranded, non-enveloped RNA virus ~7,700 nucleotides long. Poliovirus belongs to a family of viruses called Picornaviridae. The viral particle is only ~30 nm in diameter and is often considered the most significant small virus. When infected, the poliovirus can enter the central nervous system (CNS) where it replicates in and damages motor neurons. Infected neurons can be found within either the spinal cord, brain stem or motor cortex regions, all of which can lead to temporary or permanent paralysis. Once a worldwide epidemic, the introduction of the Polio vaccine in 1955 radically altered the landscape of medicine. Developed by Jonas Salk at the University of Pittsburgh, approximately 90\% of individuals receiving an injection of the inactivated polio vaccine (IPV) developed protective antibodies against the virus. The extent of protection was further increased to ~99\% with repeated injections over time. In 1961, Albert Sabin developed an oral vaccine given by mouth (OPV) containing a live but weakened (attenuated) virus. Individuals receiving the OPV also displayed the development of protective antibodies and with repeated dosages ~95\% protection. Although immune protection was higher in IPV cases, the administration benefits (drops placed in mouth vs injection with a sterile syringe) made OPV a popular choice, especially in developing countries. Influenza belongs to a family of viruses called Orthomyxoviridae. There are three common subtypes named simply Influenza A, B or C. Influenza is a segmented single-stranded enveloped RNA virus and is ~50-120 nm in diameter. Most notably, Influenza A viruses are the most pathogenic subtype of influenza and cause the most severe disease in humans. The viral envelope contains two key glycoproteins, hemagglutinins (HA) and neuraminidase (N). Hemagglutinins are heavily involved in the entry of the viral particle into a host cell, while neuraminidase proteins are involved in the budding and release of new viral particles from the host cell. For this reason, HA and N proteins are the common drug targets for therapeutic intervention. However, 16 subtypes of HA proteins and 9 subtypes of N proteins have been discovered to date and can appear in various combinations on the viral envelope. Importantly, all HA and N subtypes are not present on each virion. As such, the nomenclature (naming) of the virus is often designated based on which HA and N variant is expressed on the envelope. For example, the strain of influence responsible for the (human) Asian flu epidemic in 1957 was referred to as H2N2, while the most recent influenza epidemic in 2009 was referred to as H1N1. Due to the large number of variants, the flu vaccine is unable to vaccinate again ... Purchase answer to see full attachment