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21.4: Other Acellular Entities - Prions and Viroids - Biology

21.4: Other Acellular Entities - Prions and Viroids - Biology


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Skills to Develop

  • Describe prions and their basic properties
  • Define viroids and their targets of infection

Prions and viroids are pathogens (agents with the ability to cause disease) that have simpler structures than viruses but, in the case of prions, still can produce deadly diseases.

Prions

Prions, so-called because they are proteinaceous, are infectious particles—smaller than viruses—that contain no nucleic acids (neither DNA nor RNA). Historically, the idea of an infectious agent that did not use nucleic acids was considered impossible, but pioneering work by Nobel Prize-winning biologist Stanley Prusiner has convinced the majority of biologists that such agents do indeed exist.

Fatal neurodegenerative diseases, such as kuru in humans and bovine spongiform encephalopathy (BSE) in cattle (commonly known as “mad cow disease”) were shown to be transmitted by prions. The disease was spread by the consumption of meat, nervous tissue, or internal organs between members of the same species. Kuru, native to humans in Papua New Guinea, was spread from human to human via ritualistic cannibalism. BSE, originally detected in the United Kingdom, was spread between cattle by the practice of including cattle nervous tissue in feed for other cattle. Individuals with kuru and BSE show symptoms of loss of motor control and unusual behaviors, such as uncontrolled bursts of laughter with kuru, followed by death. Kuru was controlled by inducing the population to abandon its ritualistic cannibalism.

On the other hand, BSE was initially thought to only affect cattle. Cattle dying of the disease were shown to have developed lesions or “holes” in the brain, causing the brain tissue to resemble a sponge. Later on in the outbreak, however, it was shown that a similar encephalopathy in humans known as variant Creutzfeldt-Jakob disease (CJD) could be acquired from eating beef from animals with BSE, sparking bans by various countries on the importation of British beef and causing considerable economic damage to the British beef industry (FIgure (PageIndex{1})). BSE still exists in various areas, and although a rare disease, individuals that acquire CJD are difficult to treat. The disease can be spread from human to human by blood, so many countries have banned blood donation from regions associated with BSE.

The cause of spongiform encephalopathies, such as kuru and BSE, is an infectious structural variant of a normal cellular protein called PrP (prion protein). It is this variant that constitutes the prion particle. PrP exists in two forms, PrPc, the normal form of the protein, and PrPsc, the infectious form. Once introduced into the body, the PrPsc contained within the prion binds to PrPc and converts it to PrPsc. This leads to an exponential increase of the PrPsc protein, which aggregates. PrPsc is folded abnormally, and the resulting conformation (shape) is directly responsible for the lesions seen in the brains of infected cattle. Thus, although not without some detractors among scientists, the prion seems likely to be an entirely new form of infectious agent, the first one found whose transmission is not reliant upon genes made of DNA or RNA.

Viroids

Viroids are plant pathogens: small, single-stranded, circular RNA particles that are much simpler than a virus. They do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not, however, manufacture any proteins, and they only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.

Viroids are known to infect plants (Figure (PageIndex{2})) and are responsible for crop failures and the loss of millions of dollars in agricultural revenue each year. Some of the plants they infect include potatoes, cucumbers, tomatoes, chrysanthemums, avocados, and coconut palms.

Career Connection: Virologist

Virology is the study of viruses, and a virologist is an individual trained in this discipline. Training in virology can lead to many different career paths. Virologists are actively involved in academic research and teaching in colleges and medical schools. Some virologists treat patients or are involved in the generation and production of vaccines. They might participate in epidemiologic studies (Figure (PageIndex{3})) or become science writers, to name just a few possible careers.

If you think you may be interested in a career in virology, find a mentor in the field. Many large medical centers have departments of virology, and smaller hospitals usually have virology labs within their microbiology departments. Volunteer in a virology lab for a semester or work in one over the summer. Discussing the profession and getting a first-hand look at the work will help you decide whether a career in virology is right for you. The American Society of Virology’s website is a good resource for information regarding training and careers in virology.

Prions are infectious agents that consist of protein, but no DNA or RNA, and seem to produce their deadly effects by duplicating their shapes and accumulating in tissues. They are thought to contribute to several progressive brain disorders, including mad cow disease and Creutzfeldt-Jakob disease. Viroids are single-stranded RNA pathogens that infect plants. Their presence can have a severe impact on the agriculture industry.

pathogen
agent with the ability to cause disease
prion
infectious particle that consists of proteins that replicate without DNA or RNA
PrPc
normal prion protein
PrPsc
infectious form of a prion protein
viroid
plant pathogen that produces only a single, specific RNA

Prions , so-called because they are proteinaceous, are infectious particles—smaller than viruses—that contain no nucleic acids (neither DNA nor RNA). Historically, the idea of an infectious agent that did not use nucleic acids was considered impossible, but pioneering work by Nobel Prize-winning biologist Stanley Prusiner has convinced the majority of biologists that such agents do indeed exist.

Fatal neurodegenerative diseases, such as kuru in humans and bovine spongiform encephalopathy (BSE) in cattle (commonly known as “mad cow disease”) were shown to be transmitted by prions. The disease was spread by the consumption of meat, nervous tissue, or internal organs between members of the same species. Kuru, native to humans in Papua New Guinea, was spread from human to human via ritualistic cannibalism. BSE, originally detected in the United Kingdom, was spread between cattle by the practice of including cattle nervous tissue in feed for other cattle. Individuals with kuru and BSE show symptoms of loss of motor control and unusual behaviors, such as uncontrolled bursts of laughter with kuru, followed by death. Kuru was controlled by inducing the population to abandon its ritualistic cannibalism.

On the other hand, BSE was initially thought to only affect cattle. Cattle dying of the disease were shown to have developed lesions or “holes” in the brain, causing the brain tissue to resemble a sponge. Later on in the outbreak, however, it was shown that a similar encephalopathy in humans, known as variant Creutzfeldt-Jakob disease (CJD), could be acquired from eating beef from animals infected with BSE, sparking bans by various countries on the importation of British beef and causing considerable economic damage to the British beef industry (Figure 1). BSE still exists in various areas, and although a rare disease, individuals that acquire CJD are difficult to treat. The disease can be spread from human to human by blood, so many countries have banned blood donation from regions associated with BSE.

The cause of spongiform encephalopathies, such as kuru and BSE, is an infectious structural variant of a normal cellular protein called PrP (prion protein). It is this variant that constitutes the prion particle. PrP exists in two forms, PrP c , the normal form of the protein, and PrP sc , the infectious form. Once introduced into the body, the PrP sc contained within the prion binds to PrP c and converts it to PrP sc . This leads to an exponential increase of the PrP sc protein, which aggregates. PrP sc is folded abnormally, and the resulting conformation (shape) is directly responsible for the lesions seen in the brains of infected cattle. Thus, although not without some detractors among scientists, the prion seems likely to be an entirely new form of infectious agent, the first one found whose transmission is not reliant upon genes made of DNA or RNA.

Figure 1: Mad Cow Disease in humans. (a) Endogenous normal prion protein (PrPc) is converted into the disease-causing form (PrPsc) when it encounters this variant form of the protein. PrPsc may arise spontaneously in brain tissue, especially if a mutant form of the protein is present, or it may occur via the spread of misfolded prions consumed in food into brain tissue. (b) This prion-infected brain tissue, visualized using light microscopy, shows the vacuoles that give it a spongy texture, typical of transmissible spongiform encephalopathies. (credit b: modification of work by Dr. Al Jenny, USDA APHIS scale-bar data from Matt Russell)

Viroids

Viroids are plant pathogens: small, single-stranded, circular RNA particles that are much simpler than a virus. They do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not, however, manufacture any proteins, and they only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.

Viroids are known to infect plants (Figure) and are responsible for crop failures and the loss of millions of dollars in agricultural revenue each year. Some of the plants they infect include potatoes, cucumbers, tomatoes, chrysanthemums, avocados, and coconut palms.

These potatoes have been infected by the potato spindle tuber viroid (PSTV), which is typically spread when infected knives are used to cut healthy potatoes, which are then planted. (credit: Pamela Roberts, University of Florida Institute of Food and Agricultural Sciences, USDA ARS)


Viroids

Viroids are plant pathogens: small, single-stranded, circular RNA particles that are much simpler than a virus. They do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not, however, manufacture any proteins, and they only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.

Viroids are known to infect plants ([link]) and are responsible for crop failures and the loss of millions of dollars in agricultural revenue each year. Some of the plants they infect include potatoes, cucumbers, tomatoes, chrysanthemums, avocados, and coconut palms.

These potatoes have been infected by the potato spindle tuber viroid (PSTV), which is typically spread when infected knives are used to cut healthy potatoes, which are then planted. (credit: Pamela Roberts, University of Florida Institute of Food and Agricultural Sciences, USDA ARS)

Virologist Virology is the study of viruses, and a virologist is an individual trained in this discipline. Training in virology can lead to many different career paths. Virologists are actively involved in academic research and teaching in colleges and medical schools. Some virologists treat patients or are involved in the generation and production of vaccines. They might participate in epidemiologic studies ([link]) or become science writers, to name just a few possible careers.

This virologist is engaged in fieldwork, sampling eggs from this nest for avian influenza. (credit: Don Becker, USGS EROS, U.S. Fish and Wildlife Service)

If you think you may be interested in a career in virology, find a mentor in the field. Many large medical centers have departments of virology, and smaller hospitals usually have virology labs within their microbiology departments. Volunteer in a virology lab for a semester or work in one over the summer. Discussing the profession and getting a first-hand look at the work will help you decide whether a career in virology is right for you. The American Society of Virology’s website is a good resource for information regarding training and careers in virology.


Biology 171

By the end of this section, you will be able to do the following:

  • Describe prions and their basic properties
  • Define viroids and their targets of infection

Prions and viroids are pathogens (agents with the ability to cause disease) that have simpler structures than viruses but, in the case of prions, still can produce deadly diseases.

Prions

Prions , so-called because they are proteinaceous, are infectious particles—smaller than viruses—that contain no nucleic acids (neither DNA nor RNA). Historically, the idea of an infectious agent that did not use nucleic acids was considered impossible, but pioneering work by Nobel Prize-winning biologist Stanley Prusiner has convinced the majority of biologists that such agents do indeed exist.

Fatal neurodegenerative diseases, such as kuru in humans and bovine spongiform encephalopathy (BSE) in cattle (commonly known as “mad cow disease”) were shown to be transmitted by prions. The disease was spread by the consumption of meat, nervous tissue, or internal organs between members of the same species. Kuru, native to humans in Papua New Guinea, was spread from human to human via ritualistic cannibalism. BSE, originally detected in the United Kingdom, was spread between cattle by the practice of including cattle nervous tissue in feed for other cattle. Individuals with kuru and BSE show symptoms of loss of motor control and unusual behaviors, such as uncontrolled bursts of laughter with kuru, followed by death. Kuru was controlled by inducing the population to abandon its ritualistic cannibalism.

On the other hand, BSE was initially thought to only affect cattle. Cattle dying of the disease were shown to have developed lesions or “holes” in the brain, causing the brain tissue to resemble a sponge. Later on in the outbreak, however, it was shown that a similar encephalopathy in humans, known as variant Creutzfeldt-Jakob disease (CJD), could be acquired from eating beef from animals infected with BSE, sparking bans by various countries on the importation of British beef and causing considerable economic damage to the British beef industry ((Figure)). BSE still exists in various areas, and although a rare disease, individuals that acquire CJD are difficult to treat. The disease can be spread from human to human by blood, so many countries have banned blood donation from regions associated with BSE.

The cause of spongiform encephalopathies, such as kuru and BSE, is an infectious structural variant of a normal cellular protein called PrP (prion protein). It is this variant that constitutes the prion particle. PrP exists in two forms, PrP c , the normal form of the protein, and PrP sc , the infectious form. Once introduced into the body, the PrP sc contained within the prion binds to PrP c and converts it to PrP sc . This leads to an exponential increase of the PrP sc protein, which aggregates. PrP sc is folded abnormally, and the resulting conformation (shape) is directly responsible for the lesions seen in the brains of infected cattle. Thus, although not without some detractors among scientists, the prion seems likely to be an entirely new form of infectious agent, the first one found whose transmission is not reliant upon genes made of DNA or RNA.


Viroids

Viroids are plant pathogens: small, single-stranded, circular RNA particles that are much simpler than a virus. They do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not, however, manufacture any proteins, and they only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.

Viroids are known to infect plants ((Figure)) and are responsible for crop failures and the loss of millions of dollars in agricultural revenue each year. Some of the plants they infect include potatoes, cucumbers, tomatoes, chrysanthemums, avocados, and coconut palms.


Virologist
Virology is the study of viruses, and a virologist is an individual trained in this discipline. Training in virology can lead to many different career paths. Virologists are actively involved in academic research and teaching in colleges and medical schools. Some virologists treat patients or are involved in the generation and production of vaccines. They might participate in epidemiologic studies ((Figure)) or become science writers, to name just a few possible careers.


If you think you may be interested in a career in virology, find a mentor in the field. Many large medical centers have departments of virology, and smaller hospitals usually have virology labs within their microbiology departments. Volunteer in a virology lab for a semester or work in one over the summer. Discussing the profession and getting a first-hand look at the work will help you decide whether a career in virology is right for you. The American Society of Virology’s website is a good resource for information regarding training and careers in virology.

Section Summary

Prions are infectious agents that consist of protein, but no DNA or RNA, and seem to produce their deadly effects by duplicating their shapes and accumulating in tissues. They are thought to contribute to several progressive brain disorders, including mad cow disease and Creutzfeldt-Jakob disease. Viroids are single-stranded RNA pathogens that infect plants. Their presence can have a severe impact on the agriculture industry.

Free Response

Prions are responsible for variant Creutzfeldt-Jakob Disease, which has resulted in over 100 human deaths in Great Britain during the last 10 years. How do humans contract this disease?

This prion-based disease is transmitted through human consumption of infected meat.

How are viroids like viruses?

They both replicate in a cell, and they both contain nucleic acid.

A botanist notices that a tomato plant looks diseased. How could the botanist confirm that the agent causing disease is a viroid, and not a virus?

The botanist would need to isolate any foreign nucleic acids from infected plant cells, and confirm that an RNA molecule is the etiological agent of disease. The botanist would then need to demonstrate that the RNA can infect plant cells without a capsid, and that the RNA replicates, but is not translated to produce proteins.

Glossary


42. The table below shows the Baltimore Classification used to classify viruses based on their genetic material. What is the difference between how Group I and Group III viruses reproduce? In Group I .

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This text is based on Openstax Biology for AP Courses, Senior Contributing Authors Julianne Zedalis, The Bishop's School in La Jolla, CA, John Eggebrecht, Cornell University Contributing Authors Yael Avissar, Rhode Island College, Jung Choi, Georgia Institute of Technology, Jean DeSaix, University of North Carolina at Chapel Hill, Vladimir Jurukovski, Suffolk County Community College, Connie Rye, East Mississippi Community College, Robert Wise, University of Wisconsin, Oshkosh

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21.1 | Viral Evolution, Morphology, and Classification

By the end of this section, you will be able to:

  • Describe how viruses were first discovered and how they are detected
  • Discuss three hypotheses about how viruses evolved
  • Recognize the basic shapes of viruses
  • Understand past and emerging classification systems for viruses

Viruses are diverse entities. They vary in their structure, their replication methods, and in their target hosts. Nearly all forms of life—from bacteria and archaea to eukaryotes such as plants, animals, and fungi—have viruses that infect them. While most biological diversity can be understood through evolutionary history, such as how species have adapted to conditions and environments, much about virus origins and evolution remains unknown.

Discovery and Detection

Viruses were first discovered after the development of a porcelain filter, called the Chamberland-Pasteur filter, which could remove all bacteria visible in the microscope from any liquid sample. In 1886, Adolph Meyer demonstrated that a disease of tobacco plants, tobacco mosaic disease, could be transferred from a diseased plant to a healthy one via liquid plant extracts. In 1892, Dmitri Ivanowski showed that this disease could be transmitted in this way even after the Chamberland-Pasteur filter had removed all viable bacteria from the extract. Still, it was many years before it was proven that these “filterable” infectious agents were not simply very small bacteria but were a new type of very small, disease-causing particle.

Virions, single virus particles, are very small, about 20–250 nanometers in diameter. These individual virus particles are the infectious form of a virus outside the host cell. Unlike bacteria (which are about 100-times larger), we cannot see viruses with a light microscope, with the exception of some large virions of the poxvirus family. It was not until the development of the electron microscope in the late 1930s that scientists got their first good view of the structure of the tobacco mosaic virus (TMV) (Figure 21.1) and other viruses (Figure 21.2). The surface structure of virions can be observed by both scanning and transmission electron microscopy, whereas the internal structures of the virus can only be observed in images from a transmission electron microscope. The use of these technologies has allowed for the discovery of many viruses of all types of living organisms. They were initially grouped by shared morphology. Later, groups of viruses were classified by the type of nucleic acid they contained, DNA or RNA, and whether their nucleic acid was single- or double-stranded. More recently, molecular analysis of viral replicative cycles has further refined their classification.

Figure 21.2 In these transmission electron micrographs, (a) a virus is dwarfed by the bacterial cell it infects, while (b) these E. coli cells are dwarfed by cultured colon cells. (credit a: modification of work by U.S. Dept. of Energy, Office of Science, LBL, PBD credit b: modification of work by J.P. Nataro and S. Sears, unpub. data, CDC scale-bar data from Matt Russell)

Evolution of Viruses

Although biologists have accumulated a significant amount of knowledge about how present-day viruses evolve, much less is known about how viruses originated in the first place. When exploring the evolutionary history of most organisms, scientists can look at fossil records and similar historic evidence. However, viruses do not fossilize, so researchers must conjecture by investigating how today’s viruses evolve and by using biochemical and genetic information to create speculative virus histories.

While most findings agree that viruses don’t have a single common ancestor, scholars have yet to find a single hypothesis about virus origins that is fully accepted in the field. One such hypothesis, called devolution or the regressive hypothesis, proposes to explain the origin of viruses by suggesting that viruses evolved from free-living cells. However, many components of how this process might have occurred are a mystery. A second hypothesis (called escapist or the progressive hypothesis) accounts for viruses having either an RNA or a DNA genome and suggests that viruses originated from RNA and DNA molecules that escaped from a host cell. A third hypothesis posits a system of self-replication similar to that of other self-replicating molecules, likely evolving alongside the cells they rely on as hosts studies of some plant pathogens support this hypothesis.

As technology advances, scientists may develop and refine further hypotheses to explain the origin of viruses. The emerging field called virus molecular systematics attempts to do just that through comparisons of sequenced genetic material. These researchers hope to one day better understand the origin of viruses, a discovery that could lead to advances in the treatments for the ailments they produce.

Viral Morphology

Viruses are acellular, meaning they are biological entities that do not have a cellular structure. They therefore lack most of the components of cells, such as organelles, ribosomes, and the plasma membrane. A virion consists of a nucleic acid core, an outer protein coating or capsid, and sometimes an outer envelope made of protein and phospholipid membranes derived from the host cell. Viruses may also contain additional proteins, such as enzymes. The most obvious difference between members of viral families is their morphology, which is quite diverse. An interesting feature of viral complexity is that the complexity of the host does not correlate with the complexity of the virion. Some of the most complex virion structures are observed in bacteriophages, viruses that infect the simplest living organisms, bacteria.

Viruses come in many shapes and sizes, but these are consistent and distinct for each viral family. All virions have a nucleic acid genome covered by a protective layer of proteins, called a capsid. The capsid is made up of protein subunits called capsomeres. Some viral capsids are simple polyhedral “spheres,” whereas others are quite complex in structure.

In general, the shapes of viruses are classified into four groups: filamentous, isometric (or icosahedral), enveloped, and head and tail. Filamentous viruses are long and cylindrical. Many plant viruses are filamentous, including TMV. Isometric viruses have shapes that are roughly spherical, such as poliovirus or herpesviruses. Enveloped viruses have membranes surrounding capsids. Animal viruses, such as HIV, are frequently enveloped. Head and tail viruses infect bacteria and have a head that is similar to icosahedral viruses and a tail shape like filamentous viruses.

Many viruses use some sort of glycoprotein to attach to their host cells via molecules on the cell called viral receptors (Figure 21.3). For these viruses, attachment is a requirement for later penetration of the cell membrane, so they can complete their replication inside the cell. The receptors that viruses use are molecules that are normally found on cell surfaces and have their own physiological functions. Viruses have simply evolved to make use of these molecules for their own replication. For example, HIV uses the CD4 molecule on T lymphocytes as one of its receptors. CD4 is a type of molecule called a cell adhesion molecule, which functions to keep different types of immune cells in close proximity to each other during the generation of a T lymphocyte immune response.

Figure 21.3 The KSHV virus binds the xCT receptor on the surface of human cells. xCT receptors protect cells against stress. Stressed cells express more xCT receptors than non-stressed cells. The KSHV virion causes cells to become stressed, thereby increasing expression of the receptor to which it binds. (credit: modification of work by NIAID, NIH)

Among the most complex virions known, the T4 bacteriophage, which infects the Escherichia coli bacterium, has a tail structure that the virus uses to attach to host cells and a head structure that houses its DNA.

Adenovirus, a non-enveloped animal virus that causes respiratory illnesses in humans, uses glycoprotein spikes protruding from its capsomeres to attach to host cells. Non-enveloped viruses also include those that cause polio (poliovirus), plantar warts (papillomavirus), and hepatitis A (hepatitis A virus).

Enveloped virions like HIV, the causative agent in AIDS, consist of nucleic acid (RNA in the case of HIV) and capsid proteins surrounded by a phospholipid bilayer envelope and its associated proteins. Glycoproteins embedded in the viral envelope are used to attach to host cells. Other envelope proteins are the matrix proteins that stabilize the envelope and often play a role in the assembly of progeny virions. Chicken pox, influenza, and mumps are examples of diseases caused by viruses with envelopes. Because of the fragility of the envelope, non-enveloped viruses are more resistant to changes in temperature, pH, and some disinfectants than enveloped viruses.

Overall, the shape of the virion and the presence or absence of an envelope tell us little about what disease the virus may cause or what species it might infect, but they are still useful means to begin viral classification (Figure 21.4).

Figure 21.4 Viruses can be either complex in shape or relatively simple. This figure shows three relatively complex virions: the bacteriophage T4, with its DNA-containing head group and tail fibers that attach to host cells adenovirus, which uses spikes from its capsid to bind to host cells and HIV, which uses glycoproteins embedded in its envelope to bind to host cells. Notice that HIV has proteins called matrix proteins, internal to the envelope, which help stabilize virion shape. (credit “bacteriophage, adenovirus”: modification of work by NCBI, NIH credit “HIV retrovirus”: modification of work by NIAID, NIH)

Which of the following statements about virus structure is true?

a. All viruses are encased in a viral membrane.

b. The capsomere is made up of small protein subunits called capsids.

c. DNA is the genetic material in all viruses.

d. Glycoproteins help the virus attach to the host cell.

Types of Nucleic Acid

Unlike nearly all living organisms that use DNA as their genetic material, viruses may use either DNA or RNA as theirs. The virus core contains the genome or total genetic content of the virus. Viral genomes tend to be small, containing only those genes that encode proteins that the virus cannot get from the host cell. This genetic material may be single- or double-stranded. It may also be linear or circular. While most viruses contain a single nucleic acid, others have genomes that have several, which are called segments.

In DNA viruses, the viral DNA directs the host cell’s replication proteins to synthesize new copies of the viral genome and to transcribe and translate that genome into viral proteins. DNA viruses cause human diseases, such as chickenpox, hepatitis B, and some venereal diseases, like herpes and genital warts.

RNA viruses contain only RNA as their genetic material. To replicate their genomes in the host cell, the RNA viruses encode enzymes that can replicate RNA into DNA, which cannot be done by the host cell. These RNA polymerase enzymes are more likely to make copying errors than DNA polymerases, and therefore often make mistakes during transcription. For this reason, mutations in RNA viruses occur more frequently than in DNA viruses. This causes them to change and adapt more rapidly to their host. Human diseases caused by RNA viruses include hepatitis C, measles, and rabies.

Virus Classification

To understand the features shared among different groups of viruses, a classification scheme is necessary. As most viruses are not thought to have evolved from a common ancestor, however, the methods that scientists use to classify living things are not very useful. Biologists have used several classification systems in the past, based on the morphology and genetics of the different viruses. However, these earlier classification methods grouped viruses differently, based on which features of the virus they were using to classify them. The most commonly used classification method today is called the Baltimore classification scheme and is based on how messenger RNA (mRNA) is generated in each particular type of virus.

Past Systems of Classification

Viruses are classified in several ways: by factors such as their core content (Table 21.1 and Figure 21.3), the structure of their capsids, and whether they have an outer envelope. The type of genetic material (DNA or RNA) and its structure (single- or double-stranded, linear or circular, and segmented or non-segmented) are used to classify the virus core structures.

Figure 21.5 Viruses are classified based on their core genetic material and capsid design. (a) Rabies virus has a single-stranded RNA (ssRNA) core and an enveloped helical capsid, whereas (b) variola virus, the causative agent of smallpox, has a double-stranded DNA (dsDNA) core and a complex capsid. Rabies transmission occurs when saliva from an infected mammal enters a wound. The virus travels through neurons in the peripheral nervous system to the central nervous system where it impairs brain function, and then travels to other tissues. The virus can infect any mammal, and most die within weeks of infection. Smallpox is a human virus transmitted by inhalation of the variola virus, localized in the skin, mouth, and throat, which causes a characteristic rash. Before its eradication in 1979, infection resulted in a 30–35 percent mortality rate. (credit “rabies diagram”: modification of work by CDC “rabies micrograph”: modification of work by Dr. Fred Murphy, CDC credit “small pox micrograph”: modification of work by Dr. Fred Murphy, Sylvia Whitfield, CDC credit “smallpox photo”: modification of work by CDC scale-bar data from Matt Russell)

Viruses can also be classified by the design of their capsids (Figure 21.4 and Figure 21.5). Capsids are classified as naked icosahedral, enveloped icosahedral, enveloped helical, naked helical, and complex (Figure 21.6 and Figure 21.7). The type of genetic material (DNA or RNA) and its structure (single- or double-stranded, linear or circular, and segmented or non-segmented) are used to classify the virus core structures (Table 21.2).

Figure 21.6 Adenovirus (left) is depicted with a double-stranded DNA genome enclosed in an icosahedral capsid that is 90–100 nm across. The virus, shown clustered in the micrograph (right), is transmitted orally and causes a variety of illnesses in vertebrates, including human eye and respiratory infections. (credit “adenovirus”: modification of work by Dr. Richard Feldmann, National Cancer Institute credit “micrograph”: modification of work by Dr. G. William Gary, Jr., CDC scale-bar data from Matt Russell)

Virus Classification by Capsid Structure

Figure 21.7 Transmission electron micrographs of various viruses show their structures. The capsid of the (a) polio virus is naked icosahedral (b) the Epstein-Barr virus capsid is enveloped icosahedral (c) the mumps virus capsid is an enveloped helix (d) the tobacco mosaic virus capsid is naked helical and (e) the herpesvirus capsid is complex. (credit a: modification of work by Dr. Fred Murphy, Sylvia Whitfield credit b: modification of work by Liza Gross credit c: modification of work by Dr. F. A. Murphy, CDC credit d: modification of work by USDA ARS credit e: modification of work by Linda Stannard, Department of Medical Microbiology, University of Cape Town, South Africa, NASA scale-bar data from Matt Russell)

Baltimore Classification

The most commonly used system of virus classification was developed by Nobel Prize-winning biologist David Baltimore in the early 1970s. In addition to the differences in morphology and genetics mentioned above, the Baltimore classification scheme groups viruses according to how the mRNA is produced during the replicative cycle of the virus.

Group I viruses contain double-stranded DNA (dsDNA) as their genome. Their mRNA is produced by transcription in much the same way as with cellular DNA. Group II viruses have single-stranded DNA (ssDNA) as their genome. They convert their single-stranded genomes into a dsDNA intermediate before transcription to mRNA can occur. Group III viruses use dsRNA as their genome. The strands separate, and one of them is used as a template for the generation of mRNA using the RNA-dependent RNA polymerase encoded by the virus. Group IV viruses have ssRNA as their genome with a positive polarity. Positive polarity means that the genomic RNA can serve directly as mRNA. Intermediates of dsRNA, called replicative intermediates, are made in the process of copying the genomic RNA. Multiple, full-length RNA strands of negative polarity (complimentary to the positive-stranded genomic RNA) are formed from these intermediates, which may then serve as templates for the production of RNA with positive polarity, including both full-length genomic RNA and shorter viral mRNAs. Group V viruses contain ssRNA genomes with a negative polarity, meaning that their sequence is complementary to the mRNA. As with Group IV viruses, dsRNA intermediates are used to make copies of the genome and produce mRNA. In this case, the negative-stranded genome can be converted directly to mRNA. Additionally, full-length positive RNA strands are made to serve as templates for the production of the negative-stranded genome. Group VI viruses have diploid (two copies) ssRNA genomes that must be converted, using the enzyme reverse transcriptase, to dsDNA the dsDNA is then transported to the nucleus of the host cell and inserted into the host genome. Then, mRNA can be produced by transcription of the viral DNA that was integrated into the host genome. Group VII viruses have partial dsDNA genomes and make ssRNA intermediates that act as mRNA, but are also converted back into dsDNA genomes by reverse transcriptase, necessary for genome replication. The characteristics of each group in the Baltimore classification are summarized in Table 21.3 with examples of each group.