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5.4: Prions and Viroids - Biology

5.4: Prions and Viroids - Biology


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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 1). BSE still exists in various areas, and although a rare disease, CJD is 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 fully accepted 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 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. For example, the potato spindle tuber viroid (PSTVd), which typically spreads when infected knives cut healthy potatoes in preparation for planting, can affect potatoes and tomatoes. The symptoms of PSTVd can be seen in Figure 2.

Learning Objectives

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.


5.4: Prions and Viroids - Biology

At the beginning of this chapter, we discussed the cell theory and noted that viruses do not fit the definition of living things because they are acellular. Viruses may be as small as 20 nm or as large as 300 nm. For reference, prokaryotes are 1–10 µm, and eukaryotes are about ten times larger. Unlike eukaryotic cells, viruses lack organelles and a nucleus.

Viruses are composed of genetic material, a protein coat, and sometimes an envelope containing lipids. The genetic information may be circular or linear, single- or double-stranded, and composed of either DNA or RNA. The protein coat is known as a capsid. If an envelope is present, it will surround the capsid and is composed of phospholipids and virus-specific proteins. The envelope is very sensitive to heat, detergents, and desiccation thus, enveloped viruses are easier to kill. On the other hand, viruses that do not have an envelope are more resistant to sterilization and are likely to persist on surfaces for an extended period of time.

Because viruses cannot reproduce independently, they are considered obligate intracellular parasites. Viruses must express and replicate genetic information within a host cell because they lack ribosomes to carry out protein synthesis. After hijacking a cell’s machinery, a virus will replicate and produce viral progeny, called virions, which can be released to infect additional cells.

Bacteriophages are viruses that specifically target bacteria. They do not actually enter bacteria rather, they simply inject their genetic material, leaving the remaining structures outside the infected cell. In addition to a capsid, bacteriophages contain a tail sheath and tail fibers, as shown in Figure 1.15. The tail sheath can act like a syringe, injecting genetic material into a bacterium. The tail fibers help the bacteriophage to recognize and connect to the correct host cell.

Figure 1.15. Structure of a Bacteriophage

Viral genomes come in a variety of shapes and sizes. Some are made of only a few genes, while others have several hundred. In addition, viral genomes may be made of either DNA or RNA, and may be single- or double-stranded in both cases.

Single-stranded RNA viruses may be positive sense or negative sense. Positive sense implies that the genome may be directly translated to functional proteins by the ribosomes of the host cell, just like mRNA. Negative-sense RNA viruses are a bit more complicated: these viruses require synthesis of an RNA strand complementary to the negative-sense RNA strand, which can then be used as a template for protein synthesis. Negative-sense RNA viruses must carry an RNA replicase in the virion to ensure that the complementary strand is synthesized.

Retroviruses are enveloped, single-stranded RNA viruses in the family Retroviridae usually, the virion contains two identical RNA molecules. These viruses carry an enzyme known as reverse transcriptase, which synthesizes DNA from single-stranded RNA. The DNA then integrates into the host cell genome, where it is replicated and transcribed as if it were the host cell’s own DNA. This is a clever mechanism because the integration of the genetic material into the host cell genome allows for the cell to be infected indefinitely, and the only way to cure the infection is to kill the infected cell itself. The human immunodeficiency virus (HIV) is a retrovirus that utilizes this life cycle, which is one of the characteristics that make HIV so difficult to treat, as shown in Figure 1.16.

Figure 1.16. Life Cycle of the Human Immunodeficiency Virus (HIV)

Both retroviruses and transduction are under investigation as methods of gene therapy. It is theorized that retroviruses and transduction methods can deliver functional versions of missing or altered genes, so that the correct proteins can be synthesized and certain disease states can be alleviated. Gene therapy is discussed in Chapter 6 of MCAT Biochemistry Review.

As we have already discussed, viruses must infect a host cell and use the host cell’s machinery in order to reproduce. Here, we will discuss the viral life cycle in detail.

Viruses can only infect a specific set of cells. In order to infect a cell, the virus has to bind to specific receptors on the host cell. Without the proper receptors, a cell is essentially invisible to the virus. Once the virus binds the correct receptor, the virus and the cell are brought into close enough proximity to permit additional interactions. Enveloped viruses fuse with the plasma membrane of a cell, allowing the entry of the virion into the host cell. Sometimes a host cell may misinterpret the binding of a virus to the membrane as nutrients or other useful molecules and will actually bring the virus into the cytoplasm via endocytosis. As mentioned earlier, bacteriophages use tail fibers to anchor themselves to the cell membrane and then inject their viral genome into the host bacterium using the tail sheath. Some tail fibers even have enzymatic activity, allowing for both penetration of the cell wall and the formation of pores in the cell membrane.

HIV must bind to a receptor called CCR5 on white blood cells in order to infect them. Some people lack this receptor and are thus immune to HIV. There was recently a case in which an HIV-positive man with leukemia received a bone marrow transplant from a donor that lacked CCR5. Not only was his leukemia cured, but this transplant also resulted in remission of his HIV infection because the white blood cells from his newly acquired bone marrow were not susceptible to HIV infection.

Depending on the virus, different portions of the virion will be inserted into host cells. Enveloped viruses such as HIV fuse with the membrane and enter the cell intact, whereas bacteriophages only insert their genetic material, leaving their capsids outside the host cell.

Translation and Progeny Assembly

After infection, translation of viral genetic material must occur in order for the virus to reproduce. This requires translocation of the genetic material to the correct location in the cell. DNA viruses must go to the nucleus in order to be transcribed to mRNA. The mRNA then goes to the cytoplasm, where it is translated to proteins. Genetic material from positive-sense RNA viruses stays in the cytoplasm, where it is directly translated to protein by host cell ribosomes. Negative-sense RNA viruses require synthesis of a complementary RNA strand via RNA replicase, which can then be translated to form proteins. DNA formed through reverse transcription in retroviruses also travels to the nucleus, where it can be integrated into the host genome.

Using the ribosomes, tRNA, amino acids, and enzymes of the host cell, the viral RNA is translated into protein. Many of these proteins are structural capsid proteins and allow for creation of new virions in the cytoplasm in the host cell. Once the viral genome has been replicated, it can be packaged within the capsid. Note that the viral genome must be returned to its original form before packaging for example, retroviruses must transcribe new copies of their single-stranded RNA from the DNA that entered the host genome. A single virus may create anywhere from hundreds to many thousands of new virions within a single host cell.

Progeny Release

Viral progeny may be released in multiple ways. First, the viral invasion may initiate cell death, which results in spilling of the viral progeny. Second, the host cell may lyse as a result of being filled with extremely large numbers of virions. Lysis is actually a disadvantage for the virus because the virus can no longer use the cell to carry out its life cycle. Finally, a virus can leave the cell by fusing with its plasma membrane as shown in Figure 1.17, a process known as extrusion. This process allows for survival of the host cell, and continued use of the host cell by the virus. A virus in this state is said to be in a productive cycle.

Figure 1.17. Viral Extrusion

Lytic and Lysogenic Cycles

Depending on growth conditions and the specific virus, bacteriophages may enter a lytic or lysogenic life cycle. These two phases are similar to the lysis and productive cycle methods of progeny release discussed above.

During a lytic cycle, the bacteriophage makes maximal use of the cell’s machinery with little regard for the survival of the host cell. Once the host is swollen with new virions, the cell lyses, and other bacteria can be infected. Bacteria in the lytic phase are termed virulent.

In the event that the virus does not lyse the bacterium, it may integrate into the host genome as a provirus or prophage, beginning the lysogenic cycle. In this case, the virus will be replicated as the bacterium reproduces because it is now a part of the host’s genome. Although the virus may remain integrated into the host genome indefinitely, environmental factors (radiation, light, or chemicals) will cause the provirus to leave the genome and revert to a lytic cycle at some point. As mentioned earlier, trapping of segments of the bacterial genome can occur when the provirus leaves the genome, which allows transduction of genes from one bacterium to another. Although bacteriophages can kill a host bacterium, there may be some benefit to having them integrated in the lysogenic cycle. Infection with one strain of phage generally makes the bacterium less susceptible to superinfection (simultaneous infection) with other phages. Because the provirus is relatively innocuous, there may be some evolutionary advantage to this association. The lytic and lysogenic cycles are contrasted in Figure 1.18.

Figure 1.18. Lytic vs. Lysogenic Cycles of Bacteriophages

Prions and viroids are very small (subviral) particles that can cause disease under certain circumstances.

Prions are infectious proteins and are, thus, also nonliving things. Prions cause disease by triggering misfolding of other proteins, usually involving the conversion of a protein from an &alpha-helical structure to a &beta-pleated sheet. This drastically reduces the solubility of the protein, as well as the ability of the cell to degrade the misfolded protein. Eventually, protein aggregates form, and function of the cell is reduced. Prions are known to cause bovine spongiform encephalopathy (mad cow disease), Creutzfeldt–Jakob disease, and familial fatal insomnia in humans.

Viroids are small plant pathogens consisting of a very short circular single-stranded RNA. Viroids can bind to a large number of RNA sequences and will silence genes in the plant genome. This prevents synthesis of necessary proteins and can subsequently cause metabolic and structural derangements in the plant cell. Viroids are classically thought of as plant pathogens, but a few examples of human viroids do exist, including the hepatitis D virus (HDV). Alone, HDV is innocuous however, when coinfected with hepatitis B virus (HBV), HDV is able to exert its silencing function on human hepatocytes.

MCAT Concept Check 1.5:

Before you move on, assess your understanding of the material with these questions.

1. Why are viruses considered obligate intracellular parasites?

2. Coronavirus, which causes the common cold, is described as an enveloped, single-stranded positive-sense RNA virus. What does this description indicate about the virus?

3. Briefly describe the pathway of retroviral nucleic acids from infection of a host cell to release of viral progeny:


Viroids

Figure 2. These potatoes have been infected by the potato spindle tuber viroid. (credit: Pamela Roberts, University of Florida Institute of Food and Agricultural Sciences, USDA ARS)

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 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. For example, the potato spindle tuber viroid (PSTVd), which typically spreads when infected knives cut healthy potatoes in preparation for planting, can affect potatoes and tomatoes. The symptoms of PSTVd can be seen in Figure 2.

In Summary: Prions and Viroids

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.


Notes on Viroids and Prions

Viroids are much smaller than viruses and are also considerably simpler, for they consist of no more than a single strand of RNA.

The RNA is not enclosed in any structure, and except during infection is not asso­ciated with any other chemical substances.

The typical viroid is an RNA molecule about 50 nm in length. Though at the present time viroids are only suspected of being the agents of certain diseases in animal cells, they are known to be the cause of a number of plant diseases including spindle tuber disease in potatoes.

Prions:

Generally, infectious agents are either viroids, vi­ruses, prokaryotic cells (e.g., bacteria), or eukaryotic cells (e.g., certain protists). What these infectious agents have in common is that their identity is defined by the nucleic acid that each carries. Although there is still considerable debate on the matter, it now appears that there may be an exception to this rule.

Scrapie (a disease of goats and sheep) and a disease of the ner­vous system in humans called Creutzfeldt-Jakob dis­ease) appear to be caused by agents consisting only of protein the agents of these diseases are called prions. The protein comprising a prion has a molecular weight between 50,000 and 100,000, corresponding to a parti­cle size that is 100 times smaller than the smallest vi­ruses.


108 Other Acellular Entities: Prions and Viroids

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.

Review Questions

Which of the following is not associated with prions?

Which statement is true of viroids?

  1. They are single-stranded RNA particles.
  2. They reproduce only outside of the cell.
  3. They produce proteins.
  4. They affect both plants and animals.

Critical Thinking Questions

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


Study Notes on Prions

Prion is an acronym for ‘proteinaceous infectious particle.’ In the mid-1960s, Tikvah Alper and co-workers reported that nucleic acid was unlikely to be a component of the infectious agent that causes scrapie disease. In 1967, J. S. Griffith speculated that the scrapie agent might be a protein capable of ‘self-replication’ without nucleic acid.

However, Stanley B. Prusiner, a Neurologist at the University of California at San Francisco, was the first in the early 1980’s to successfully purify the infectious agent and to show that it consists mostly of proteins (technically, it is a glycoprotein, because it has a sugar group attached). He coined the term prion in 1982 for the new pathogen consisting solely of protein, responsible for neurodegenerative diseases called Transmissible Spongiform Encephalopathies (TSEs).

These include scrapie disease in sheep, bovine spongiform encephalopath (BSE or made cow disease) in cattle, Creutzfeldt-Jakob Disease (CJD) and Kuru in humans. He chose this name to distinguish this new pathogen from virus and viroid’s.

Prusiner was awarded the noble prize in medicine for a revolutionary theory ‘the prion hypothesis. In 2007 biochemist Surachai Supattapon and co-workers produced purified infectious prions (PrPc co-purified lipids, and a synthetic polyanionic molecule). In 2010 Jiyan. Ma and co-workers purified infectious prions. In 2011, it was demonstrated that prions can be degraded by lichens.

Prions are something unique existing somewhere in the border zone between living things and non-living matter. Prion, an abnormal from of normal cell protein (PrP) accumulate in brain and progressively damage and destroy brain cells. Prion protein can be transmitted in other individuals of the same or closely related species, by injection or ingestion of infected tissue and appear to be transmissible between species that are not closely related e.g., between cattle and humans.

Proteins showing prion type behaviour are also found in some fungi. As of 2010, there are 8 known prion proteins in fungi (7 in Saccharomyces cerevisae and 1 is in Podospora anserina). These has been useful in helping to understand mammalian prions. Fungal prions do not appear to cause disease in hosts (non-lethal prions).

2. Structure of Prions:

The prions are exclusively composed of sialogycoprotein called prion protein (PrP). They contain no nucleic acid. This protein is found throughout the body even in healthy people and animals. However, PrP found in infections particles has a different structure and is resistant to proteases, the enzyme in the body that can normally break down proteins.

The normal form of protein is PrPc while the infections form is called Pr Psc (the c refers to cellular or common PrP while the sc refer to scrapie, a prion disease occurring in sheep). PrPc is a normal protein found in the membrane of cells.

It has 209 amino acids (in humans), one disulfide bond, a molecular mass of 35-36 KDa and a mainly alpha-helical structure. The infectious isoform of PrP known as PrPSc, is able to convert normal PrPc proteins into infectious isoform by changing their conformation, or shape, this in turn, alters the way, the prion interconnect. Although the exact 3D structure of PrPSc is not known it has a higher proportion of B-sheet structure in place of the normal a-helix structure.

3. Multiplication of Prions:

Prions multiply by transmitting a misfold protein state. When prion enters a healthy organism, it induces existing properly folded proteins to into disease associated prion form. The prion acts as a template to guide misfolding of more proteins into prion form. These newly formed prions can then go on to convert more proteins themselves, this triggers a chain of reaction that produces a large amount of the prion forms. To-explain this Heterodimer model is given.

Heterodimer Model:

This model tries to explain how prions replicate in a protein only manner. Single PrPsc molecule binds to a single PrPc molecule and catalyzes its conversion into PrPsc. The two PrPsc molecules then come apart and can go on to convert more PrPc (Fig. 3). An alternative model assumes that PrPsc exists only as fibrils, and that fibril ends bind PrPc and convert it into PrPsc (Fig. 4).

4. Prion Diseases:

Prion diseases (also called transmissible spongiform encephalopathy) are very rare: All most all known prion diseases are neurologic diseases. Creutz Feldt-Jacob disease, make up about 85% of the cases. There are about 1 to 1.5 cases per one million people per year.

Human Prion Diseases:

Creutzfeldt-Jacob Disease (Bovine Spongiform Encephalopathy):

A person can get the disease by eating of BSE (Bovine spongiform encephalopathy) infected beef having a blood transfusion, from a person with the disease, injection of human growth hormone extracted from bodies with the disease, or through infected surgical instruments.

Patients suffer from Ataxia or disequilibrium (a patient cannot stand or walk well because he cannot maintain his equilibrium. This is because of a disease in cerebellum), dementia or loss of mentality (progressive loss of cognitive functions) usually die after one year.

This disease is seen people living in New Guinea who eat the brains of dead people. Patients suffer from ataxia, dementia and inability in moving their eyes. Patients usually die within two years.

Gerstmann-Straussler-Scheinker Syndrome:

Very rare syndrome, presents with ataxia and dementia Animal prion diseases.


Viroids

Figure 2: 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 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 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.

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 3]) or become science writers, to name just a few possible careers.

Figure 3: 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.


Viroids

Figure 2. These potatoes have been infected by the potato spindle tuber viroid, which is typically spreads when infected knives cut healthy potatoes, which are then planted. (credit: Pamela Roberts, University of Florida Institute of Food and Agricultural Sciences, USDA ARS)

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 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

Figure 3. 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)

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 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.


RNAs That Behave Like Prions

The term "prion" was originally coined to describe the proteinaceous infectious agents involved in mammalian neurological disorders. More recently, a prion has been defined as a nonchromosomal, protein-based genetic element that is capable of converting the copies of its own benign variant into the prion form, with the new phenotypic effects that can be transmitted through the cytoplasm. Some prions are toxic to the cell, are able to aggregate and/or form amyloid structures, and may be infectious in the wild, but none of those traits are seen as an integral property of all prions. We propose that the definition of prion should be expanded, to include the inducible transmissible entities undergoing autocatalytic conversion and consisting of RNA rather than protein. We show that when seen in this framework, some naturally occurring RNAs, including ribozymes, riboswitches, viroids, viroid-like retroelements, and PIWI-interacting RNAs (piRNAs), possess several of the characteristic properties of prions.


Watch the video: Viroids: Possibly the Smallest Pathogens on Earth (February 2023).