Virus Intelligent Design: Origin, Morphology, Classification, Infections, Hosts, Treatment by Owen Borville BIO 21 October 6, 2024
The first viruses were discovered in the 1890s by Russian microbiologist Dmitry I. Ivanovsky and Dutch microbiologist and botanist Martinus W. Beijerinck. However, scientists didn't see viruses with their own eyes until the 1930s when the electron microscope was invented. The first virus to be seen was the tobacco mosaic virus (TMV), which was crystallized and purified by Wendell Stanley in 1935 and visualized with an electron microscope in 1939.
Key milestones in the history of virology: 1915: Frederick Twort discovered bacteriophage, the viruses that attack bacteria. 1928: Fred Griffith provided the first evidence that DNA formed genes. 1935: Wendell Stanley found that the TMV was mostly made of protein. 1939: Stanley and Max Lauffer separated the TMV into protein and nucleic acid, which was identified as RNA by Hubert S. Loring. 1952: Hershey and Chase showed that the nucleic acid portion of a virus carried the genetic material and was responsible for infectivity. 1954: Watson and Crick discovered the exact structure of DNA.
Virons are very small, single virus particles 20-250 nanometers in diameter. Some can be 1000 nanometers in diameter.
The origin of viruses is uncertain, because they do not fossilize and don't have a single common ancestor. Evolutionist-based scientists are not certain about the origin of viruses, but several hypotheses have been proposed with little or no evidence. Viruses seem to be the result of "de-evolution", which would contradict evolutionist theory, or the result of incomplete evolution of cells. However, the fact that they still exist after the "claimed millions and billions of years of evolution" is difficult to explain without a shorter timeline.
Viral Morphology
Viruses are non-cellular biological phenomena that do not have cellular structure such as organelles, ribosomes, and plasma membranes. 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, within the capsid or attached to the viral genome. Bacteriophages are complex viruses that infect the simplest living organisms, bacteria.
All virions have a nucleic acid genome covered by a protective capsid. The proteins of the capsid are encoded in the viral genome, and are called capsomeres. Viral capsids shapes can vary and can be helical, polyhedral, or have a complex shape. Many viruses use some sort of glycoprotein to attach to their host cells via molecules on the cell called viral receptors, and this attachment must be used for penetration into the host cell membrane.
Glycoproteins embedded in the viral envelope with nucleic acids 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. Viruses can use DNA or RNA for their genetic material.
The virus core contains the genome, the total genetic content of the virus, which is usually small because the virus can also obtain genetic material from its host. 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.
RNA viruses contain only RNA as their genetic material. To replicate their genomes in the host cell, the RNA viruses must encode their own enzymes that can replicate RNA into RNA or, in the retroviruses, into DNA. Mutations in RNA viruses occur more commonly than in DNA viruses.
Virus Classification: viruses can be classified by genome structure: Viruses can be classified according to their core genetic material and capsid design.
RNA: Rabies virus, retroviruses DNA: Herpesviruses, smallpox virus
Single-stranded: Rabies virus, retroviruses Double-stranded: Herpesviruses, smallpox virus
Linear: Rabies virus, retroviruses, herpesviruses, smallpox virus Circular: Papillomaviruses, many bacteriophages
Non-segmented: genome consists of a single segment of genetic material: Parainfluenza viruses Segmented: genome is divided into multiple segments: Influenza viruses
Capsid Classification and Examples:
Naked icosahedral: Hepatitis A virus, polioviruses
Enveloped icosahedral: Epstein-Barr virus, herpes simplex virus, rubella virus, yellow fever virus, HIV-1
Enveloped helical: Influenza viruses, mumps virus, measles virus, rabies virus
Naked helical: Tobacco mosaic virus
Complex with many proteins; some have combinations of icosahedral and helical capsid structures: Herpesviruses, smallpox virus, hepatitis B virus, T4 bacteriophage
The Baltimore Classification of viruses by Nobel laurate David Baltimore in the 1970s classifies viruses by morphology, genetics, and in addition to how the mRNA is produced during the replicative cycle of the virus.
Group Characteristics Mode of mRNA Production and Examples:
I Double-stranded DNA: mRNA is transcribed directly from the DNA template. Herpes simplex (herpesvirus)
II Single-stranded DNA: DNA is converted to double-stranded form before RNA is transcribed. Canine parvovirus (parvovirus)
III Double-stranded RNA: mRNA is transcribed from the RNA genome. Childhood gastroenteritis (rotavirus)
IV Single stranded RNA (+): Genome functions as mRNA. Common cold (picornavirus)
V Single stranded RNA (-): mRNA is transcribed from the RNA. genome Rabies (rhabdovirus)
VI Single stranded RNA viruses with reverse transcriptase: Reverse transcriptase makes DNA from the RNA genome; DNA is then incorporated in the host genome; mRNA is transcribed from the incorporated DNA. Human immunodeficiency virus (HIV)
VII Double stranded DNA viruses with reverse transcriptase: The viral genome is double-stranded DNA, but viral DNA is replicated through an RNA intermediate; the RNA may serve directly as mRNA or as a template to make mRNA. Hepatitis B virus (hepadnavirus)
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, using the enzymes of the host cell.
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, which 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 (complementary 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.
Steps of Virus Infections and Hosts
Specific host cells that a virus must occupy and use to replicate are called permissive, due to a surface molecule called the viral receptor on the host cell surface to allow the virus to attach. The virus uses its host cell processes to replicate and the viral replication cycle can produce dramatic biochemical and structural changes in the host cell, including cell damage, known as cytopathic effects leading to possible destruction of the cell. Cells can be destroyed by lysis bursting or apoptosis programmed cell death. Many animal viruses like HIV leave the infected cells of the immune system by a process known as budding.
A virus attaches to a specific receptor site on the host cell membrane through attachment proteins in the capsid or via glycoproteins embedded in the viral envelope.
Viruses enter the host cell with or without the viral capsid. Plant and animal viruses enter by endocytosis, where the cell membrane surrounds and engulfs the entire virus, or fuses directly with the membrane.
The replication mechanism of viruses depends on the viral genome among DNA, mRNA, and RNA using host cell proteins and enzymes to replicate viral DNA and transcribe viral mRNA, then viral protein synthesis.
The last stage of viral replication is regress, where new virions are released from the host organism and are able to infect adjacent cells and continue the replication process.
So the viral replication process includes: attachment to host, virus enters cell, viral contents are released, viral mRNA is used to make viral proteins, and new virus components are produced in the host cell.
Types of Virus Hosts:
Viruses that infect bacteria are called bacteriophages, most of which use host enzymes for DNA replication and RNA transcription. When a bacteriophage infection results in new virions, the infection is called productive. If the virions are released by bursting the cell, this replication is called lytic cycle. If the virus remains in the cell without being released, it is a lysogenic cycle, and the viral genome is incorporated into the genome of the host cell. A prophage is when the phage DNA is incorporated into the host cell genome. Latency is when viruses can exist in nervous tissue for long periods of time without producing new virions, only to leave latency periodically and cause lesions in the skin where the virus replicates.
Plant Viruses commonly have single stranded RNA genomes. The transfer of a virus from one plant to another is known as horizontal transmission, whereas the inheritance of a virus from a parent is called vertical transmission. Plant viruses usually can only enter plant cells that have damaged cell walls from environmental processes.
Symptoms of plant viral diseases include hyperplasia, the abnormal proliferation of cells that causes the appearance of plant tumors known as galls. Hypoplasia is decreased cell growth in plant leaves, causing thinning and yellowing. Cell necrosis is when viruses directly kill plant cells, causing dead or black stems, leaves, or fruit. Other symptoms of plant viruses are abnormal growth patterns and discoloration.
Animal viruses do not have to penetrate the cell wall to affect and infect the host cell. Non-enveloped viruses may also be taken into the host cell in two ways, including by the normal cell process of receptor-mediated endocytosis. In addition, capsid proteins in non-enveloped viruses can undergo shape changes after binding to the receptor, creating channels in the host cell membrane.
Enveloped viruses also have two ways to enter cells after binding to their receptors: receptor-mediated endocytosis and fusion. The receptor-mediated endocytosis in enveloped viruses is similar to non-enveloped virions. Fusion only occurs with enveloped virions. Receptor-mediated endocytosis is the cellular process in which specific molecules are internalized by binding to receptors on the cell surface. In fusion, special fusion proteins in their envelopes to cause the envelope to fuse with the plasma membrane of the cell, thus releasing the genome and capsid of the virus into the cell cytoplasm.
Acute disease in humans is when symptoms get increasingly worse for a short period followed by the elimination of the virus from the body by the immune system and eventual recovery from the infection. Chronic infections are long-term viral infections. Some viruses only cause intermittent symptoms. Asymptomatic infections are when viruses cause disease by producing infections without any symptoms in the host. A latent viral infection is a type of persistent viral infection where a virus lies dormant in a cell without causing symptoms. Some animal-infecting viruses can cause cancer and are called oncogenic viruses, which cause unregulated cell growth by interfering with the host cells by introducing or interfering with genes and genetic material.
Vaccination is the primary method of controlling viral diseases. Vaccines used in vaccination may be prepared using live viruses, killed viruses, or molecular subunits of the virus. Live viral vaccines are designed in the laboratory to cause few symptoms in recipients while giving them protective immunity against future infections.
Live vaccines are usually more effective than killed vaccines, however the live vaccines have a low risk of returning to their disease-causing form (back mutations). Live vaccines are commonly made by weakening the wild-type or disease-causing virus by growing it in the laboratory in tissues or at temperatures different from what the virus is accustomed to in the host. The virus vaccines can adapt to new conditions and create back mutations, causing new disease. Therefore, there are some risks with viral vaccines and these vaccines are under continuous development by scientists. Some viruses have higher mutation rates than others. Some vaccines can be used to treat active viral infections.
Development of antiviral drugs target only the virus by inhibiting only viral DNA replication. These antiviral drugs are designed to be effective against a specific virus. Viruses have been used in gene therapy to treat genetic diseases. Oncolytic viruses are designed in the laboratory to attack and destroy cancer cells. Phage therapy uses viruses called phages to treat bacterial infections. Phages are natural predators of bacteria, but can be used to fight bacterial infections, such as with drug-resistant bacteria.
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 are a type of protein smaller than a virus with no nucleic acids that can cause normal proteins in the brain to fold incorrectly. Prion diseases can affect both humans and animals. They are sometimes spread to humans by infected meat products. In many cases, the source of the abnormal protein is unknown. Prion diseases are transmissible, untreatable, and fatal brain diseases of mammals. The cause of disease from prions is highly unusual.
Viroids are plant pathogens as they are small, single-stranded, circular RNA particles that are much simpler than a virus. Viroids do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not manufacture any proteins and only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.
The first viruses were discovered in the 1890s by Russian microbiologist Dmitry I. Ivanovsky and Dutch microbiologist and botanist Martinus W. Beijerinck. However, scientists didn't see viruses with their own eyes until the 1930s when the electron microscope was invented. The first virus to be seen was the tobacco mosaic virus (TMV), which was crystallized and purified by Wendell Stanley in 1935 and visualized with an electron microscope in 1939.
Key milestones in the history of virology: 1915: Frederick Twort discovered bacteriophage, the viruses that attack bacteria. 1928: Fred Griffith provided the first evidence that DNA formed genes. 1935: Wendell Stanley found that the TMV was mostly made of protein. 1939: Stanley and Max Lauffer separated the TMV into protein and nucleic acid, which was identified as RNA by Hubert S. Loring. 1952: Hershey and Chase showed that the nucleic acid portion of a virus carried the genetic material and was responsible for infectivity. 1954: Watson and Crick discovered the exact structure of DNA.
Virons are very small, single virus particles 20-250 nanometers in diameter. Some can be 1000 nanometers in diameter.
The origin of viruses is uncertain, because they do not fossilize and don't have a single common ancestor. Evolutionist-based scientists are not certain about the origin of viruses, but several hypotheses have been proposed with little or no evidence. Viruses seem to be the result of "de-evolution", which would contradict evolutionist theory, or the result of incomplete evolution of cells. However, the fact that they still exist after the "claimed millions and billions of years of evolution" is difficult to explain without a shorter timeline.
Viral Morphology
Viruses are non-cellular biological phenomena that do not have cellular structure such as organelles, ribosomes, and plasma membranes. 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, within the capsid or attached to the viral genome. Bacteriophages are complex viruses that infect the simplest living organisms, bacteria.
All virions have a nucleic acid genome covered by a protective capsid. The proteins of the capsid are encoded in the viral genome, and are called capsomeres. Viral capsids shapes can vary and can be helical, polyhedral, or have a complex shape. Many viruses use some sort of glycoprotein to attach to their host cells via molecules on the cell called viral receptors, and this attachment must be used for penetration into the host cell membrane.
Glycoproteins embedded in the viral envelope with nucleic acids 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. Viruses can use DNA or RNA for their genetic material.
The virus core contains the genome, the total genetic content of the virus, which is usually small because the virus can also obtain genetic material from its host. 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.
RNA viruses contain only RNA as their genetic material. To replicate their genomes in the host cell, the RNA viruses must encode their own enzymes that can replicate RNA into RNA or, in the retroviruses, into DNA. Mutations in RNA viruses occur more commonly than in DNA viruses.
Virus Classification: viruses can be classified by genome structure: Viruses can be classified according to their core genetic material and capsid design.
RNA: Rabies virus, retroviruses DNA: Herpesviruses, smallpox virus
Single-stranded: Rabies virus, retroviruses Double-stranded: Herpesviruses, smallpox virus
Linear: Rabies virus, retroviruses, herpesviruses, smallpox virus Circular: Papillomaviruses, many bacteriophages
Non-segmented: genome consists of a single segment of genetic material: Parainfluenza viruses Segmented: genome is divided into multiple segments: Influenza viruses
Capsid Classification and Examples:
Naked icosahedral: Hepatitis A virus, polioviruses
Enveloped icosahedral: Epstein-Barr virus, herpes simplex virus, rubella virus, yellow fever virus, HIV-1
Enveloped helical: Influenza viruses, mumps virus, measles virus, rabies virus
Naked helical: Tobacco mosaic virus
Complex with many proteins; some have combinations of icosahedral and helical capsid structures: Herpesviruses, smallpox virus, hepatitis B virus, T4 bacteriophage
The Baltimore Classification of viruses by Nobel laurate David Baltimore in the 1970s classifies viruses by morphology, genetics, and in addition to how the mRNA is produced during the replicative cycle of the virus.
Group Characteristics Mode of mRNA Production and Examples:
I Double-stranded DNA: mRNA is transcribed directly from the DNA template. Herpes simplex (herpesvirus)
II Single-stranded DNA: DNA is converted to double-stranded form before RNA is transcribed. Canine parvovirus (parvovirus)
III Double-stranded RNA: mRNA is transcribed from the RNA genome. Childhood gastroenteritis (rotavirus)
IV Single stranded RNA (+): Genome functions as mRNA. Common cold (picornavirus)
V Single stranded RNA (-): mRNA is transcribed from the RNA. genome Rabies (rhabdovirus)
VI Single stranded RNA viruses with reverse transcriptase: Reverse transcriptase makes DNA from the RNA genome; DNA is then incorporated in the host genome; mRNA is transcribed from the incorporated DNA. Human immunodeficiency virus (HIV)
VII Double stranded DNA viruses with reverse transcriptase: The viral genome is double-stranded DNA, but viral DNA is replicated through an RNA intermediate; the RNA may serve directly as mRNA or as a template to make mRNA. Hepatitis B virus (hepadnavirus)
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, using the enzymes of the host cell.
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, which 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 (complementary 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.
Steps of Virus Infections and Hosts
Specific host cells that a virus must occupy and use to replicate are called permissive, due to a surface molecule called the viral receptor on the host cell surface to allow the virus to attach. The virus uses its host cell processes to replicate and the viral replication cycle can produce dramatic biochemical and structural changes in the host cell, including cell damage, known as cytopathic effects leading to possible destruction of the cell. Cells can be destroyed by lysis bursting or apoptosis programmed cell death. Many animal viruses like HIV leave the infected cells of the immune system by a process known as budding.
A virus attaches to a specific receptor site on the host cell membrane through attachment proteins in the capsid or via glycoproteins embedded in the viral envelope.
Viruses enter the host cell with or without the viral capsid. Plant and animal viruses enter by endocytosis, where the cell membrane surrounds and engulfs the entire virus, or fuses directly with the membrane.
The replication mechanism of viruses depends on the viral genome among DNA, mRNA, and RNA using host cell proteins and enzymes to replicate viral DNA and transcribe viral mRNA, then viral protein synthesis.
The last stage of viral replication is regress, where new virions are released from the host organism and are able to infect adjacent cells and continue the replication process.
So the viral replication process includes: attachment to host, virus enters cell, viral contents are released, viral mRNA is used to make viral proteins, and new virus components are produced in the host cell.
Types of Virus Hosts:
Viruses that infect bacteria are called bacteriophages, most of which use host enzymes for DNA replication and RNA transcription. When a bacteriophage infection results in new virions, the infection is called productive. If the virions are released by bursting the cell, this replication is called lytic cycle. If the virus remains in the cell without being released, it is a lysogenic cycle, and the viral genome is incorporated into the genome of the host cell. A prophage is when the phage DNA is incorporated into the host cell genome. Latency is when viruses can exist in nervous tissue for long periods of time without producing new virions, only to leave latency periodically and cause lesions in the skin where the virus replicates.
Plant Viruses commonly have single stranded RNA genomes. The transfer of a virus from one plant to another is known as horizontal transmission, whereas the inheritance of a virus from a parent is called vertical transmission. Plant viruses usually can only enter plant cells that have damaged cell walls from environmental processes.
Symptoms of plant viral diseases include hyperplasia, the abnormal proliferation of cells that causes the appearance of plant tumors known as galls. Hypoplasia is decreased cell growth in plant leaves, causing thinning and yellowing. Cell necrosis is when viruses directly kill plant cells, causing dead or black stems, leaves, or fruit. Other symptoms of plant viruses are abnormal growth patterns and discoloration.
Animal viruses do not have to penetrate the cell wall to affect and infect the host cell. Non-enveloped viruses may also be taken into the host cell in two ways, including by the normal cell process of receptor-mediated endocytosis. In addition, capsid proteins in non-enveloped viruses can undergo shape changes after binding to the receptor, creating channels in the host cell membrane.
Enveloped viruses also have two ways to enter cells after binding to their receptors: receptor-mediated endocytosis and fusion. The receptor-mediated endocytosis in enveloped viruses is similar to non-enveloped virions. Fusion only occurs with enveloped virions. Receptor-mediated endocytosis is the cellular process in which specific molecules are internalized by binding to receptors on the cell surface. In fusion, special fusion proteins in their envelopes to cause the envelope to fuse with the plasma membrane of the cell, thus releasing the genome and capsid of the virus into the cell cytoplasm.
Acute disease in humans is when symptoms get increasingly worse for a short period followed by the elimination of the virus from the body by the immune system and eventual recovery from the infection. Chronic infections are long-term viral infections. Some viruses only cause intermittent symptoms. Asymptomatic infections are when viruses cause disease by producing infections without any symptoms in the host. A latent viral infection is a type of persistent viral infection where a virus lies dormant in a cell without causing symptoms. Some animal-infecting viruses can cause cancer and are called oncogenic viruses, which cause unregulated cell growth by interfering with the host cells by introducing or interfering with genes and genetic material.
Vaccination is the primary method of controlling viral diseases. Vaccines used in vaccination may be prepared using live viruses, killed viruses, or molecular subunits of the virus. Live viral vaccines are designed in the laboratory to cause few symptoms in recipients while giving them protective immunity against future infections.
Live vaccines are usually more effective than killed vaccines, however the live vaccines have a low risk of returning to their disease-causing form (back mutations). Live vaccines are commonly made by weakening the wild-type or disease-causing virus by growing it in the laboratory in tissues or at temperatures different from what the virus is accustomed to in the host. The virus vaccines can adapt to new conditions and create back mutations, causing new disease. Therefore, there are some risks with viral vaccines and these vaccines are under continuous development by scientists. Some viruses have higher mutation rates than others. Some vaccines can be used to treat active viral infections.
Development of antiviral drugs target only the virus by inhibiting only viral DNA replication. These antiviral drugs are designed to be effective against a specific virus. Viruses have been used in gene therapy to treat genetic diseases. Oncolytic viruses are designed in the laboratory to attack and destroy cancer cells. Phage therapy uses viruses called phages to treat bacterial infections. Phages are natural predators of bacteria, but can be used to fight bacterial infections, such as with drug-resistant bacteria.
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 are a type of protein smaller than a virus with no nucleic acids that can cause normal proteins in the brain to fold incorrectly. Prion diseases can affect both humans and animals. They are sometimes spread to humans by infected meat products. In many cases, the source of the abnormal protein is unknown. Prion diseases are transmissible, untreatable, and fatal brain diseases of mammals. The cause of disease from prions is highly unusual.
Viroids are plant pathogens as they are small, single-stranded, circular RNA particles that are much simpler than a virus. Viroids do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not manufacture any proteins and only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.