Which of the Following Pathogens Can Not Reproduce Without a Host and Consists of Dna and Rna?

We normally recall of pathogens in hostile terms—every bit invaders that attack our bodies. But a pathogen or a parasite, like any other organism, is simply trying to live and procreate. Living at the expense of a host organism is a very attractive strategy, and information technology is possible that every living organism on earth is subject to some blazon of infection or parasitism (Figure 25-ane). A human host is a nutrient-rich, warm, and moist surroundings, which remains at a uniform temperature and constantly renews itself. It is not surprising that many microorganisms accept evolved the ability to survive and reproduce in this desirable niche. In this department, we discuss some of the common features that microorganisms must have in club to exist infectious. We so explore the wide multifariousness of organisms that are known to cause disease in humans.

Effigy 25-i

Parasitism at many levels. (A) Scanning electron micrograph of a flea. The flea is a common parasite of mammals—including dogs, cats, rats, and humans. It drinks the blood of its host. Flea bites spread bubonic plague by passing the pathogenic (more...)

Pathogens Have Evolved Specific Mechanisms for Interacting with Their Hosts

The man body is a complex and thriving ecosystem. It contains about 10¹³ human cells and also about 10¹⁴ bacterial, fungal, and protozoan cells, which correspond thousands of microbial species. These microbes, called the normal flora, are usually limited to sure areas of the trunk, including the skin, mouth, large intestine, and vagina. In addition, humans are always infected with viruses, near of which rarely, if e'er, get symptomatic. If it is normal for u.s. to live in such shut intimacy with a broad variety of microbes, how is it that some of them are capable of causing us illness or expiry?

Pathogens are usually singled-out from the normal flora. Our normal microbial inhabitants only cause trouble if our immune systems are weakened or if they proceeds access to a usually sterile office of the body (for case, when a bowel perforation enables the gut flora to enter the peritoneal crenel of the abdomen, causing peritonitis). In contrast, defended pathogens do not require that the host be immunocompromised or injured. They have developed highly specialized mechanisms for crossing cellular and biochemical barriers and for eliciting specific responses from the host organism that contribute to the survival and multiplication of the pathogen.

In order to survive and multiply in a host, a successful pathogen must be able to: (1) colonize the host; (ii) find a nutritionally compatible niche in the host body; (3) avoid, subvert, or circumvent the host innate and adaptive allowed responses; (four) replicate, using host resource; and (v) go out and spread to a new host. Nether severe selective force per unit area to induce but the correct host cell responses to reach this complex set of tasks, pathogens take evolved mechanisms that maximally exploit the biology of their host organisms. Many of the pathogens we hash out in this chapter are practiced and applied cell biologists. Nosotros tin can larn a great deal of cell biology by observing them.

The Signs and Symptoms of Infection May Be Caused by the Pathogen or by the Host'due south Responses

Although we tin easily understand why infectious microorganisms would evolve to reproduce in a host, it is less clear why they would evolve to cause illness. 1 explanation may exist that, in some cases, the pathological responses elicited by microorganisms enhance the efficiency of their spread or propagation and hence clearly accept a selective reward for the pathogen. The virus-containing lesions on the genitalia caused by herpes simplex infection, for instance, facilitate direct spread of the virus from an infected host to an uninfected partner during sexual contact. Similarly, diarrheal infections are efficiently spread from patient to caretaker. In many cases, however, the induction of disease has no apparent advantage for the pathogen.

Many of the symptoms and signs that we associate with infectious disease are direct manifestations of the host's immune responses in action. Some hallmarks of bacterial infection, including the swelling and redness at the site of infection and the production of pus (mainly dead white claret cells), are the direct result of immune system cells attempting to destroy the invading microorganisms. Fever, too, is a defensive response, as the increase in body temperature tin can inhibit the growth of some microorganisms. Thus, agreement the biological science of an infectious disease requires an appreciation of the contributions of both pathogen and host.

Pathogens Are Phylogenetically Various

Many types of pathogens cause disease in humans. The most familiar are viruses and bacteria. Viruses cause diseases ranging from AIDS and smallpox to the common common cold. They are essentially fragments of nucleic acid (Dna or RNA) instructions, wrapped in a protective vanquish of proteins and (in some cases) membrane (Effigy 25-2A). They use the basic transcription and translation mechanism of their host cells for their replication.

Figure 25-two

Pathogens in many forms. (A) The construction of the protein coat, or capsid, of poliovirus. This virus was once a common crusade of paralysis, only the disease (poliomyelitis) has been about eradicated past widespread vaccination. (B) The bacterium Vibrio cholerae (more than...)

Of all the bacteria we come across in our lives, only a pocket-sized minority are dedicated pathogens. Much larger and more circuitous than viruses, bacteria are unremarkably free-living cells, which perform most of their bones metabolic functions themselves, relying on the host primarily for diet (Effigy 25-2B).

Another infectious agents are eucaryotic organisms. These range from single-celled fungi and protozoa (Figure 25-2C), through large complex metazoa such as parasitic worms. One of the nearly mutual infectious diseases on the planet, shared by about a billion people at present, is an infestation in the gut past Ascaris lumbricoides. This nematode closely resembles its cousin Caenorhabditis elegans, which is widely used as a model organism for genetic and developmental biological inquiry (discussed in Chapter 21). C. elegans, nevertheless, is only near 1 mm in length, whereas Ascaris can accomplish xxx cm (Effigy 25-2D).

Some rare neurodegenerative diseases, including mad cow disease, are caused by an unusual type of infectious particle called a prion, which is made but of protein. Although the prion contains no genome, it can nevertheless replicate and impale the host.

Even within each class of pathogen, at that place is hit diversity. Viruses vary tremendously in their size, shape, and content (DNA versus RNA, enveloped or not, and then on), and the aforementioned is true for the other pathogens. The ability to cause disease (pathogenesis) is a lifestyle choice, not a legacy shared simply amidst close relatives (Figure 25-3).

Figure 25-3

Phylogenetic diversity of pathogens. This diagram shows the similarities among 16S ribosomal RNA for cellular life forms (leaner, archaea, and eucaryotes). Each branch is labeled with the name of a representative fellow member of that group, and the length (more than...)

Each individual pathogen causes disease in a different style, which makes information technology challenging to understand the basic biological science of infection. But, when because the interactions of infectious agents with their hosts, some mutual themes of pathogenesis emerge. These mutual themes are the focus of this chapter. First, we innovate the basic features of each of the major types of pathogens that exploit features of host cell biological science. Then, we examine in turn the mechanisms that pathogens use to command their hosts and the innate mechanisms that hosts use to command pathogens.

Bacterial Pathogens Carry Specialized Virulence Genes

Bacteria are small and structurally uncomplicated, compared to the vast majority of eucaryotic cells. Nearly can be classified broadly past their shape every bit rods, spheres, or spirals and by their cell-surface properties. Although they lack the elaborate morphological variety of eucaryotic cells, they display a surprising assortment of surface appendages that enable them to swim or to adhere to desirable surfaces (Figure 25-iv). Their genomes are correspondingly elementary, typically on the order of i,000,000–5,000,000 nucleotide pairs in size (compared to 12,000,000 for yeast and more than than 3,000,000,000 for humans).

Effigy 25-four

Bacterial shapes and cell-surface structures. Bacteria are classified into 3 different shapes: (A) spheres (cocci), (B) rods (bacilli), and (C) spiral cells (spirochetes). (D) They are also classified equally Gram-positive or Gram-negative. Bacteria such (more...)

Equally emphasized above, only a minority of bacterial species have adult the power to cause disease in humans. Some of those that do crusade disease can only replicate inside the cells of the homo body and are called obligate pathogens. Others replicate in an environmental reservoir such equally water or soil and simply cause disease if they happen to run across a susceptible host; these are chosen facultative pathogens. Many bacteria are normally benign but have a latent ability to cause disease in an injured or immunocompromised host; these are called opportunistic pathogens.

Some bacterial pathogens are fastidious in their option of host and volition only infect a single species or a group of related species, whereas others are generalists. Shigella flexneri, for example, which causes epidemic dysentery (bloody diarrhea) in areas of the earth lacking a make clean water supply, will only infect humans and other primates. By dissimilarity, the closely related bacterium Salmonella enterica, which is a common crusade of food poisoning in humans, can also infect many other vertebrates, including chickens and turtles. A champion generalist is the opportunistic pathogen Pseudomonas aeruginosa, which is capable of causing disease in plants as well as animals.

The meaning differences betwixt a virulent pathogenic bacterium and its closest nonpathogenic relative may result from a very small number of genes. Genes that contribute to the ability of an organism to cause disease are called virulence genes. The proteins they encode are called virulence factors. Virulence genes are frequently clustered together, either in groups on the bacterial chromosome called pathogenicity islands or on extrachromosomal virulence plasmids (Effigy 25-five). These genes may besides exist carried on mobile bacteriophages (bacterial viruses). It seems therefore that a pathogen may arise when groups of virulence genes are transferred together into a previously avirulent bacterium. Consider, for example, Vibrio cholerae—the bacterium that causes cholera. Several of the genes encoding the toxins that cause the diarrhea in cholera are carried on a mobile bacteriophage (Effigy 25-6). Of the hundreds of strains of Vibrio cholerae found in lakes in the wild, the only ones that cause human disease are those that have get infected with this virus.

Effigy 25-five

Genetic differences between pathogens and nonpathogens. Nonpathogenic Escherichia coli has a single circular chromosome. E. coli is very closely related to two types of food-borne pathogens—Shigella flexneri, which causes dysentery, and Salmonella (more than...)

Figure 25-6

Genetic arrangement of Vibrio cholerae. (A) Vibrio cholerae is unusual in having two circular chromosomes rather than one. The two chromosomes have singled-out origins of replication (oriC_one and oriC₂). Three loci in pathogenic strains of 5. cholerae are (more...)

Many virulence genes encode proteins that interact directly with host cells. Two of the genes carried past the Vibrio cholerae phage, for instance, encode two subunits of cholera toxin. The B subunit of this secreted, toxic protein binds to a glycolipid component of the plasma membrane of the epithelial cells in the gut of a person who has consumed Vibrio cholerae in contaminated water. The B subunit transfers the A subunit through the membrane into the epithelial cell cytoplasm. The A subunit is an enzyme that catalyzes the transfer of an ADP-ribose moiety from NAD to the trimeric 1000 poly peptide K_s, which normally activates adenylyl cyclase to make cyclic AMP (discussed in Chapter 15). ADP-ribosylation of the Thousand poly peptide results in an overaccumulation of circadian AMP and an ion imbalance, leading to the massive watery diarrhea associated with cholera. The infection is then spread by the fecal-oral route by contaminated food and water.

Some pathogenic bacteria use several independent mechanisms to crusade toxicity to the cells of their host. Anthrax, for example, is an astute infectious illness of sheep, cattle, other herbivores, and occasionally humans. It is usually caused by contact with spores of the Gram-positive bacterium, Bacillus anthracis. Dissimilar cholera, anthrax has never been observed to spread directly from one infected person to some other. Fallow spores can survive in soil for long periods of fourth dimension and are highly resistant to adverse environmental conditions, including oestrus, ultraviolet and ionizing radiation, pressure, and chemical agents. After the spores are inhaled, ingested, or rubbed into breaks in the skin, the spores germinate, and the bacteria begin to replicate. Growing bacteria secrete two toxins, chosen lethal toxin and edema toxin. Either toxin solitary is sufficient to cause signs of infection. Similar the A and B subunits of cholera toxin, both toxins are fabricated of two subunits. The B subunit is identical between lethal toxin and edema toxin, and it binds to a host cell-surface receptor to transfer the 2 different A subunits into host cells. The A subunit of edema toxin is an adenylyl cyclase that directly converts host prison cell ATP into circadian AMP. This causes an ion imbalance that can lead to accumulation of extracellular fluid (edema) in the infected pare or lung. The A subunit of lethal toxin is a zinc protease that cleaves several members of the MAP kinase kinase family (discussed in Affiliate xv). Injection of lethal toxin into the bloodstream of an animal causes shock and death. The molecular mechanisms and the sequence of events leading to decease in anthrax remain uncertain.

These examples illustrate a common theme amid virulence factors. They are frequently either toxic proteins (toxins) that straight interact with important host structural or signaling proteins to elicit a host cell response that is beneficial to pathogen colonization or replication, or they are proteins that are needed to deliver such toxins to their host cell targets. One mutual and specially efficient delivery mechanism, chosen the type Three secretion organisation, acts like a tiny syringe that injects toxic proteins from the cytoplasm of an extracellular bacterium direct into the cytoplasm of an adjacent host jail cell (Figure 25-7). At that place is a remarkable caste of structural similarity between the type Three syringe and the base of a bacterial flagellum (come across Figure 15-67), and many of the proteins in the two structures are clearly homologous.

Figure 25-7

Type Iii secretion systems that can deliver virulence factors into the cytoplasm of host cells. (A) Electron micrographs of purified type III apparatuses. About 2 dozen proteins are necessary to make the complete structure, which is seen in the 3 (more...)

Considering bacteria class a kingdom distinct from the eucaryotes they infect (come across Figure 25-iii), much of their basic machinery for DNA replication, transcription, translation, and fundamental metabolism is quite different from that of their host. These differences enable united states to find antibacterial drugs that specifically inhibit these processes in leaner, without disrupting them in the host. Nearly of the antibiotics that nosotros apply to treat bacterial infections are pocket-size molecules that inhibit macromolecular synthesis in bacteria by targeting bacterial enzymes that are either singled-out from their eucaryotic counterparts or that are involved in pathways, such every bit cell wall biosynthesis, that are absent in humans (Effigy 25-8 and Table six-3).

Effigy 25-8

Antibiotic targets. Despite the large number of antibiotics bachelor, they have a narrow range of targets, which are highlighted in yellow. A few representative antibiotics in each class are listed. All antibiotics used to care for man infections autumn (more...)

Fungal and Protozoan Parasites Have Complex Life Cycles with Multiple Forms

Pathogenic fungi and protozoan parasites are eucaryotes. It is therefore more difficult to find drugs that will kill them without killing the host. Consequently, antifungal and antiparasitic drugs are often less effective and more toxic than antibiotics. A second characteristic of fungal and parasitic infections that makes them hard to treat is the tendency of the infecting organisms to switch among several different forms during their life cycles. A drug that is constructive at killing one form is frequently ineffective at killing another form, which therefore survives the treatment.

The fungal co-operative of the eucaryotic kingdom includes both unicellular yeasts (such as Saccharomyces cerevisiae and Schizosaccharomyces pombe) and filamentous, multicellular molds (like those plant on moldy fruit or bread). Most of the important pathogenic fungi exhibit dimorphism—the ability to grow in either yeast or mold form. The yeast-to-mold or mold-to-yeast transition is ofttimes associated with infection. Histoplasma capsulatum, for example, grows as a mold at depression temperature in the soil, only it switches to a yeast form when inhaled into the lung, where it can cause the disease histoplasmosis (Figure 25-9).

Figure 25-ix

Dimorphism in the pathogenic fungus Histoplasma capsulatum. (A) At depression temperature in the soil, Histoplasma grows as a filamentous fungus. (B) Afterwards being inhaled into the lung of a mammal, Histoplasma undergoes a morphological switch triggered past the (more...)

Protozoan parasites take more elaborate life cycles than do fungi. These cycles frequently require the services of more one host. Malaria is the nigh common protozoal disease, infecting 200–300 million people every twelvemonth and killing i–3 million of them. It is caused by four species of Plasmodium, which are transmitted to humans by the bite of the female of any of 60 species of Anopheles mosquito. Plasmodium falciparum—the most intensively studied of the malaria-causing parasites—exists in no fewer than eight distinct forms, and it requires both the man and musquito hosts to complete its sexual cycle (Figure 25-x). Gametes are formed in the bloodstream of infected humans, but they can only fuse to grade a zygote in the gut of the mosquito. Three of the Plasmodium forms are highly specialized to invade and replicate in specific tissues—the insect gut lining, the human liver, and the human ruddy blood cell.

Effigy 25-10

The complex life wheel of malaria. (A) The sexual cycle of Plasmodium falciparum requires passage between a human being host and an insect host. (B)-(D) Blood smears from people infected with malaria, showing three different forms of the parasite that appear (more...)

Because malaria is so widespread and devastating, it has acted equally a strong selective pressure on human being populations in areas of the globe that harbor the Anopheles musquito. Sickle cell anemia, for example, is a recessive genetic disorder acquired past a point mutation in the factor that encodes the hemoglobin β concatenation, and information technology is common in areas of Africa with a high incidence of the most serious class of malaria (caused by Plasmodium falciparum). The malarial parasites abound poorly in red blood cells from either homozygous sickle cell patients or healthy heterozygous carriers, and, as a effect, malaria is seldom found among carriers of this mutation. For this reason, malaria has maintained the sickle cell mutation at high frequency in these regions of Africa.

Viruses Exploit Host Cell Mechanism for All Aspects of Their Multiplication

Bacteria, fungi, and eucaryotic parasites are cells themselves. Even when they are obligate parasites, they utilize their own machinery for Dna replication, transcription, and translation, and they provide their own sources of metabolic energy. Viruses, by dissimilarity, are the ultimate hitchhikers, carrying lilliputian more than than information in the form of nucleic acrid. The information is largely replicated, packaged, and preserved by the host cells (Figure 25-xi). Viruses have a small genome, fabricated up of a single nucleic acrid blazon—either DNA or RNA—which, in either example, may be single-stranded or double-stranded. The genome is packaged in a poly peptide coat, which in some viruses is further enclosed by a lipid envelope.

Effigy 25-11

A unproblematic viral life wheel. The hypothetical virus shown consists of a small double-stranded DNA molecule that codes for only a single viral capsid protein. No known virus is this simple.

Viruses replicate in various ways. In general, replication involves (1) disassembly of the infectious virus particle, (ii) replication of the viral genome, (iii) synthesis of the viral proteins by the host cell translation machinery, and (iv) reassembly of these components into progeny virus particles. A single virus particle (a virion) that infects a unmarried host cell can produce thousands of progeny in the infected cell. Such biggy viral multiplication is often enough to kill the host jail cell: the infected cell breaks open (lyses) and thereby allows the progeny viruses access to nearby cells. Many of the clinical manifestations of viral infection reflect this cytolytic outcome of the virus. Both the cold sores formed by herpes simplex virus and the lesions caused by the smallpox virus, for example, reverberate the killing of the epidermal cells in a local area of infected pare.

Viruses come in a wide multifariousness of shapes and sizes, and, unlike cellular life forms, they cannot be systematically classified by their relatedness into a single phylogenetic tree. Because of their tiny sizes, consummate genome sequences accept been obtained for near all clinically of import viruses. Poxviruses are among the largest, up to 450 nm long, which is virtually the size of some small bacteria. Their genome of double-stranded DNA consists of virtually 270,000 nucleotide pairs. At the other finish of the size scale are parvoviruses, which are less than 20 nm long and have a single-stranded Deoxyribonucleic acid genome of under 5000 nucleotides (Figure 25-12). The genetic information in a virus can be carried in a diverseness of unusual nucleic acrid forms (Figure 25-13).

Figure 25-12

Examples of viral morphology. As shown, viruses vary greatly in both size and shape.

Figure 25-13

Schematic drawings of several types of viral genomes. The smallest viruses incorporate only a few genes and can have an RNA or a Dna genome. The largest viruses comprise hundreds of genes and take a double-stranded DNA genome. The peculiar ends (as well every bit (more...)

The capsid that encloses the viral genome is made of one or several proteins, bundled in regularly repeating layers and patterns. In enveloped viruses, the capsid itself is enclosed by a lipid bilayer membrane that is caused in the process of budding from the host cell plasma membrane (Figure 25-14). Whereas nonenveloped viruses usually leave an infected prison cell past lysing it, an enveloped virus can leave the cell past budding, without disrupting the plasma membrane and, therefore, without killing the prison cell. These viruses can cause chronic infections, and some tin help transform an infected prison cell into a cancer cell.

Figure 25-14

Conquering of a viral envelope. (A) Electron micrograph of an animal jail cell from which six copies of an enveloped virus (Semliki forest virus) are budding. (B) Schematic view of the envelope assembly and budding processes. The lipid bilayer that surrounds (more...)

Despite this diversity, all viral genomes encode three types of proteins: proteins for replicating the genome, proteins for packaging the genome and delivering it to more host cells, and proteins that modify the structure or function of the host cell to suit the needs of the virus (Figure 25-15). In the second section of this affiliate, we focus primarily on this third class of viral proteins.

Figure 25-15

A map of the HIV genome. This retroviral genome consists of about 9000 nucleotides and contains nine genes, the locations of which are shown in green and cerise. Three of the genes (green) are common to all retroviruses: gag encodes capsid proteins, env (more...)

Since nigh of the critical steps in viral replication are performed by host jail cell machinery, the identification of effective antiviral drugs is specially problematic. Whereas the antibody tetracycline specifically poisons bacterial ribosomes, for example, it will not be possible to notice a drug that specifically poisons viral ribosomes, as viruses use the ribosomes of the host cell to make their proteins. The best strategy for containing viral diseases is to prevent them past vaccination of the potential hosts. Highly successful vaccination programs have finer eliminated smallpox from the planet, and the eradication of poliomyelitis is imminent (Figure 25-16).

Effigy 25-16

Eradication of a viral disease through vaccination. The graph shows number of cases of poliomyelitis reported per year in the United States. The arrows indicate the timing of the introduction of the Salk vaccine (inactivated virus given by injection) (more than...)

Prions Are Infectious Proteins

All information in biological systems is encoded by structure. We are used to thinking of biological information in the form of nucleic acid sequences (equally in our clarification of viral genomes), simply the sequence itself is a shorthand lawmaking for describing nucleic acid construction. The replication and expression of the information encoded in DNA and RNA are strictly dependent on the structure of these nucleic acids and their interactions with other macromolecules. The propagation of genetic data primarily requires that the information be stored in a structure that can be duplicated from unstructured precursors. Nucleic acid sequences are the simplest and most robust solution that organisms have found to the trouble of faithful structural replication.

Nucleic acids are not the only solution, however. Prions are infectious agents that are replicated in the host past copying an abnormal poly peptide structure. They can occur in yeasts, and they cause diverse neurodegenerative diseases in mammals. The near well-known infection caused by prions is bovine spongiform encephalopathy (BSE, or mad cow disease), which occasionally spreads to humans who eat infected parts of the cow (Figure 25-17). Isolation of the infectious prions that cause the illness scrapie in sheep, followed by years of painstaking laboratory characterization of scrapie-infected mice, eventually established that the protein itself is infectious.

Figure 25-17

Neural degeneration in a prion infection. This micrograph shows a slice from the encephalon of a person who died of kuru. Kuru is a human prion affliction, very similar to BSE, that was spread from one person to another by ritual mortuary practices in New Guinea. (more than...)

Intriguingly, the infectious prion protein is made by the host, and its amino acid sequence is identical to a normal host protein. Moreover, the prion and normal forms of the protein are indistinguishable in their posttranslational modifications. The just difference between them appears to be in their folded three-dimensional structure. The misfolded prion protein tends to amass, and it has the remarkable capacity to cause the normal protein to adopt its misfolded prion conformation and thereby to become infectious (see Figure 6-89). This ability of the prion to convert the normal host protein to misfolded prion protein is equivalent to the prion's having replicated itself in the host. If eaten by another susceptible host, these newly-misfolded prions can transmit the infection.

It is non known how normal proteins are usually able to notice the single, right, folded conformation, amid the billions of other possibilities, without becoming stuck in dead-end intermediates (discussed in Chapters 3 and vi). Prions are a expert example of how poly peptide folding tin can go dangerously wrong. Merely, why are the prion diseases and so uncommon? What are the constraints that determine whether a misfolded protein will acquit like a prion, or but become refolded or degraded by the cell that made it? We exercise non even so have answers to these questions, and the study of prions remains an area of intense research.

Summary

Infectious diseases are caused by pathogens, which include bacteria, fungi, protozoa, worms, viruses, and fifty-fifty infectious proteins called prions. Pathogens of all classes must accept mechanisms for entering their host and for evading immediate devastation by the host allowed organisation. Most bacteria are not pathogenic. Those that are contain specific virulence genes that mediate interactions with the host, eliciting particular responses from the host cells that promote the replication and spread of the pathogen. Pathogenic fungi, protozoa, and other eucaryotic parasites typically pass through several different forms during the course of infection; the ability to switch amongst these forms is unremarkably required for the parasites to exist able to survive in a host and crusade disease. In some cases, such as malaria, parasites must pass sequentially through several host species to consummate their life cycles. Unlike bacteria and eucaryotic parasites, viruses have no metabolism of their ain and no intrinsic power to produce the proteins encoded by their Deoxyribonucleic acid or RNA genomes. They rely entirely on subverting the mechanism of the host cell to produce their proteins and to replicate their genomes. Prions, the smallest and simplest infectious agents, contain no nucleic acid; instead, they are rare, aberrantly folded proteins that happen to catalyze the misfolding of proteins in the host that share their primary amino acid sequence.

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Source: https://www.ncbi.nlm.nih.gov/books/NBK26917/