What Is An Organism That Carries And Transmits Pathogens To Humans Or Other Animals?

We normally think of pathogens in hostile terms—as 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 it is possible that every living organism on earth is field of study to some type of infection or parasitism (Figure 25-ane). A human being host is a nutrient-rich, warm, and moist environment, which remains at a compatible temperature and constantly renews itself. Information technology is not surprising that many microorganisms take evolved the ability to survive and reproduce in this desirable niche. In this section, we talk over some of the common features that microorganisms must have in order to be infectious. We and so explore the broad diversity of organisms that are known to cause illness in humans.

Effigy 25-1

Parasitism at many levels. (A) Scanning electron micrograph of a flea. The flea is a mutual 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 human being trunk is a complex and thriving ecosystem. It contains almost ten^xiii human being cells and also virtually 10¹⁴ bacterial, fungal, and protozoan cells, which represent thousands of microbial species. These microbes, called the normal flora, are commonly limited to certain areas of the body, including the skin, mouth, big intestine, and vagina. In addition, humans are ever infected with viruses, about of which rarely, if e'er, become symptomatic. If it is normal for us to alive in such close intimacy with a wide variety of microbes, how is it that some of them are capable of causing us illness or death?

Pathogens are usually distinct from the normal flora. Our normal microbial inhabitants only cause trouble if our allowed systems are weakened or if they gain access to a commonly sterile part of the body (for instance, when a bowel perforation enables the gut flora to enter the peritoneal cavity 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 lodge to survive and multiply in a host, a successful pathogen must be able to: (ane) colonize the host; (2) discover a nutritionally compatible niche in the host body; (3) avoid, subvert, or circumvent the host innate and adaptive allowed responses; (4) replicate, using host resources; and (5) exit and spread to a new host. Nether severe selective force per unit area to induce only the correct host cell responses to accomplish this circuitous set of tasks, pathogens have evolved mechanisms that maximally exploit the biological science of their host organisms. Many of the pathogens we discuss in this chapter are practiced and applied cell biologists. We can learn a great deal of cell biology by observing them.

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

Although we can easily understand why infectious microorganisms would evolve to reproduce in a host, it is less articulate why they would evolve to cause disease. One caption may be that, in some cases, the pathological responses elicited past microorganisms raise the efficiency of their spread or propagation and hence clearly take a selective reward for the pathogen. The virus-containing lesions on the ballocks caused past 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, nevertheless, the consecration 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 blood cells), are the straight result of immune system cells attempting to destroy the invading microorganisms. Fever, too, is a defensive response, every bit the increment in torso temperature tin inhibit the growth of some microorganisms. Thus, understanding the biology of an communicable diseases requires an appreciation of the contributions of both pathogen and host.

Pathogens Are Phylogenetically Diverse

Many types of pathogens cause disease in humans. The virtually familiar are viruses and bacteria. Viruses cause diseases ranging from AIDS and smallpox to the common cold. They are substantially fragments of nucleic acid (DNA or RNA) instructions, wrapped in a protective shell of proteins and (in some cases) membrane (Figure 25-2A). They utilise the basic transcription and translation machinery of their host cells for their replication.

Effigy 25-2

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

Of all the bacteria we run across in our lives, just a small minority are defended pathogens. Much larger and more than complex than viruses, bacteria are usually free-living cells, which perform most of their basic metabolic functions themselves, relying on the host primarily for nutrition (Figure 25-2B).

Another infectious agents are eucaryotic organisms. These range from single-celled fungi and protozoa (Figure 25-2C), through large circuitous metazoa such as parasitic worms. One of the almost common 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 research (discussed in Chapter 21). C. elegans, however, is only about 1 mm in length, whereas Ascaris can reach thirty cm (Figure 25-2D).

Some rare neurodegenerative diseases, including mad cow disease, are acquired by an unusual type of infectious particle chosen a prion, which is fabricated only of protein. Although the prion contains no genome, it can nevertheless replicate and kill the host.

Even inside each form of pathogen, there is hitting diversity. Viruses vary tremendously in their size, shape, and content (DNA versus RNA, enveloped or non, and so on), and the same is true for the other pathogens. The power to crusade disease (pathogenesis) is a lifestyle choice, not a legacy shared only amongst close relatives (Figure 25-3).

Figure 25-3

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

Each individual pathogen causes disease in a different way, which makes information technology challenging to sympathize the basic biology of infection. Simply, when considering the interactions of infectious agents with their hosts, some mutual themes of pathogenesis sally. These mutual themes are the focus of this chapter. First, we introduce the bones features of each of the major types of pathogens that exploit features of host cell biology. Then, we examine in plough the mechanisms that pathogens use to control their hosts and the innate mechanisms that hosts employ to command pathogens.

Bacterial Pathogens Carry Specialized Virulence Genes

Bacteria are minor and structurally simple, compared to the vast bulk of eucaryotic cells. Most tin be classified broadly by their shape as rods, spheres, or spirals and by their cell-surface properties. Although they lack the elaborate morphological multifariousness of eucaryotic cells, they display a surprising array of surface appendages that enable them to swim or to attach to desirable surfaces (Figure 25-four). Their genomes are correspondingly unproblematic, typically on the guild of 1,000,000–v,000,000 nucleotide pairs in size (compared to 12,000,000 for yeast and more than 3,000,000,000 for humans).

Effigy 25-4

Bacterial shapes and cell-surface structures. Leaner are classified into three different shapes: (A) spheres (cocci), (B) rods (bacilli), and (C) screw cells (spirochetes). (D) They are besides classified as Gram-positive or Gram-negative. Bacteria such (more than...)

As emphasized higher up, only a minority of bacterial species have adult the power to cause disease in humans. Some of those that exercise cause disease can only replicate inside the cells of the man body and are chosen obligate pathogens. Others replicate in an environmental reservoir such as water or soil and simply cause illness if they happen to meet a susceptible host; these are called facultative pathogens. Many bacteria are normally benign but have a latent power to crusade disease in an injured or immunocompromised host; these are called opportunistic pathogens.

Some bacterial pathogens are fastidious in their choice of host and will only infect a single species or a group of related species, whereas others are generalists. Shigella flexneri, for instance, which causes epidemic dysentery (bloody diarrhea) in areas of the globe defective a make clean h2o supply, will only infect humans and other primates. By contrast, the closely related bacterium Salmonella enterica, which is a mutual crusade of nutrient 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 likewise as animals.

The meaning differences between a virulent pathogenic bacterium and its closest nonpathogenic relative may result from a very small-scale number of genes. Genes that contribute to the ability of an organism to cause disease are called virulence genes. The proteins they encode are chosen 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-v). These genes may also be 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 (Figure 25-6). Of the hundreds of strains of Vibrio cholerae plant in lakes in the wild, the but ones that crusade man illness are those that have get infected with this virus.

Figure 25-5

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...)

Figure 25-6

Genetic organization of Vibrio cholerae. (A) Vibrio cholerae is unusual in having two circular chromosomes rather than i. The 2 chromosomes have distinct origins of replication (oriC_ane and oriC₂). Three loci in pathogenic strains of Five. cholerae are (more...)

Many virulence genes encode proteins that interact straight with host cells. Two of the genes carried by the Vibrio cholerae phage, for example, encode two subunits of cholera toxin. The B subunit of this secreted, toxic poly peptide 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 One thousand poly peptide G_southward, which normally activates adenylyl cyclase to make cyclic AMP (discussed in Chapter 15). ADP-ribosylation of the G poly peptide results in an overaccumulation of cyclic AMP and an ion imbalance, leading to the massive watery diarrhea associated with cholera. The infection is then spread by the fecal-oral road by contaminated nutrient and water.

Some pathogenic bacteria use several independent mechanisms to cause toxicity to the cells of their host. Anthrax, for example, is an acute infectious disease of sheep, cattle, other herbivores, and occasionally humans. Information technology is usually acquired by contact with spores of the Gram-positive bacterium, Bacillus anthracis. Unlike cholera, anthrax has never been observed to spread directly from i infected person to another. Dormant spores can survive in soil for long periods of time and are highly resistant to adverse environmental conditions, including oestrus, ultraviolet and ionizing radiations, pressure, and chemic agents. After the spores are inhaled, ingested, or rubbed into breaks in the skin, the spores germinate, and the leaner begin to replicate. Growing bacteria secrete two toxins, called lethal toxin and edema toxin. Either toxin lonely 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 jail cell-surface receptor to transfer the two unlike A subunits into host cells. The A subunit of edema toxin is an adenylyl cyclase that directly converts host cell ATP into circadian AMP. This causes an ion imbalance that can lead to accumulation of extracellular fluid (edema) in the infected peel or lung. The A subunit of lethal toxin is a zinc protease that cleaves several members of the MAP kinase kinase family (discussed in Chapter 15). Injection of lethal toxin into the bloodstream of an animal causes shock and decease. The molecular mechanisms and the sequence of events leading to death in anthrax remain uncertain.

These examples illustrate a common theme among virulence factors. They are frequently either toxic proteins (toxins) that directly interact with of import host structural or signaling proteins to elicit a host cell response that is benign to pathogen colonization or replication, or they are proteins that are needed to evangelize such toxins to their host prison cell targets. One common and particularly efficient delivery mechanism, called the type 3 secretion system, acts like a tiny syringe that injects toxic proteins from the cytoplasm of an extracellular bacterium directly into the cytoplasm of an side by side host cell (Figure 25-7). In that location is a remarkable degree of structural similarity between the type 3 syringe and the base of a bacterial flagellum (encounter Figure 15-67), and many of the proteins in the two structures are conspicuously homologous.

Figure 25-7

Blazon Iii secretion systems that can evangelize virulence factors into the cytoplasm of host cells. (A) Electron micrographs of purified type Three apparatuses. About two dozen proteins are necessary to make the consummate structure, which is seen in the 3 (more...)

Because bacteria course a kingdom distinct from the eucaryotes they infect (run across Figure 25-3), much of their basic machinery for DNA replication, transcription, translation, and key metabolism is quite different from that of their host. These differences enable us to find antibacterial drugs that specifically inhibit these processes in bacteria, without disrupting them in the host. Most of the antibiotics that we utilize to treat bacterial infections are small molecules that inhibit macromolecular synthesis in leaner by targeting bacterial enzymes that are either distinct from their eucaryotic counterparts or that are involved in pathways, such as cell wall biosynthesis, that are absent in humans (Figure 25-8 and Table 6-iii).

Figure 25-8

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

Fungal and Protozoan Parasites Have Complex Life Cycles with Multiple Forms

Pathogenic fungi and protozoan parasites are eucaryotes. Information technology is therefore more difficult to detect drugs that volition 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 difficult to treat is the tendency of the infecting organisms to switch among several different forms during their life cycles. A drug that is effective at killing i form is oft ineffective at killing another grade, which therefore survives the handling.

The fungal branch of the eucaryotic kingdom includes both unicellular yeasts (such every bit Saccharomyces cerevisiae and Schizosaccharomyces pombe) and filamentous, multicellular molds (similar those establish on moldy fruit or staff of life). Most of the important pathogenic fungi showroom dimorphism—the ability to abound in either yeast or mold form. The yeast-to-mold or mold-to-yeast transition is frequently associated with infection. Histoplasma capsulatum, for example, grows every bit a mold at low temperature in the soil, but it switches to a yeast form when inhaled into the lung, where it can crusade 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 equally a filamentous fungus. (B) Afterwards being inhaled into the lung of a mammal, Histoplasma undergoes a morphological switch triggered by the (more...)

Protozoan parasites have more elaborate life cycles than do fungi. These cycles frequently require the services of more than than one host. Malaria is the most common protozoal disease, infecting 200–300 one thousand thousand people every twelvemonth and killing one–3 meg of them. It is caused by 4 species of Plasmodium, which are transmitted to humans past the bite of the female of whatsoever of threescore species of Anopheles mosquito. Plasmodium falciparum—the most intensively studied of the malaria-causing parasites—exists in no fewer than eight distinct forms, and information technology requires both the human and mosquito hosts to complete its sexual cycle (Figure 25-x). Gametes are formed in the bloodstream of infected humans, only they tin only fuse to form 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 reddish claret jail cell.

Effigy 25-10

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

Because malaria is so widespread and devastating, it has acted as a strong selective pressure level on human populations in areas of the world that harbor the Anopheles musquito. Sickle cell anemia, for example, is a recessive genetic disorder caused past a point mutation in the gene that encodes the hemoglobin β chain, and information technology is common in areas of Africa with a high incidence of the most serious form of malaria (caused by Plasmodium falciparum). The malarial parasites grow poorly in red claret cells from either homozygous sickle cell patients or good for you heterozygous carriers, and, as a event, 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 Prison cell Machinery for All Aspects of Their Multiplication

Bacteria, fungi, and eucaryotic parasites are cells themselves. Even when they are obligate parasites, they use their ain machinery for DNA replication, transcription, and translation, and they provide their own sources of metabolic energy. Viruses, by dissimilarity, are the ultimate hitchhikers, carrying little more information in the grade of nucleic acid. The information is largely replicated, packaged, and preserved past the host cells (Figure 25-xi). Viruses have a small genome, made up of a single nucleic acid type—either Deoxyribonucleic acid or RNA—which, in either case, may be single-stranded or double-stranded. The genome is packaged in a protein coat, which in some viruses is farther enclosed by a lipid envelope.

Figure 25-11

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

Viruses replicate in various means. In full general, replication involves (one) disassembly of the infectious virus particle, (2) replication of the viral genome, (3) synthesis of the viral proteins by the host jail cell translation machinery, and (4) 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 prison cell. Such prodigious viral multiplication is ofttimes enough to kill the host cell: the infected jail cell breaks open up (lyses) and thereby allows the progeny viruses access to nearby cells. Many of the clinical manifestations of viral infection reflect this cytolytic effect of the virus. Both the common cold sores formed by herpes simplex virus and the lesions caused by the smallpox virus, for example, reflect the killing of the epidermal cells in a local surface area of infected skin.

Viruses come in a broad multifariousness of shapes and sizes, and, unlike cellular life forms, they cannot exist systematically classified by their relatedness into a single phylogenetic tree. Because of their tiny sizes, consummate genome sequences have been obtained for nearly all clinically important viruses. Poxviruses are among the largest, upwardly to 450 nm long, which is about the size of some small bacteria. Their genome of double-stranded DNA consists of near 270,000 nucleotide pairs. At the other terminate of the size calibration are parvoviruses, which are less than 20 nm long and have a single-stranded DNA genome of under 5000 nucleotides (Figure 25-12). The genetic data in a virus can be carried in a variety of unusual nucleic acid 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 contain hundreds of genes and accept a double-stranded DNA genome. The peculiar ends (as well every bit (more...)

The capsid that encloses the viral genome is fabricated of 1 or several proteins, arranged in regularly repeating layers and patterns. In enveloped viruses, the capsid itself is enclosed past a lipid bilayer membrane that is acquired in the process of budding from the host prison cell plasma membrane (Figure 25-14). Whereas nonenveloped viruses unremarkably leave an infected jail cell past lysing it, an enveloped virus tin leave the jail cell by budding, without disrupting the plasma membrane and, therefore, without killing the cell. These viruses can cause chronic infections, and some tin can help transform an infected jail cell into a cancer prison cell.

Figure 25-14

Acquisition of a viral envelope. (A) Electron micrograph of an animal cell from which half-dozen copies of an enveloped virus (Semliki woods virus) are budding. (B) Schematic view of the envelope associates and budding processes. The lipid bilayer that surrounds (more...)

Despite this variety, all viral genomes encode three types of proteins: proteins for replicating the genome, proteins for packaging the genome and delivering information technology to more host cells, and proteins that modify the structure or office of the host cell to suit the needs of the virus (Figure 25-fifteen). In the second department 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 red. Three of the genes (greenish) are mutual to all retroviruses: gag encodes capsid proteins, env (more...)

Since most of the critical steps in viral replication are performed by host prison cell machinery, the identification of constructive antiviral drugs is particularly problematic. Whereas the antibiotic tetracycline specifically poisons bacterial ribosomes, for example, information technology will not be possible to notice a drug that specifically poisons viral ribosomes, equally viruses utilise the ribosomes of the host prison cell to brand their proteins. The best strategy for containing viral diseases is to prevent them by vaccination of the potential hosts. Highly successful vaccination programs accept effectively eliminated smallpox from the planet, and the eradication of poliomyelitis is imminent (Figure 25-16).

Figure 25-16

Eradication of a viral illness through vaccination. The graph shows number of cases of poliomyelitis reported per year in the United states. The arrows betoken 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 past construction. We are used to thinking of biological data in the form of nucleic acid sequences (as in our clarification of viral genomes), just the sequence itself is a shorthand code for describing nucleic acid structure. The replication and expression of the information encoded in Dna and RNA are strictly dependent on the construction of these nucleic acids and their interactions with other macromolecules. The propagation of genetic information primarily requires that the information exist stored in a structure that can be duplicated from unstructured precursors. Nucleic acid sequences are the simplest and most robust solution that organisms have plant to the problem of faithful structural replication.

Nucleic acids are non the merely solution, all the same. Prions are infectious agents that are replicated in the host by copying an aberrant poly peptide structure. They tin can occur in yeasts, and they cause various neurodegenerative diseases in mammals. The near well-known infection caused past prions is bovine spongiform encephalopathy (BSE, or mad cow disease), which occasionally spreads to humans who swallow infected parts of the moo-cow (Figure 25-17). Isolation of the infectious prions that crusade the disease scrapie in sheep, followed past years of painstaking laboratory characterization of scrapie-infected mice, somewhen established that the protein itself is infectious.

Effigy 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 disease, very similar to BSE, that was spread from 1 person to another by ritual mortuary practices in New Republic of guinea. (more...)

Intriguingly, the infectious prion protein is made past the host, and its amino acrid sequence is identical to a normal host protein. Moreover, the prion and normal forms of the protein are indistinguishable in their posttranslational modifications. The but difference betwixt them appears to be in their folded 3-dimensional structure. The misfolded prion poly peptide tends to aggregate, and it has the remarkable chapters to cause the normal protein to adopt its misfolded prion conformation and thereby to become infectious (see Effigy 6-89). This ability of the prion to catechumen 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 not known how normal proteins are usually able to find the single, correct, folded conformation, among the billions of other possibilities, without becoming stuck in expressionless-end intermediates (discussed in Chapters 3 and 6). Prions are a good case of how protein folding tin go dangerously wrong. Only, why are the prion diseases so uncommon? What are the constraints that determine whether a misfolded protein will conduct like a prion, or simply get refolded or degraded by the jail cell that made it? We do not nonetheless have answers to these questions, and the study of prions remains an area of intense enquiry.

Summary

Infectious diseases are caused by pathogens, which include bacteria, fungi, protozoa, worms, viruses, and even infectious proteins called prions. Pathogens of all classes must have mechanisms for entering their host and for evading immediate devastation past the host allowed system. Nigh 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 amid these forms is normally required for the parasites to be able to survive in a host and cause disease. In some cases, such every bit malaria, parasites must laissez passer 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 ability to produce the proteins encoded by their DNA or RNA genomes. They rely entirely on subverting the machinery of the host cell to produce their proteins and to replicate their genomes. Prions, the smallest and simplest infectious agents, contain no nucleic acrid; 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.

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

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