what term refers to the preference of a pathogen for a particular part of the body?

We commonly call back of pathogens in hostile terms—as invaders that attack our bodies. But a pathogen or a parasite, like any other organism, is just trying to live and procreate. Living at the expense of a host organism is a very bonny strategy, and it is possible that every living organism on earth is subject to some blazon of infection or parasitism (Figure 25-1). A human host is a nutrient-rich, warm, and moist environment, which remains at a compatible temperature and constantly renews itself. It is not surprising that many microorganisms take evolved the ability to survive and reproduce in this desirable niche. In this department, we hash out some of the mutual features that microorganisms must have in order to be infectious. We then explore the wide variety of organisms that are known to crusade disease in humans.

Figure 25-one

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 trunk is a circuitous and thriving ecosystem. Information technology contains about 10¹³ human cells and too near 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 pare, rima oris, large intestine, and vagina. In addition, humans are ever infected with viruses, nearly of which rarely, if ever, become symptomatic. If information technology is normal for u.s. to alive in such shut intimacy with a wide variety of microbes, how is it that some of them are capable of causing united states illness or decease?

Pathogens are usually distinct from the normal flora. Our normal microbial inhabitants only cause trouble if our immune systems are weakened or if they gain access to a normally sterile part of the trunk (for example, when a bowel perforation enables the gut flora to enter the peritoneal cavity of the abdomen, causing peritonitis). In contrast, defended pathogens do non require that the host exist 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; (two) detect a nutritionally uniform niche in the host body; (three) avoid, subvert, or circumvent the host innate and adaptive immune responses; (4) replicate, using host resource; and (5) exit and spread to a new host. Under severe selective pressure to induce just the correct host cell responses to accomplish this circuitous set of tasks, pathogens have evolved mechanisms that maximally exploit the biology of their host organisms. Many of the pathogens we discuss in this chapter are skillful and practical prison cell biologists. Nosotros can acquire a not bad bargain of cell biology by observing them.

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

Although we tin easily sympathise why infectious microorganisms would evolve to reproduce in a host, information technology is less articulate why they would evolve to cause disease. Ane caption may be that, in some cases, the pathological responses elicited by microorganisms enhance the efficiency of their spread or propagation and hence conspicuously have a selective advantage for the pathogen. The virus-containing lesions on the ballocks caused by herpes simplex infection, for example, 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 flagman. In many cases, still, the induction of disease has no apparent reward for the pathogen.

Many of the symptoms and signs that we associate with communicable diseases are directly manifestations of the host's immune responses in activity. 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 direct result of allowed arrangement cells attempting to destroy the invading microorganisms. Fever, too, is a defensive response, as the increase in torso temperature can inhibit the growth of some microorganisms. Thus, understanding 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 affliction in humans. The most familiar are viruses and leaner. Viruses crusade diseases ranging from AIDS and smallpox to the mutual common cold. They are essentially fragments of nucleic acid (Deoxyribonucleic acid or RNA) instructions, wrapped in a protective beat out of proteins and (in some cases) membrane (Figure 25-2A). They employ the basic transcription and translation machinery of their host cells for their replication.

Figure 25-2

Pathogens in many forms. (A) The construction of the poly peptide coat, or capsid, of poliovirus. This virus was once a common cause of paralysis, just the affliction (poliomyelitis) has been most eradicated by widespread vaccination. (B) The bacterium Vibrio cholerae (more...)

Of all the leaner nosotros encounter in our lives, only a pocket-sized minority are dedicated pathogens. Much larger and more complex than viruses, bacteria are unremarkably 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 complex metazoa such every bit parasitic worms. Ane of the virtually common infectious diseases on the planet, shared by about a billion people at present, is an infestation in the gut by 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 30 cm (Figure 25-2nd).

Some rare neurodegenerative diseases, including mad cow disease, are caused by an unusual blazon of infectious particle chosen a prion, which is fabricated only of protein. Although the prion contains no genome, it can even so replicate and impale the host.

Fifty-fifty within each class of pathogen, there is striking diversity. Viruses vary tremendously in their size, shape, and content (Deoxyribonucleic acid versus RNA, enveloped or non, and and so on), and the same is true for the other pathogens. The ability to cause disease (pathogenesis) is a lifestyle choice, not a legacy shared merely among close relatives (Figure 25-3).

Figure 25-iii

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 member of that group, and the length (more...)

Each individual pathogen causes illness in a different manner, which makes it challenging to understand the bones biology of infection. But, when considering the interactions of infectious agents with their hosts, some common themes of pathogenesis sally. These mutual themes are the focus of this chapter. Beginning, nosotros introduce the basic features of each of the major types of pathogens that exploit features of host cell biological science. Then, nosotros examine in plow the mechanisms that pathogens utilize to control their hosts and the innate mechanisms that hosts use to control pathogens.

Bacterial Pathogens Carry Specialized Virulence Genes

Bacteria are pocket-sized and structurally simple, compared to the vast majority of eucaryotic cells. Most can exist classified broadly past their shape as rods, spheres, or spirals and past their cell-surface backdrop. Although they lack the elaborate morphological variety of eucaryotic cells, they brandish a surprising array of surface appendages that enable them to swim or to attach to desirable surfaces (Figure 25-4). Their genomes are correspondingly simple, typically on the order of 1,000,000–5,000,000 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. Bacteria are classified into three dissimilar shapes: (A) spheres (cocci), (B) rods (bacilli), and (C) spiral cells (spirochetes). (D) They are besides classified as Gram-positive or Gram-negative. Leaner such (more...)

Every bit emphasized above, only a minority of bacterial species have developed the ability to cause disease in humans. Some of those that do crusade disease can but replicate within the cells of the human body and are chosen obligate pathogens. Others replicate in an environmental reservoir such as h2o or soil and merely crusade disease if they happen to see a susceptible host; these are called facultative pathogens. Many bacteria are normally beneficial merely 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 choice of host and will 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 world defective a clean water supply, will merely infect humans and other primates. By dissimilarity, the closely related bacterium Salmonella enterica, which is a mutual cause of nutrient poisoning in humans, tin 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 significant differences between a virulent pathogenic bacterium and its closest nonpathogenic relative may consequence from a very modest 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 likewise 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-half dozen). Of the hundreds of strains of Vibrio cholerae found in lakes in the wild, the only ones that cause human disease are those that accept go infected with this virus.

Figure 25-5

Genetic differences betwixt pathogens and nonpathogens. Nonpathogenic Escherichia coli has a single round chromosome. Due east. coli is very closely related to 2 types of food-borne pathogens—Shigella flexneri, which causes dysentery, and Salmonella (more...)

Effigy 25-half dozen

Genetic arrangement of Vibrio cholerae. (A) Vibrio cholerae is unusual in having two circular chromosomes rather than one. The 2 chromosomes have distinct origins of replication (oriC₁ and oriC₂). Iii loci in pathogenic strains of V. cholerae are (more than...)

Many virulence genes encode proteins that collaborate directly with host cells. Two of the genes carried by the Vibrio cholerae phage, for case, 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 jail cell cytoplasm. The A subunit is an enzyme that catalyzes the transfer of an ADP-ribose moiety from NAD to the trimeric One thousand protein G_s, which normally activates adenylyl cyclase to make cyclic AMP (discussed in Affiliate 15). ADP-ribosylation of the G protein results in an overaccumulation of cyclic AMP and an ion imbalance, leading to the massive watery diarrhea associated with cholera. The infection is so spread past the fecal-oral route past contaminated food and h2o.

Some pathogenic bacteria utilise 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. It is commonly caused by contact with spores of the Gram-positive bacterium, Bacillus anthracis. Different cholera, anthrax has never been observed to spread directly from 1 infected person to another. Dormant spores tin can survive in soil for long periods of time 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 leaner secrete two toxins, called 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 made 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 cyclic AMP. This causes an ion imbalance that can atomic number 82 to accumulation of extracellular fluid (edema) in the infected skin 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 animate being causes stupor and death. The molecular mechanisms and the sequence of events leading to death in anthrax remain uncertain.

These examples illustrate a common theme amidst virulence factors. They are oftentimes either toxic proteins (toxins) that direct interact with important 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 deliver such toxins to their host cell targets. 1 mutual and particularly efficient commitment mechanism, called the blazon III secretion system, acts like a tiny syringe that injects toxic proteins from the cytoplasm of an extracellular bacterium directly into the cytoplasm of an adjacent host cell (Figure 25-7). At that place is a remarkable degree of structural similarity betwixt the blazon Three syringe and the base of a bacterial flagellum (see Figure 15-67), and many of the proteins in the two structures are conspicuously homologous.

Figure 25-seven

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

Because bacteria form a kingdom singled-out from the eucaryotes they infect (see Figure 25-three), much of their basic machinery for Deoxyribonucleic acid replication, transcription, translation, and fundamental 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 use to treat bacterial infections are small molecules that inhibit macromolecular synthesis in bacteria 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 Tabular array half-dozen-3).

Figure 25-eight

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

Fungal and Protozoan Parasites Have Complex Life Cycles with Multiple Forms

Pathogenic fungi and protozoan parasites are eucaryotes. It is therefore more hard 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 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 ane grade is often 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 constitute on moldy fruit or bread). Almost 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 oft associated with infection. Histoplasma capsulatum, for example, grows as a mold at low temperature in the soil, but information technology switches to a yeast form when inhaled into the lung, where it tin can crusade the disease histoplasmosis (Figure 25-9).

Figure 25-ix

Dimorphism in the pathogenic mucus Histoplasma capsulatum. (A) At low temperature in the soil, Histoplasma grows as a filamentous fungus. (B) After existence inhaled into the lung of a mammal, Histoplasma undergoes a morphological switch triggered by the (more...)

Protozoan parasites take more elaborate life cycles than do fungi. These cycles frequently require the services of more than one host. Malaria is the most mutual protozoal disease, infecting 200–300 1000000 people every year and killing 1–3 million of them. Information technology is acquired by four species of Plasmodium, which are transmitted to humans past the bite of the female person 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 human and musquito hosts to complete its sexual cycle (Figure 25-x). Gametes are formed in the bloodstream of infected humans, but they tin but fuse to form a zygote in the gut of the musquito. Three of the Plasmodium forms are highly specialized to invade and replicate in specific tissues—the insect gut lining, the human being liver, and the human ruddy claret jail cell.

Figure 25-10

The circuitous life cycle 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 announced (more...)

Because malaria is and so widespread and devastating, it has acted as a strong selective pressure on homo populations in areas of the world that harbor the Anopheles mosquito. Sickle cell anemia, for case, is a recessive genetic disorder caused by a point mutation in the gene that encodes the hemoglobin β chain, and it is common in areas of Africa with a high incidence of the most serious form of malaria (caused past Plasmodium falciparum). The malarial parasites grow poorly in ruby-red blood cells from either homozygous sickle cell patients or salubrious heterozygous carriers, and, as a result, malaria is seldom constitute among carriers of this mutation. For this reason, malaria has maintained the sickle jail cell mutation at high frequency in these regions of Africa.

Viruses Exploit Host Jail cell Mechanism for All Aspects of Their Multiplication

Bacteria, fungi, and eucaryotic parasites are cells themselves. Even when they are obligate parasites, they use their own machinery for DNA replication, transcription, and translation, and they provide their own sources of metabolic energy. Viruses, by contrast, are the ultimate hitchhikers, carrying picayune more than information in the course of nucleic acrid. The information is largely replicated, packaged, and preserved by the host cells (Figure 25-eleven). Viruses have a small genome, made up of a single nucleic acrid type—either DNA or RNA—which, in either case, may exist single-stranded or double-stranded. The genome is packaged in a protein glaze, which in some viruses is further enclosed by a lipid envelope.

Effigy 25-11

A simple viral life cycle. The hypothetical virus shown consists of a small double-stranded Deoxyribonucleic acid molecule that codes for only a unmarried viral capsid protein. No known virus is this simple.

Viruses replicate in diverse ways. In general, replication involves (ane) disassembly of the infectious virus particle, (two) replication of the viral genome, (3) synthesis of the viral proteins by the host cell translation mechanism, and (4) reassembly of these components into progeny virus particles. A single virus particle (a virion) that infects a single host prison cell tin can produce thousands of progeny in the infected cell. Such prodigious viral multiplication is often enough to kill the host 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 effect of the virus. Both the 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 expanse of infected pare.

Viruses come in a wide diversity of shapes and sizes, and, different cellular life forms, they cannot exist systematically classified past their relatedness into a single phylogenetic tree. Because of their tiny sizes, complete genome sequences have been obtained for nearly all clinically important viruses. Poxviruses are amidst the largest, up to 450 nm long, which is about the size of some modest bacteria. Their genome of double-stranded DNA consists of virtually 270,000 nucleotide pairs. At the other end of the size calibration are parvoviruses, which are less than twenty nm long and accept a unmarried-stranded DNA genome of under 5000 nucleotides (Figure 25-12). The genetic data in a virus tin can be carried in a multifariousness of unusual nucleic acrid forms (Figure 25-13).

Figure 25-12

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

Figure 25-13

Schematic drawings of several types of viral genomes. The smallest viruses contain only a few genes and can have an RNA or a DNA genome. The largest viruses contain hundreds of genes and have a double-stranded Deoxyribonucleic acid genome. The peculiar ends (equally well as (more...)

The capsid that encloses the viral genome is made of one or several proteins, arranged in regularly repeating layers and patterns. In enveloped viruses, the capsid itself is enclosed by 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 usually exit an infected jail cell past lysing it, an enveloped virus can leave the jail cell by budding, without disrupting the plasma membrane and, therefore, without killing the prison cell. These viruses can cause chronic infections, and some tin can assist transform an infected cell into a cancer cell.

Figure 25-14

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

Despite this variety, 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 alter the structure or office of the host cell to suit the needs of the virus (Figure 25-fifteen). In the 2d section of this chapter, we focus primarily on this 3rd class of viral proteins.

Figure 25-15

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

Since most of the disquisitional steps in viral replication are performed past host cell mechanism, the identification of effective antiviral drugs is particularly problematic. Whereas the antibody tetracycline specifically poisons bacterial ribosomes, for example, it volition not be possible to notice a drug that specifically poisons viral ribosomes, every bit viruses use the ribosomes of the host cell to make their proteins. The best strategy for containing viral diseases is to prevent them by vaccination of the potential hosts. Highly successful vaccination programs have effectively eliminated smallpox from the planet, and the eradication of poliomyelitis is imminent (Effigy 25-16).

Figure 25-xvi

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...)

Prions Are Infectious Proteins

All data in biological systems is encoded past structure. We are used to thinking of biological data in the form of nucleic acid sequences (every bit in our description of viral genomes), merely 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 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 construction that tin be duplicated from unstructured precursors. Nucleic acid sequences are the simplest and near robust solution that organisms accept found to the problem of faithful structural replication.

Nucleic acids are not the only solution, however. Prions are infectious agents that are replicated in the host by copying an aberrant protein structure. They can occur in yeasts, and they crusade various 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 disease scrapie in sheep, followed past years of painstaking laboratory characterization of scrapie-infected mice, somewhen established that the protein itself is infectious.

Figure 25-17

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

Intriguingly, the infectious prion poly peptide 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 duplicate in their posttranslational modifications. The only difference between them appears to be in their folded three-dimensional structure. The misfolded prion protein tends to aggregate, and information technology has the remarkable capacity to crusade the normal poly peptide to prefer its misfolded prion conformation and thereby to become infectious (encounter Effigy 6-89). This power of the prion to convert the normal host poly peptide to misfolded prion poly peptide is equivalent to the prion's having replicated itself in the host. If eaten past another susceptible host, these newly-misfolded prions can transmit the infection.

It is not known how normal proteins are usually able to notice the single, correct, folded conformation, among the billions of other possibilities, without condign stuck in dead-end intermediates (discussed in Chapters 3 and half dozen). Prions are a good example of how protein folding can go dangerously incorrect. But, why are the prion diseases so uncommon? What are the constraints that determine whether a misfolded protein will behave similar a prion, or simply go refolded or degraded by the cell that made it? We practice not however have answers to these questions, and the report 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 by the host immune organisation. About 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 power to switch amongst these forms is usually required for the parasites to be able to survive in a host and crusade affliction. In some cases, such equally malaria, parasites must pass sequentially through several host species to consummate their life cycles. Unlike bacteria and eucaryotic parasites, viruses accept no metabolism of their own and no intrinsic ability to produce the proteins encoded past 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, incorporate no nucleic acid; instead, they are rare, aberrantly folded proteins that happen to catalyze the misfolding of proteins in the host that share their principal amino acid sequence.

bowlingbrines41.blogspot.com

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