What Is The Area Of Biology That Studies The Nucleic Acid Makeup Of An Organism?

Nosotros normally call back of pathogens in hostile terms—as invaders that attack our bodies. Just a pathogen or a parasite, similar any other organism, is but 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 world is subject to some type of infection or parasitism (Effigy 25-1). A human host is a nutrient-rich, warm, and moist environment, which remains at a uniform temperature and constantly renews itself. It is not surprising that many microorganisms have evolved the power to survive and reproduce in this desirable niche. In this section, we discuss some of the common features that microorganisms must have in order to exist infectious. We and so explore the wide variety of organisms that are known to crusade disease in humans.

Figure 25-ane

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 than...)

Pathogens Take Evolved Specific Mechanisms for Interacting with Their Hosts

The homo body is a complex and thriving ecosystem. It contains about ten¹³ human cells and too about 10^xiv bacterial, fungal, and protozoan cells, which represent thousands of microbial species. These microbes, called the normal flora, are usually limited to certain areas of the torso, including the skin, mouth, large intestine, and vagina. In improver, humans are always infected with viruses, almost of which rarely, if ever, become symptomatic. If it is normal for u.s. to alive in such close intimacy with a wide diversity of microbes, how is it that some of them are capable of causing u.s. illness or death?

Pathogens are usually singled-out from the normal flora. Our normal microbial inhabitants but cause problem if our allowed systems are weakened or if they gain access to a unremarkably 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, dedicated pathogens do non require that the host be immunocompromised or injured. They take adult 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 gild to survive and multiply in a host, a successful pathogen must be able to: (1) colonize the host; (2) find 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. Under severe selective pressure to induce only the correct host cell responses to accomplish this complex ready of tasks, pathogens take evolved mechanisms that maximally exploit the biology of their host organisms. Many of the pathogens we discuss in this chapter are skilful and practical cell biologists. We tin acquire a peachy deal of jail cell biology past observing them.

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

Although nosotros tin can easily understand why infectious microorganisms would evolve to reproduce in a host, it is less clear why they would evolve to cause disease. One explanation may exist that, in some cases, the pathological responses elicited by microorganisms heighten the efficiency of their spread or propagation and hence clearly take a selective advantage for the pathogen. The virus-containing lesions on the genitalia acquired by canker 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, however, the consecration of affliction has no credible reward for the pathogen.

Many of the symptoms and signs that we acquaintance with communicable diseases 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, as well, is a defensive response, as the increase in trunk temperature can inhibit the growth of some microorganisms. Thus, understanding the biology of an infectious disease requires an appreciation of the contributions of both pathogen and host.

Pathogens Are Phylogenetically Diverse

Many types of pathogens cause disease in humans. The most familiar are viruses and leaner. Viruses cause diseases ranging from AIDS and smallpox to the common common cold. They are essentially fragments of nucleic acrid (DNA or RNA) instructions, wrapped in a protective vanquish 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-two

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

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

Some other infectious agents are eucaryotic organisms. These range from single-celled fungi and protozoa (Figure 25-2C), through large circuitous metazoa such equally parasitic worms. I of the nigh mutual infectious diseases on the planet, shared past 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 equally a model organism for genetic and developmental biological research (discussed in Affiliate 21). C. elegans, even so, is only about 1 mm in length, whereas Ascaris tin can reach 30 cm (Figure 25-2D).

Some rare neurodegenerative diseases, including mad cow affliction, 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.

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

Effigy 25-iii

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

Each individual pathogen causes disease in a dissimilar mode, which makes information technology challenging to understand the basic biology of infection. Simply, when because the interactions of infectious agents with their hosts, some common themes of pathogenesis sally. These common themes are the focus of this affiliate. First, we innovate the basic features of each of the major types of pathogens that exploit features of host cell biology. So, we examine in turn the mechanisms that pathogens use to command their hosts and the innate mechanisms that hosts utilise to control pathogens.

Bacterial Pathogens Acquit Specialized Virulence Genes

Bacteria are small and structurally uncomplicated, compared to the vast majority of eucaryotic cells. Most can exist classified broadly past their shape as rods, spheres, or spirals and by their cell-surface backdrop. Although they lack the elaborate morphological variety of eucaryotic cells, they display a surprising array of surface appendages that enable them to swim or to adhere to desirable surfaces (Effigy 25-4). Their genomes are correspondingly simple, typically on the club 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).

Figure 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 also classified every bit Gram-positive or Gram-negative. Bacteria such (more...)

As emphasized above, only a minority of bacterial species take developed the ability to cause disease in humans. Some of those that do cause disease can only replicate inside the cells of the homo body and are chosen obligate pathogens. Others replicate in an environmental reservoir such as water or soil and but cause disease if they happen to encounter a susceptible host; these are called facultative pathogens. Many leaner are normally beneficial just have a latent power to crusade affliction in an injured or immunocompromised host; these are called opportunistic pathogens.

Some bacterial pathogens are fastidious in their pick of host and will simply 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 lacking a make clean water supply, will just infect humans and other primates. By contrast, the closely related bacterium Salmonella enterica, which is a common cause of food poisoning in humans, can likewise 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 significant differences between a virulent pathogenic bacterium and its closest nonpathogenic relative may result from a very small number of genes. Genes that contribute to the power of an organism to crusade disease are called virulence genes. The proteins they encode are called virulence factors. Virulence genes are oft 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-six). 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-five

Genetic differences between pathogens and nonpathogens. Nonpathogenic Escherichia coli has a unmarried circular chromosome. E. coli is very closely related to 2 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 one. The two chromosomes have distinct origins of replication (oriC₁ and oriC₂). Three loci in pathogenic strains of Five. cholerae are (more...)

Many virulence genes encode proteins that collaborate directly with host cells. Two of the genes carried by the Vibrio cholerae phage, for example, encode 2 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 G poly peptide Chiliad_{due south}, which ordinarily activates adenylyl cyclase to make cyclic AMP (discussed in Chapter 15). ADP-ribosylation of the 1000 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 and so spread by the fecal-oral route by contaminated nutrient and water.

Some pathogenic bacteria use several independent mechanisms to cause toxicity to the cells of their host. Anthrax, for case, is an astute infectious disease of sheep, cattle, other herbivores, and occasionally humans. Information technology is commonly acquired past contact with spores of the Gram-positive bacterium, Bacillus anthracis. Unlike cholera, anthrax has never been observed to spread directly from one infected person to another. Dormant spores can survive in soil for long periods of time and are highly resistant to adverse environmental weather, including estrus, ultraviolet and ionizing radiation, pressure, and chemical agents. Later the spores are inhaled, ingested, or rubbed into breaks in the skin, the spores germinate, and the leaner brainstorm to replicate. Growing bacteria secrete two toxins, chosen lethal toxin and edema toxin. Either toxin lonely is sufficient to cause signs of infection. Like 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 information technology binds to a host cell-surface receptor to transfer the ii different A subunits into host cells. The A subunit of edema toxin is an adenylyl cyclase that direct converts host cell ATP into cyclic AMP. This causes an ion imbalance that can lead 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 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 death in anthrax remain uncertain.

These examples illustrate a common theme among virulence factors. They are frequently either toxic proteins (toxins) that directly collaborate with of import host structural or signaling proteins to arm-twist 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 particularly efficient delivery mechanism, called the blazon 3 secretion system, acts like a tiny syringe that injects toxic proteins from the cytoplasm of an extracellular bacterium direct into the cytoplasm of an adjacent host cell (Figure 25-7). There is a remarkable caste of structural similarity betwixt the type III syringe and the base of a bacterial flagellum (encounter Figure fifteen-67), and many of the proteins in the two structures are clearly homologous.

Figure 25-vii

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

Because leaner course a kingdom distinct from the eucaryotes they infect (see Effigy 25-3), much of their basic machinery for Dna replication, transcription, translation, and fundamental metabolism is quite unlike from that of their host. These differences enable united states to find antibacterial drugs that specifically inhibit these processes in bacteria, without disrupting them in the host. Most of the antibiotics that we apply to care for bacterial infections are small 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 equally cell wall biosynthesis, that are absent in humans (Figure 25-8 and Table vi-3).

Effigy 25-eight

Antibiotic targets. Despite the large number of antibiotics bachelor, they take a narrow range of targets, which are highlighted in yellow. A few representative antibiotics in each form are listed. All antibiotics used to treat human infections fall (more than...)

Fungal and Protozoan Parasites Accept Complex Life Cycles with Multiple Forms

Pathogenic fungi and protozoan parasites are eucaryotes. It is therefore more than hard to detect drugs that will impale them without killing the host. Consequently, antifungal and antiparasitic drugs are oft less constructive and more toxic than antibiotics. A 2nd feature of fungal and parasitic infections that makes them difficult to care for is the tendency of the infecting organisms to switch amid several unlike forms during their life cycles. A drug that is effective at killing one form is oft ineffective at killing another form, which therefore survives the treatment.

The fungal branch of the eucaryotic kingdom includes both unicellular yeasts (such as Saccharomyces cerevisiae and Schizosaccharomyces pombe) and filamentous, multicellular molds (similar those found 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 frequently associated with infection. Histoplasma capsulatum, for case, grows as a mold at depression temperature in the soil, but it switches to a yeast grade when inhaled into the lung, where it can crusade the affliction histoplasmosis (Figure 25-ix).

Figure 25-ix

Dimorphism in the pathogenic fungus Histoplasma capsulatum. (A) At low 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 by the (more...)

Protozoan parasites have more elaborate life cycles than practice fungi. These cycles frequently crave the services of more than ane host. Malaria is the most common protozoal disease, infecting 200–300 million people every yr and killing i–three 1000000 of them. It is caused by four species of Plasmodium, which are transmitted to humans by the bite of the female of whatever of lx species of Anopheles mosquito. Plasmodium falciparum—the nigh intensively studied of the malaria-causing parasites—exists in no fewer than eight distinct forms, and it requires both the human being and musquito hosts to complete its sexual wheel (Figure 25-10). Gametes are formed in the bloodstream of infected humans, simply they can 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 being liver, and the man red claret jail cell.

Figure 25-10

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

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

Bacteria, fungi, and eucaryotic parasites are cells themselves. Fifty-fifty when they are obligate parasites, they use their ain machinery for Deoxyribonucleic acid replication, transcription, and translation, and they provide their own sources of metabolic free energy. Viruses, past contrast, are the ultimate hitchhikers, carrying fiddling more than data in the form of nucleic acrid. The information is largely replicated, packaged, and preserved by the host cells (Figure 25-11). Viruses have a small genome, fabricated upwardly of a single nucleic acid type—either DNA or RNA—which, in either case, may exist unmarried-stranded or double-stranded. The genome is packaged in a protein coat, which in some viruses is further enclosed past a lipid envelope.

Effigy 25-xi

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

Viruses replicate in diverse means. In general, replication involves (1) disassembly of the infectious virus particle, (2) replication of the viral genome, (3) synthesis of the viral proteins past the host cell translation mechanism, and (4) reassembly of these components into progeny virus particles. A unmarried virus particle (a virion) that infects a single host prison cell can produce thousands of progeny in the infected prison cell. Such biggy viral multiplication is often enough to kill the host prison 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 acquired by the smallpox virus, for case, reverberate the killing of the epidermal cells in a local expanse of infected skin.

Viruses come in a wide multifariousness of shapes and sizes, and, dissimilar cellular life forms, they cannot exist systematically classified by their relatedness into a single phylogenetic tree. Because of their tiny sizes, complete genome sequences take been obtained for most all clinically important viruses. Poxviruses are among the largest, up to 450 nm long, which is about the size of some small bacteria. Their genome of double-stranded Deoxyribonucleic acid consists of about 270,000 nucleotide pairs. At the other end of the size scale are parvoviruses, which are less than 20 nm long and have a single-stranded Dna genome of nether 5000 nucleotides (Effigy 25-12). The genetic information in a virus tin exist carried in a variety of unusual nucleic acid forms (Figure 25-13).

Effigy 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 simply 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 (every bit well as (more...)

The capsid that encloses the viral genome is fabricated of one 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 jail cell plasma membrane (Figure 25-14). Whereas nonenveloped viruses normally go out an infected cell past lysing information technology, an enveloped virus can leave the cell past budding, without disrupting the plasma membrane and, therefore, without killing the cell. These viruses can crusade chronic infections, and some can help transform an infected cell into a cancer cell.

Figure 25-xiv

Acquisition of a viral envelope. (A) Electron micrograph of an beast cell from which vi 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 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 function of the host prison cell to suit the needs of the virus (Effigy 25-15). In the second section of this chapter, nosotros focus primarily on this 3rd class of viral proteins.

Figure 25-fifteen

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 greenish and ruby. 3 of the genes (green) are common to all retroviruses: gag encodes capsid proteins, env (more...)

Since about of the disquisitional steps in viral replication are performed by host cell machinery, the identification of effective antiviral drugs is particularly problematic. Whereas the antibiotic tetracycline specifically poisons bacterial ribosomes, for example, it will not be possible to find 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 by vaccination of the potential hosts. Highly successful vaccination programs have effectively eliminated smallpox from the planet, and the eradication of poliomyelitis is imminent (Figure 25-16).

Figure 25-sixteen

Eradication of a viral disease through vaccination. The graph shows number of cases of poliomyelitis reported per twelvemonth 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 information in biological systems is encoded past structure. We are used to thinking of biological information in the form of nucleic acrid sequences (as in our description of viral genomes), merely the sequence itself is a shorthand code for describing nucleic acrid 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 construction that can be duplicated from unstructured precursors. Nucleic acrid sequences are the simplest and virtually robust solution that organisms take plant to the trouble of faithful structural replication.

Nucleic acids are non the but solution, yet. Prions are infectious agents that are replicated in the host by copying an aberrant protein construction. They can occur in yeasts, and they cause various neurodegenerative diseases in mammals. The most well-known infection caused by prions is bovine spongiform encephalopathy (BSE, or mad cow affliction), which occasionally spreads to humans who eat infected parts of the moo-cow (Figure 25-17). Isolation of the infectious prions that cause the affliction scrapie in sheep, followed by years of painstaking laboratory label of scrapie-infected mice, eventually established that the poly peptide 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 like to BSE, that was spread from one person to another by ritual mortuary practices in New Republic of guinea. (more...)

Intriguingly, the infectious prion protein is fabricated by the host, and its amino acid sequence is identical to a normal host poly peptide. 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 it has the remarkable capacity to cause the normal poly peptide to prefer its misfolded prion conformation and thereby to become infectious (run into Figure 6-89). This ability of the prion to convert the normal host protein to misfolded prion poly peptide 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 unremarkably able to find the unmarried, correct, folded conformation, amid the billions of other possibilities, without becoming stuck in expressionless-end intermediates (discussed in Chapters 3 and half-dozen). Prions are a skilful case of how poly peptide folding tin go dangerously wrong. Only, why are the prion diseases and then uncommon? What are the constraints that determine whether a misfolded protein will deport like a prion, or simply get refolded or degraded by the jail cell that fabricated information technology? We exercise not notwithstanding accept answers to these questions, and the study of prions remains an area of intense inquiry.

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 destruction by the host immune system. Almost leaner 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 unlike forms during the form of infection; the ability to switch amidst these forms is commonly required for the parasites to exist able to survive in a host and cause illness. In some cases, such as malaria, parasites must pass sequentially through several host species to complete their life cycles. Dissimilar bacteria and eucaryotic parasites, viruses have no metabolism of their own and no intrinsic ability to produce the proteins encoded by their Deoxyribonucleic acid 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 chief amino acid sequence.

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

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