Prokaryotes and Viruses Biology Textbook PDF

By the late 1800s, the germ theory of disease had demonstrated that microscopic organisms such as bacteria were agents of infectious disease. However, it was soon discovered that some diseases could be transmitted by submicroscopic particles not visible via a light microscope (Figure 6.37). It was n...

By the late 1800s, the germ theory of disease had demonstrated that microscopic organisms such as bacteria were agents of infectious disease. However, it was soon discovered that some diseases could be transmitted by submicroscopic particles not visible via a light microscope (Figure 6.37). It was not until the development of the electron microscope in the 1930s that scientists were able to visualize these particles and to identify them as viruses. **Figure 6.37** Relative sizes of cells, bacteria, and viruses. Since the development of the electron microscope, many types of viruses and other infectious particles (eg, prions, viroids) have been identified as causative agents for disease in all types of organisms, including bacteria and archaea. Although viruses have some features in common with living organisms, viruses do not conform to the cell theory and therefore are not considered cells or living organisms (Table 6.2). Like cells, viruses contain genetic material and undergo evolution and [natural selection](javascript:void(0)). However, unlike cellular genomes, which consist of DNA, viral genomes are more diverse and may be made up of either DNA or RNA. Viruses do not carry out metabolism on their own; rather, they require host resources to carry out viral activities. Because viral reproduction is impossible without a host cell, viruses are considered **obligate intracellular parasites**. This lesson provides an overview of the basic features of viruses, including viral structures and genomes. A close-up of a virus AI-generated content may be incorrect. Chapter 6: Prokaryotes and Viruses 251 **Table 6.2** A comparison of viral, prokaryotic, and eukaryotic features. 6.4.01 Viral Structures Viral genetic material is typically protected by a protein coat called a **capsid**. Capsids are composed of protein subunits known as **capsomeres**, to which protein **spikes** may be attached. Most capsids are formed from identical capsomeres, but some viruses contain capsids composed of multiple capsomere types. Viral capsids are a primary determinant of viral morphology; for example, some viral capsids are **polyhedral** (eg, in the shape of an icosahedron), with many faces. Capsids may also be **helical**, with the viral genome covered by capsomeres that create a rod-like or filamentous shape (Figure 6.38). **Figure 6.38** Capsid morphologies.  A diagram of a cylinder AI-generated content may be incorrect. Chapter 6: Prokaryotes and Viruses 252 Viruses with more elaborate structures are called **complex viruses**. For example, a bacteriophage (ie, virus that infects only bacteria) has a polyhedral structure known as a **head** with additional structures attached. The head contains the virus\'s genetic information and is attached to a helical structure called the **tail sheath**. Additional structures (eg, tail fibers) are attached to the tail sheath (Figure 6.38). **Naked viruses** are coated solely by a capsid, while **enveloped viruses** are covered by an additional layer called a **viral envelope**, which is derived from the plasma membrane of the host cell (Figure 6.39). The viral envelope is composed of a phospholipid bilayer that contains embedded proteins and glycoproteins (protein **spikes**). Proteins embedded in the viral envelope may be derived from both the host organism and the virus (see Concept 6.5.02). Whether the virus is enveloped or naked, the proteins present on the outer surface of the virus mediate its entry into the host cell. Although enveloped viruses contain a membrane derived from the host cell, this membrane is not considered a plasma membrane, and enveloped viruses are not considered cells. **Figure 6.39** An enveloped virus. 6.4.02 Viral Genomes Like cells, viruses contain [nucleic acids](javascript:void(0)); however, unlike cellular organisms, viruses are not limited to double-stranded DNA genomes. Viral genomes are small compared to prokaryotic genomes, with relatively few genes, and may be composed of either single- or double-stranded DNA or RNA. Viral genomes may be either circular or linear, and may be segmented (ie, composed of more than one nucleic acid molecule). Because viruses lack typical cellular structures and metabolic pathways, viruses are most often classified by genome type. All viruses must use host cell [translation](javascript:void(0)) machinery (see Concept 2.3.05) for the synthesis and trafficking of viral proteins. However, some viruses contain virally encoded DNA and RNA polymerase enzymes, ensuring their ability to replicate and express viral genes under a variety of conditions. For example, RNA viruses must encode the necessary enzymes for replication and [transcription](javascript:void(0)) of RNA molecules because host enzymes use double-stranded DNA templates for replication and transcription.  Chapter 6: Prokaryotes and Viruses 253 **DNA Viruses** Upon infection with a **double-stranded DNA (dsDNA) virus**, viral DNA is typically imported into the host nucleus, where the replication and transcription of viral genes occurs in a process similar to the expression of host genes (Figure 6.40). However, some DNA viruses are known to carry out replication and transcription in the cytoplasm. **Figure 6.40** Examples of viral replication and gene expression in DNA viruses. **Single-stranded DNA viruses (ssDNA viruses)** use a single-stranded DNA genome as a template to synthesize a complementary DNA strand. Subsequently, host or viral RNA polymerases can be used to transcribe viral genes. ssDNA viruses must use the dsDNA template to synthesize a single-stranded DNA copy of the genome before final virus assembly (Figure 6.40). **RNA Viruses** Host RNA polymerase enzymes require a double-stranded DNA template for transcription, so RNA viruses must use virally encoded RNA polymerase enzymes (RNA-dependent RNA polymerases) to transcribe viral RNA. **Single-stranded RNA viruses (ssRNA viruses)** may be classified as either **positive (+)** or **negative (−) sense** (Figure 6.41). A diagram of a virus AI-generated content may be incorrect. Chapter 6: Prokaryotes and Viruses 254 **Figure 6.41** RNA virus genome naming conventions. As depicted in Figure 6.41, positive (+) sense RNA is similar in sequence and directionality to host cell mRNA. Therefore, positive (+) sense RNA can be translated directly by host ribosomes without further modification (see Chapter 2 for a review of gene expression mechanisms). For any type of RNA virus, a positive (+) sense RNA is *required* by the host ribosome to synthesize the correct viral proteins. Therefore, in the case of negative (−) sense RNA, a complementary positive (+) sense copy must be synthesized using the (−) ssRNA strand as a template before translation can take place. For replication of a (+) ssRNA genome, a complementary (−) ssRNA strand must be synthesized and used as a template to generate more (+) ssRNA to be packaged into new virions (ie, complete, infectious virus particles). Conversely, for replication of a (−) ssRNA genome, the complementary (+) ssRNA synthesized for viral protein translation is also used to generate more copies of the (−) ssRNA genome for final viral assembly (Figure 6.42).  Chapter 6: Prokaryotes and Viruses 255 **Figure 6.42** Examples of viral replication and gene expression in RNA viruses. **Double-stranded RNA viruses (dsRNA viruses)** are denatured upon host cell entry, and the (+) ssRNA strand can be translated directly by host ribosomes to synthesize viral proteins. Each strand is used as a template to synthesize complementary (+) ssRNA and (−) ssRNA strands that hybridize to create a complete dsRNA genome prior to final virus assembly (Figure 6.42). Viral replication and gene expression for each viral genome type are summarized in Table 6.3. A diagram of a virus Description automatically generated Chapter 6: Prokaryotes and Viruses 256 **Table 6.3** Viral replication and gene expression categorized by genome type. **Type of genome** **How is the viral genome replicated?** **How are viral genes expressed?** **dsDNA** Host or viral DNA polymerase replicates both strands to make more dsDNA copies. Host or viral RNA polymerase uses dsDNA as a template to transcribe viral mRNA. **ssDNA** Host or viral DNA polymerase synthesizes complementary ssDNA strand to make dsDNA; dsDNA is then used as a template to make more ssDNA copies. Complementary ssDNA strand is synthesized and used as a template by host or viral RNA polymerase to transcribe viral mRNA. **(+) ssRNA** Viral RNA polymerase synthesizes complementary (−) ssRNA strand to use as a template to make more (+) ssRNA copies. (+) ssRNA strand used directly during translation; (−) ssRNA can be used as a template by viral RNA polymerase to transcribe (+) ssRNA. **(−) ssRNA** Viral RNA polymerase synthesizes complementary (+) ssRNA for use as a template to make more (−) ssRNA copies. Viral RNA polymerase uses (−) ssRNA strand as a template to transcribe (+) ssRNA for translation. **dsRNA** Viral RNA polymerase use (+) ssRNA strand as a template to make (−) ssRNA and vice versa. (+) ssRNA strand used directly during translation; (−) ssRNA can be used as a template by viral RNA polymerase to transcribe more (+) ssRNA copies. **Concept Check 6.5** A scientist has purified viral RNA being translated by host ribosomes in an infected cell. A portion of the viral RNA sequence was determined to be the following: 5′-AAAUGUGUGCCGAAAUGUUGA-3′. If the identified virus has a (−) ssRNA genome, what is its sequence? [**Solution**](javascript:void(0))  **Viral Life Cycles** Introduction As obligate intracellular parasites, viruses are metabolically inactive when outside of a host cell. The viral life cycle begins when a virus enters a host cell. In the host cell, the virus can utilize host cell machinery and resources to replicate and release fully formed viral progeny (**virions**) to infect other host cells. The viral life cycle is comprised of the activities involved from host cell viral entry to exit. This lesson highlights the life cycles of both bacterial and animal viruses, with special consideration paid to retroviruses, a type of animal virus. 6.5.01 Bacteriophages **Bacteriophages** (also known simply as **phages**) are viruses that exclusively infect bacteria. Bacteriophages, which typically contain DNA genomes, are capsid coated and, unlike animal viruses, cannot be enveloped due to the rigidity of bacterial cell walls. Some bacteriophages have an elaborate capsid coating (see Concept 6.4.01). Bacteriophages most often replicate through a cycle known as the **lytic replication cycle**, the steps of which are described as follows and shown in Figure 6.43: 1.**Attachment**: Phage tail fibers attach to the host bacterial cell surface. 2.**Entry**: The phage uses its tail sheath to inject the viral genome into the bacterial cytosol. Only the viral genome enters the cell, and the empty phage remains on the cell exterior. 3.**Synthesis**: Viral enzymes target the bacterial genome for degradation and promote synthesis of viral proteins needed to replicate and assemble new phages. 4.**Assembly**: Viral components (eg, capsid head, tail sheath, tail fibers) are assembled, and viral genomes are packaged inside. 5.**Release**: The host cell lyses (ie, bursts), and the fully assembled virions are released. Chapter 6: Prokaryotes and Viruses 258 **Figure 6.43** Lytic replication cycle of bacteriophages. Some bacteriophages are able to switch between a lytic replication cycle and an alternative cycle called the **lysogenic replication cycle**. During **lysogeny**, bacteriophages are able to enter a latent (ie, inactive) phase for a variable period of time by incorporating viral DNA into a host chromosome, forming what is known as a **prophage** (ie, viral genetic material recombined into a host chromosome). Expression of most viral genes is repressed, keeping the prophage from stimulating the synthesis and release of new virions. With each new bacterial division (ie, via binary fission), prophage DNA is replicated along with the bacterial chromosome, and the prophage remains latent within the bacterial population. Under certain conditions, the phage DNA may be excised from the bacterial chromosome, initiating a lytic replication cycle, as shown in Figure 6.44. In some cases, a small piece of the bacterial chromosome may be excised along with the prophage DNA and transferred to the next host via transduction (see Concept 6.3.03). A diagram of a cell AI-generated content may be incorrect. Chapter 6: Prokaryotes and Viruses 259 **Figure 6.44** Lysogenic replication cycle of bacteriophages. 6.5.02 Animal Viruses Generally, animal virus life cycles follow the same basic steps as the life cycles of bacteriophages (see Concept 6.5.01), which include attachment, entry, synthesis, assembly, and release. However, due to fundamental differences between prokaryotic and eukaryotic cell biology, there are some significant differences between the life cycles of animal viruses and bacteriophages, as summarized in Table 6.4. **Table 6.4** Similarities and differences between animal viruses and bacteriophages. **Bacteriophages** **Animal viruses** **Host cell entry** Direct penetration Direct penetration Endocytosis Membrane fusion **Synthesis and assembly** Host cytoplasm Host cytoplasm Host cellular compartments (eg, nucleus, endoplasmic reticulum, Golgi apparatus) **Host cell release** Host cell lysis Host cell lysis Exocytosis Budding  Chapter 6: Prokaryotes and Viruses 260 Both bacteriophages and animal viruses bind to specific host cell receptor sites complementary to structures found on the outermost virion surface. Unlike bacteriophages, animal viruses may be surrounded by a viral envelope derived from the plasma membrane of the previous host (see Concept 6.4.01). In addition, both capsid-coated and enveloped animal viruses often have glycoprotein **spikes** on the outermost viral surface to mediate host attachment. Animal virus entry may take place via three mechanisms, as depicted in Figure 6.45: Naked virions may enter the cell via **direct penetration**. Insertion of the viral genome into the host cell leaves an empty capsid on the host cell surface. The entire virion (naked or enveloped) may enter the cell intact via **endocytosis**. Enveloped virions may enter the cell via **membrane fusion**, in which the viral envelope and host plasma membrane fuse, releasing the capsid-coated virus into the host cytoplasm. Upon entry, viruses that enter the cell through endocytosis or membrane fusion must be **uncoated**, which occurs either within a phagolysosome after endocytosis or within the cytoplasm after membrane fusion. **Figure 6.45** Mechanisms of animal virus entry into host cells. Depending on genome type, the viral genome may be imported into the host cell nucleus to initiate viral replication and gene expression, or these processes may take place within the host cytosol. In either case, DNA replication and transcription may be mediated by host or virally encoded enzymes. Viral proteins may be synthesized by cytosolic ribosomes, or they may be synthesized by ribosomes on the rough endoplasmic reticulum and trafficked through the endomembrane system (Figure 6.46). A diagram of a virus AI-generated content may be incorrect. Chapter 6: Prokaryotes and Viruses 261 **Figure 6.46** Example of viral assembly utilizing host protein synthesis and trafficking machinery. Naked virions exit the cell via **lysis** (resulting in host cell death) or **exocytosis**, whereas enveloped viruses are released by **budding** (Figure 6.47). In many cases, viral exit via exocytosis or budding does not result in host cell death. During budding, the assembled virus travels to and pushes through the plasma membrane, creating a membrane coating (ie, viral envelope) around the virion. Prior to budding, viral glycoproteins (spikes) are trafficked to the host plasma membrane via the endomembrane system; therefore, the complete viral envelope includes viral glycoproteins, enabling viral attachment to the next host cell.  Chapter 6: Prokaryotes and Viruses 262 **Figure 6.47** Mechanisms of animal virus exit from host cells. 6.5.03 Retroviruses While it is possible for some DNA viruses to integrate into host cell genomes, most RNA viruses have no mechanism for integration. However, a subgroup of positive sense single-stranded RNA \[(+) ssRNA\] animal viruses known as **retroviruses** can convert RNA genomes into linear double-stranded DNA (dsDNA), which can then be integrated into host cell DNA. Carrying out this unique viral life cycle requires **reverse transcription** from RNA to DNA (ie, the opposite of traditional [transcription](javascript:void(0))) and integration of the viral genome into the host chromosome. The virally encoded enzyme **reverse transcriptase** (an RNA-dependent DNA polymerase) catalyzes the conversion of retroviral (+) ssRNA to dsDNA in the host cytosol upon viral entry and uncoating. The dsDNA copy is then imported into the nucleus, where the viral DNA integrates into a random region of the host cell\'s chromosome with the assistance of another virally encoded enzyme known as **integrase**. Subsequently, a (+) ssRNA viral genome can be transcribed by host RNA polymerase and packaged into viral progeny, which then exit the cell via budding, as shown in Figure 6.48. A virus that integrates into host cell DNA is known as a **provirus** and is replicated along with host DNA during the [cell cycle](javascript:void(0)), bearing some resemblance to bacteriophage lysogeny (see Concept 6.5.01). Descendants of the original infected host cell containing the provirus are also infected. A diagram of a virus AI-generated content may be incorrect. Chapter 6: Prokaryotes and Viruses 263 **Figure 6.48** Retroviral life cycle. A subclass of transposable elements (see Concept 6.3.04) known as **retrotransposons** are thought to have originated from retroviruses because retrotransposons move via mRNA intermediates using retroviral mechanisms. For example, transposable elements known as autonomous retrotransposons are able to move from one location to another in the genome via reverse transcription of an mRNA intermediate. In addition to inverted repeats, autonomous retrotransposons contain genes for the enzymes reverse transcriptase and integrase. Retrotransposon DNA is transcribed in the nucleus to form mRNA, which is  Chapter 6: Prokaryotes and Viruses 264 transported into the cytosol where translation of retrotransposon encoded genes (eg, reverse transcriptase, integrase) occurs. Retrotransposon mRNA is then converted back into dsDNA by reverse transcriptase and integrated into a new site within the genome by integrase in a process similar to the retroviral life cycle (Figure 6.49). **Figure 6.49** Retrotransposons can move to new locations in the genome using a mechanism similar to the retroviral life cycle. A diagram of a transtransparent AI-generated content may be incorrect. **Sub-Viral Particles** Introduction In addition to viruses (described in Lessons 6.4 and 6.5), several other types of nonliving infectious agents have been discovered, including **viroids** and **prions**. A viroid is composed of a small, naked RNA molecule with no capsid coat and is not known to code for proteins, while prions are self-replicating proteins that do not contain any genetic material. While the typical features of cells and viruses are not present in these subviral particles, they are still considered infectious and are able to cause disease in some cases. This lesson summarizes the major features of viroids and prions. 6.6.01 Viroids **Viroids** are subviral infectious particles consisting of a short, circular single-stranded RNA molecule with no accompanying protein capsid (Figure 6.50). Viroids contain regions that exhibit self-complementarity, resulting in double-stranded regions within their circular RNA genome. Viroid genomes do not typically code for proteins and viroid replication is thought to occur via host RNA polymerases through a mechanism unique to viroids. When infecting host cells, viroids can bind host RNA sequences via complementary base pairing, resulting in host gene silencing. Most known viroids infect plants; however, hepatitis D virus shows some similarity to known viroids and is an example of a viroid-like virus capable of infecting humans and causing disease. **Figure 6.50** Viroids are subviral infectious particles that lack a capsid coat. 6.6.02 Prions A **prion** (also known as **PrPSc**) is a misfolded version of a cell surface protein known as **PrPC** (ie, wild-type PrP). Prions can catalyze the misfolding of additional wild-type PrP proteins, resulting in self-propagating protein aggregates that are able to cause disease. Unlike living organisms, viruses, and viroids, prions do not contain genetic material (ie, DNA or RNA).  Chapter 6: Prokaryotes and Viruses 266 Because wild-type PrP proteins are highly expressed in the cells of the [central nervous system](javascript:void(0)), prion diseases in humans are often neurodegenerative. Misfolded prions can arise by the spontaneous conversion of the wild-type PrP protein structure to a prion form. Some prion diseases affecting humans, such as Creutzfeldt-Jakob disease (CJD) and fatal familial insomnia, may also be heritable (ie, caused by genetic mutations). Humans and animals may also acquire an infectious form of CJD (vCJD) by consuming (ie, becoming inoculated with) products containing prions from cattle with bovine spongiform encephalopathy (BSE), sometimes known as mad cow disease. Prions act as infectious agents by inducing changes in the [secondary structure](javascript:void(0)) of other wild-type PrP proteins, resulting in the production of more prions. These structural changes to wild-type PrP proteins occur post-translationally and involve the refolding of α-helices to form β-pleated sheets (Figure 6.51). **Figure 6.51** Prions induce wild-type PrP proteins to misfold, increasing prion numbers By inducing wild-type PrP proteins to change conformation, prions perpetuate their own replication, increasing the number of prion proteins without initiating new gene expression. Because the misfolded prion proteins are less soluble than wild-type PrP proteins, the newly formed prions aggregate, and amyloid fibrils are formed. When prion aggregation reaches a critical threshold, cellular functions are disrupted, resulting in disease (Figure 6.51). A screenshot of a cell division AI-generated content may be incorrect. **Have you mastered this Lesson?** Mark this lesson as complete and continue to the next.