Learning Objective Check Your Understanding




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13: Viruses, Viroids, and Prions

Learning Objective

Check Your Understanding

13-1 Differentiate a virus from a bacterium.

How could the small size of viruses have helped researchers detect viruses before the invention of the electron microscope?

13-2 Describe the chemical and physical structure of both an enveloped and a nonenveloped virus.

Diagram a nonenveloped polyhedral virus that has spikes.

13-3 Define viral species.

How does a virus species differ from a bacterial species?

13-4 Give an example of a family, genus, and common name for a virus.

Attach the proper endings to Papilloma- to show the family and genus that includes HPV, the cause of cervical cancer.

13-5 Describe how bacteriophages are cultured.

What is the plaque method?

13-6 Describe how animal viruses are cultured.

Why are continuous cell lines of more practical use than primary cell lines for culturing viruses?

13-7 List three techniques used to identify viruses.

What tests could you use to identify influenza virus in a patient?

13-8 Describe the lytic cycle of T-even bacteriophages.

How do bacteriophages get nucleotides and amino acids if they don’t have any metabolic enzymes?

13-9 Describe the lysogenic cycle of bacteriophage lambda.

Vibrio cholerae produces toxin and is capable of causing cholera only when it is lysogenic. What does this mean?

13-10 Compare and contrast the multiplication cycle of DNA and RNA-containing animal viruses.

Describe the principal events of attachment, entry, uncoating, biosynthesis, maturation, and release of an enveloped DNA-containing virus.

13-11 Define oncogene and transformed cell.

What is a provirus?

13-12 Discuss the relationship between DNA- and RNA-containing viruses and cancer.

How can an RNA virus cause cancer if it doesn’t have DNA to insert into a cell’s genome?

13-13 Provide an example of a patent viral infection.

Is shingles a persistent or latent infection?

13-14 Differentiate persistent viral infections from latent viral infections.

Is shingles a persistent or latent infection?

13-15 Discuss how a protein can be infectious.

Contrast viroids and prions, and for each name a disease it causes.

13-16 Differentiate virus, viroid, and prion.

Contrast viroids and prions, and for each name a disease it causes.

13-17 Describe the lytic cycle for a plant virus.

How do plant viruses enter host cells?


Chapter Summary

General Characteristics of Viruses (pp. 368–369)

1. Depending on one’s viewpoint, viruses may be regarded as exceptionally complex aggregations of nonliving chemicals or as exceptionally simple living microbes.

2. Viruses contain a single type of nucleic acid (DNA or RNA) and a protein coat, sometimes enclosed by an envelope composed of lipids, proteins, and carbohydrates.

3. Viruses are obligatory intracellular parasites. They multiply by using the host cell’s synthesizing machinery to cause the synthesis of specialized elements that can transfer the viral nucleic acid to other cells.



Host Range (pp. 368–369)

4. Host range refers to the spectrum of host cells in which a virus can multiply.

5. Most viruses infect only specific types of cells in one host species.

6. Host range is determined by the specific attachment site on the host cell’s surface and the availability of host cellular factors.



Viral Size (p. 369)

7. Viral size is ascertained by electron microscopy.

8. Viruses range from 20 to 1000 nm in length.

Viral Structure (pp. 370–373)

1. A virion is a complete, fully developed viral particle composed of nucleic acid surrounded by a coat.



Nucleic Acid (pp. 371–372)

2. Viruses contain either DNA or RNA, never both, and the nucleic acid may be single- or double-stranded, linear or circular, or divided into several separate molecules.

3. The proportion of nucleic acid in relation to protein in viruses ranges from about 1% to about 50%.

Capsid and Envelope (pp. 372–373)

4. The protein coat surrounding the nucleic acid of a virus is called the capsid.

5. The capsid is composed of subunits, capsomeres, which can be a single type of protein or several types.

6. The capsid of some viruses is enclosed by an envelope consisting of lipids, proteins, and carbohydrates.

7. Some envelopes are covered with carbohydrate-protein complexes called spikes.

General Morphology (p. 373)

8. Helical viruses (for example, Ebola virus) resemble long rods, and their capsids are hollow cylinders surrounding the nucleic acid.

9. Polyhedral viruses (for example, adenovirus) are many-sided. Usually the capsid is an icosahedron.

10. Enveloped viruses are covered by an envelope and are roughly spherical but highly pleomorphic. There are also enveloped helical viruses (for example, influenza virus) and enveloped polyhedral viruses (for example, Simplexvirus).

11. Complex viruses have complex structures. For example, many bacteriophages have a polyhedral capsid with a helical tail attached.

Taxonomy of Viruses (pp. 373–374)

1. Classification of viruses is based on type of nucleic acid, strategy for replication, and morphology.

2. Virus family names end in -viridae; genus names end in -virus.

3. A viral species is a group of viruses sharing the same genetic information and ecological niche.



Isolation, Cultivation, and Identification of Viruses (pp. 374–379)

1. Viruses must be grown in living cells.

2. The easiest viruses to grow are bacteriophages.

Growing Bacteriophages in the Laboratory (pp. 374, 377)

3. The plaque method mixes bacteriophages with host bacteria and nutrient agar.

4. After several viral multiplication cycles, the bacteria in the area surrounding the original virus are destroyed; the area of lysis is called a plaque.

5. Each plaque originates with a single viral particle; the concentration of viruses is given as plaque-forming units.



Growing Animal Viruses in the Laboratory (pp. 377–379)

6. Cultivation of some animal viruses requires whole animals.

7. Simian AIDS and feline AIDS provide models for studying human AIDS.

8. Some animal viruses can be cultivated in embryonated eggs.

9. Cell cultures are cells growing in culture media in the laboratory.

10. Primary cell lines and embryonic diploid cell lines grow for a short time in vitro.

11. Continuous cell lines can be maintained in vitro indefinitely.

12. Viral growth can cause cytopathic effects in the cell culture.



Viral Identification (p. 379)

13. Serological tests are used most often to identify viruses.

14. Viruses may be identified by RFLPs and PCR.

Viral Multiplication (pp. 379–389)

1. Viruses do not contain enzymes for energy production or protein synthesis.

2. For a virus to multiply, it must invade a host cell and direct the host’s metabolic machinery to produce viral enzymes and components.

Multiplication of Bacteriophages (pp. 379–382)

3. During the lytic cycle, a phage causes the lysis and death of a host cell.

4. Some viruses can either cause lysis or have their DNA incorporated as a prophage into the DNA of the host cell. The latter situation is called lysogeny.

5. During the attachment phase of the lytic cycle, sites on the phage’s tail fibers attach to complementary receptor sites on the bacterial cell.

6. In penetration, phage lysozyme opens a portion of the bacterial cell wall, the tail sheath contracts to force the tail core through the cell wall, and phage DNA enters the bacterial cell. The capsid remains outside.

7. In biosynthesis, transcription of phage DNA produces mRNA coding for proteins necessary for phage multiplication. Phage DNA is replicated, and capsid proteins are produced. During the eclipse period, separate phage DNA and protein can be found.

8. During maturation, phage DNA and capsids are assembled into complete viruses.

9. During release, phage lysozyme breaks down the bacterial cell wall, and the new phages are released.

10. During the lysogenic cycle, prophage genes are regulated by a repressor coded for by the prophage. The prophage is replicated each time the cell divides.

11. Exposure to certain mutagens can lead to excision of the prophage and initiation of the lytic cycle.

12. Because of lysogeny, lysogenic cells become immune to reinfection with the same phage and may undergo phage conversion.

13. A lysogenic phage can transfer bacterial genes from one cell to another through transduction. Any genes can be transferred in generalized transduction, and specific genes can be transferred in specialized transduction.



Multiplication of Animal Viruses (pp. 382–389)

14. Animal viruses attach to the plasma membrane of the host cell.

15. Entry occurs by endocytosis or fusion.

16. Animal viruses are uncoated by viral or host cell enzymes.

17. The DNA of most DNA viruses is released into the nucleus of the host cell. Transcription of viral DNA and translation produce viral DNA and, later, capsid proteins. Capsid proteins are synthesized in the cytoplasm of the host cell.

18. DNA viruses include members of the families Adenoviridae, Poxviridae, Herpesviridae, Papovaviridae, and Hepadnaviridae.

19. Multiplication of RNA viruses occurs in the cytoplasm of the host cell. RNA-dependent RNA polymerase synthesizes a double-stranded RNA.

20. Picornaviridae + strand RNA acts as mRNA and directs the synthesis of RNA-dependent RNA polymerase.

21. Togaviridae + strand RNA acts as a template for RNA-dependent RNA polymerase, and mRNA is transcribed from a new – RNA strand.

22. Rhabdoviridae – strand RNA is a template for viral RNA-dependent RNA polymerase, which transcribes mRNA.

23. Reoviridae are digested in host cell cytoplasm to release mRNA for viral biosynthesis.

24. Retroviridae reverse transcriptase (RNA-dependent DNA polymerase) transcribes DNA from RNA.

25. After maturation, viruses are released. One method of release (and envelope formation) is budding. Nonenveloped viruses are released through ruptures in the host cell membrane.

Viruses and Cancer (pp. 389)

1. The earliest relationship between cancer and viruses was demonstrated in the early 1900s, when chicken leukemia and chicken sarcoma were transferred to healthy animals by cell-free filtrates.



The Transformation of Normal Cells into Tumor Cells (pp. 390–391)

2. When activated, oncogenes transform normal cells into cancerous cells.

3. Viruses capable of producing tumors are called oncogenic viruses.

4. Several DNA viruses and retroviruses are oncogenic.

5. The genetic material of oncogenic viruses becomes integrated into the host cell’s DNA.

6. Transformed cells lose contact inhibition, contain virus-specific antigens (TSTA and T antigen), exhibit chromosome abnormalities, and can produce tumors when injected into susceptible animals.



DNA Oncogenic Viruses (p. 391)

7. Oncogenic viruses are found among the Adenoviridae, Herpesviridae, Poxviridae, and Papovaviridae.

8. The EB virus, a herpesvirus, causes Burkitt’s lymphoma and nasopharyngeal carcinoma. Hepadnavirus causes liver cancer.

RNA Oncogenic Viruses (p. 391)

9. Among the RNA viruses, only retroviruses seem to be oncogenic.

10. HTLV-1 and HTLV-2 have been associated with human leukemia and lymphoma.

11. The virus’s ability to produce tumors is related to the production of reverse transcriptase. The DNA synthesized from the viral RNA becomes incorporated as a provirus into the host cell’s DNA.

12. A provirus can remain latent, can produce viruses, or can transform the host cell.

Latent Viral Infections (p. 392)

1. A latent viral infection is one in which the virus remains in the host cell for long periods without producing an infection.

2. Examples are cold sores and shingles.

Persistent Viral Infections (p. 392)

1. Persistent viral infections are disease processes that occur over a long period and are generally fatal.

2. Persistent viral infections are caused by conventional viruses; viruses accumulate over a long period.

Prions (pp. 392–393)

1. Prions are infectious proteins first discovered in the 1980s.

2. Prion diseases, such as CJD and mad cow disease, all involve the degeneration of brain tissue.

3. Prion diseases are the result of an altered protein; the cause can be a mutation in the normal gene for PrPC or contact with an altered protein (PrPSc).



Plant Viruses and Viroids (pp. 393–395)

1. Plant viruses must enter plant hosts through wounds or with invasive parasites, such as insects.

2. Some plant viruses also multiply in insect (vector) cells.

3. Viroids are infectious pieces of RNA that cause some plant diseases, such as potato spindle tuber disease.



The Loop

Specialized transduction is described in this chapter; generalized transduction is described in Chapter 8. Diseases caused by viruses are described in Part Four.



Answers

Review

1. Viruses absolutely require living host cells to multiply.

2. A virus has the following properties:

a. Contains DNA or RNA;

b. Has a protein coat surrounding the nucleic acid;

c. Multiplies inside a living cell using the synthetic machinery of the cell; and

d. Causes the synthesis of virions. A virion is a fully developed virus particle that transfers the viral nucleic acid to other cells and initiates multiplication.

3. The capsid of a helical virus is a hollow cylinder with a helical shape, which surrounds the nucleic acid (see Figure 13.4). An example of a helical virus is tobacco mosaic virus. Polyhedral viruses are many-sided (Figure 13.2). A polyhedral virus in the shape of an icosahedron is adenovirus. Polyhedral or helical viruses surrounded by an envelope are called enveloped viruses. An example of an enveloped helical virus is Influenzavirus (Figure 13.3), and herpes simplex is an enveloped polyhedral virus.

4.

5. Both produce double-stranded RNA, with the – strand being the template for more + strands. + strands act as mRNA in both virus groups.

6. Antibiotic treatment of S. aureus can activate phage genes that encode P-V leukocidin.

7. a. Viruses cannot easily be observed in host tissues. Viruses cannot easily be cultured in order to be inoculated into a new host. Additionally, viruses are specific for their hosts and cells, making it difficult to substitute a laboratory animal for the third step of Koch’s postulates.

b. Some viruses can infect cells without inducing cancer. Cancer may not develop until long after infection. Cancers do not seem to be contagious.

8. a. subacute sclerosing panencephalitis

b. common viruses

c. persistent

9. a. plant cell walls

b. vectors such as sap-sucking insects

c. plant protoplasts and insect cell cultures

Critical Thinking

1. Outside living cells, viruses are inert. They cannot ingest and metabolize nutrients, and they cannot reproduce. These are descriptions one might use for chemicals, not living organisms. However, inside a living cell, viruses can multiply. Clinically, because they cause infection and disease, they might be considered alive.

2. A virus is small and cannot hold as much DNA as a cell. Genes that code for proteins that serve two functions conserve space on a viral nucleic acid.

3. These two diseases provide animal models for the study of acquired immunodeficiencies and treatments. Study of the viruses (SIV and FIV) can provide more information regarding the evolution of retroviruses.

4. A prophage, provirus, or plasmid begins as a strand of DNA outside the cell’s chromosome that can be integrated into the chromosome. Like a plasmid, a prophage carries genes that can be used by the cell but are not essential. Prophages and proviruses are replicated with the cell’s chromosome and remain in progeny cells. Prophage DNA will form a circle and replicate itself in the cell’s cytoplasm. Unlike a plasmid, prophages and proviruses are not transferred in conjugation, and when they replicate themselves, viruses are produced that can destroy the host cell.

Clinical Applications

1. Cytomegalovirus. No bacteria or fungi were seen, which suggests a viral cause.

2. Herpes simplex virus. Presence of antibodies against this virus would confirm the etiology.

3. Hepatitis; these people acquired hepatitis A virus from contaminated ice-slushes.

Picornaviridae

Hepatitis A virus Ingestion +RNA, ss Nonenveloped


Hepadnaviridae (uses reverse transcriptase)

Hepatitis B Virus Injection DNA, ds Enveloped

Flaviviridae

Hepatitis C Virus Injection +RNA, ss Enveloped



Case Study: Encephalitis, Texas

Background

On May 30, a 22-year-old man complained of right hand weakness.

On June 1, he complained of right arm numbness.

On June 2, he exhibited several episodes of staring and unresponsiveness lasting 10 to 15 seconds. He consulted a physician in Mexico, who prescribed an unknown medication. That evening, he presented himself to a hospital emergency room in Texas complaining of right hand pain. He had been punctured by a catfish fin earlier in the week, so, based on this information, he was treated with ceftriaxone and tetanus toxoid.

On June 3, when he returned to the emergency room complaining of spasms, he was hyperventilating and had a white blood cell (WBC) count of 11,100 per µl. Although he was discharged after reporting some improvement, he began to have intermittent episodes of rigidity, breath holding, hallucinations, and difficulty swallowing. Eventually he refused liquids. That evening, he was admitted to the intensive-care unit of another hospital in Texas with a preliminary diagnosis of either encephalitis or tetanus. Manifestations included frequent spasms of the face, mouth, and neck; stuttering speech; hyperventilation; and a temperature of 37.8°C. His WBC count was 17,100 mm3 with granulocytosis. He was sedated and observed.

On the morning of June 4, the patient was confused, disoriented, and areflexic (without reflexes). Although his neck was supple, muscle tonus was increased in his upper extremities. Analysis of cerebrospinal fluid indicated slightly elevated protein, slightly elevated glucose, and 1 WBC per 100 µl. An electroencephalogram showed abnormal activity. Because he had uncontrolled oral secretions, he was intubated. His temperature rose to 41.7°C, and he was sweating profusely.

On June 5, the man died.

The patient had worked as a phlebotomist for a blood bank and had donated blood on May 22. His platelets had been transfused before he became ill, but the remainder of his blood products were destroyed.



Questions

1. What was the purpose of the ceftriaxone? The tetanus toxoid?

2. What is granulocytosis?

3. What is the most likely cause of the man’s illness and death?

4. What other information do you need to be sure?

5. How could he have been treated?

6. How should the recipient of the platelets be treated?

The Solution

1. To prevent tetanus.

2. An increase in granulocytes (neutrophils, eosinophils, and basophils).

3. Rabies. On June 4, the patient’s supervisor from work reported to hospital authorities that the man had suffered a bat bite on the right index finger. CSF, serum, and skin biopsy were tested for rabies; all of these samples were negative. Postmortem samples of brain tissue were positive for rabies by direct immunofluorescent antibody test.

4. A fluorescent-antibody test would confirm the diagnosis of rabies.

5. Treatment with antibodies against rabies (rabies immune globulin) before the symptoms began could have saved him.

6. With rabies immune globulin.

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