The Characteristics and Classification of Viruses, Viroids, and Prions

1. Chapter 13 Characterizing and Classifying Viruses, Viroids, and Prions

2. Cause many infections of humans, animals, plants, and bacteria • Cannot carry out any metabolic pathway • Neither grow nor respond to the environment • Cannot reproduce independently • Recruit the cell’s metabolic pathways to increase their numbers • Cause most of the diseases that plague the industrialized world • Virus – miniscule, acellular, infectious agent having one or several pieces of either DNA or RNA • No cytoplasmic membrane, cytosol, organelles (with one exception) • Have extracellular and intracellular state Characteristics of Viruses

3. Extracellular State • Called virion • Protein coat (capsid) surrounding nucleic acid • Nucleic acid and capsid also called nucleocapsid • Some have phospholipid envelope • Outermost layer provides protection and recognition sites for host cells • Intracellular State • Capsid removed • Virus exists as nucleic acid Characteristics of Viruses

4. [INSERT FIGURE 13.1] Characteristics of Viruses

5. Genetic Material of Viruses • Show more variety in nature of their genomes than do cells • May be DNA or RNA, but never both • Primary way scientists categorize and classify viruses • Can be dsDNA, ssDNA, dsRNA, ssRNA • May be linear and composed of several segments or single and circular • Much smaller than genomes of cells Characteristics of Viruses

6. Hosts of Viruses • Most viruses infect only particular host’s cells • Due to affinity of viral surface proteins or glycoproteins for complementary proteins or glycoproteins on host cell surface • May be so specific they only infect particular kind of cell in a particular host • Generalists – infect many kinds of cells in many different hosts

7. [INSERT FIGURE 13.4] Size of Viruses

8. Capsid Morphology • Capsids – protein coats that provide protection for viral nucleic acid and means of attachment to host’s cells • Capsid composed of proteinaceous subunits called capsomeres • Some capsids composed of single type of capsomere; others composed of multiple types

9. Complex shape of a bacteriophage • Notice helical capsid inside envelope • Notice polyhedral capsid inside envelope Shapes of Viruses

10. The Viral Envelope • Not all viruses have envelopes • Acquired from host cell during viral replication or release; envelope is portion of membrane system of host • Composed of phospholipid bilayer and proteins; some proteins are virally coded glycoproteins (spikes) • Envelope’s proteins and glycoproteins often play role in host recognition

11. [INSERT TABLE 13.1]

12. Classification of VirusesBased on type of nucleic acid, presence of envelope, shape, and size

13. [INSERT TABLE 13.2] • = negative sense: complimentary for mRNA, cannot be directly translated • + = positive sense: equivalent to mRNA

14. Dependent on hosts’ organelles and enzymes to produce new virions • Replication cycle usually results in death and lysis of host cell → lytic replication • Stages of lytic replication cycle • Attachment • Entry • Synthesis • Assembly • Release Viral Replication of Bacteriophages

15. [INSERT FIGURE 13.8] Viral Replication of Bacteriophages

16. [INSERT FIGURE 13.9] Viral Replication

17. Lysogeny • Modified replication cycle • Infected host cells grow and reproduce normally for generations before they lyse • Temperate phages • Prophages – inactive phages • Lysogenic conversion results when phages carry genes that alter phenotype of a bacterium

18. [INSERT FIGURE 13.11] Viral Replication - Bacteriophages

19. Viral Replication Animation: Temperate Bacteriophages

20. Replication of Animal Viruses • Same basic replication pathway as bacteriophages • Differences result from • Presence of envelope around some viruses • Eukaryotic nature of animal cells • Lack of cell wall in animal cells • Attachment of animal viruses • Chemical attraction • Animal viruses do not have tails or tail fibers • Have glycoprotein spikes or other attachment molecules that mediate attachment Viral Replication of Animal Viruses

21. [INSERT FIGURE 13.12] Viral Replication of Animal Viruses

22. Replication of Animal Viruses • Synthesis of animal viruses • Each type of animal virus requires different strategy depending on its nucleic acid • DNA viruses often enter the nucleus • RNA viruses often replicated in the cytoplasm • Must consider • How mRNA is synthesized? • What serves as template for nucleic acid replication? Viral Replication of Animal Viruses

23. dsDNA Viruses – similar to normal replication of host cellular DNA • ssDNA – in humans are paroviruses • Host enzymes produce complimentary strand of DNA to make dsDNA • +ssRNA – example is poliovirus • can act directly as mRNA • Retroviruses - +ssRNA but don’t use it as mRNA, HIV • Use their reverse transcriptase to make DNA intermediate • -ssRNA – rabies and flu • Not recognized by host ribosome • Has to use it’s RNA-dependent RNA transcriptase to make +RNA • dsRNA – rotavirus • Unwinds, + strand acts immediately as mRNA, +RNA is transcribed by RNA polymerase

24. Replication of Animal Viruses • Assembly and release of animal viruses • Most DNA viruses assemble in and are released from nucleus into cytosol • Most RNA viruses develop solely in cytoplasm • Number of viruses produced and released depends on type of virus and size and initial health of host cell • Enveloped viruses cause persistent infections • Are released by “budding”, do not lyse cell right away so cause long lasting infection • Naked viruses are released by exocytosis or may cause lysis and death of host cell

25. Viral Replication Animation: Animal Viruses

26. Replication of Animal Viruses • Latency of animal viruses • Similar to lysogeny of bacteriophages but there are differences • Some latent viruses do not become incorporated into host chromosome • When provirus (latent virus) is incorporated into host DNA, condition is permanent, becomes physical part of host’s chromosome • When animal viruses remain dormant in host cells • May be prolonged for years with no viral activity, signs, or symptoms Viral Replication of Animal Viruses

27. [INSERT TABLE 13.4] Viral Replication Comparison

28. Normally, animal’s genes dictate that some cells can no longer divide and those that can divide are prevented from unlimited division • Genes for cell division are “turned off” or genes that inhibit division are “turned on” • Neoplasia – uncontrolled cell division in multicellular animal; mass of neoplastic cells is tumor • Benign vs. malignant tumors • Metastasis • Cancers The Role of Viruses In Cancer

30. Environmental factors that contribute to the activation of oncogenes • Ultraviolet light • Radiation • Carcinogens • Viruses • Viruses cause 20-25% of human cancers in several ways • Some carry copies of oncogenes as part of their genomes • Some promote oncogenes already present in host • Some interfere with tumor repression when they insert into host’s repressor gene • Several specific DNA and RNA viruses are known to cause ~15% of human cancers • Burkitt’s lymphoma • Hodgkin’s disease • Kaposi’s sarcoma • Cervical cancer

31. Culturing Viruses in the Laboratory • Has to be done using cells • Live organisms – bacterial cultures, lab plants or animals • Cell culture • Bacteria, plant, animal • Embryonated chicken eggs are great – large cell, free of microbes, contain nourishing yolk

32. Characteristics of Viroids • Extremely small, circular pieces of RNA that are infectious and pathogenic in plants • Similar to RNA viruses, but lack capsid • May appear linear due to H bonding • No animal diseases are known as of yet Other Parasitic Particles: Viroids and Prions

33. Characteristics of Prions • Proteinaceous infectious agents • Composed of single protein PrP • All mammals contain gene that codes for primary sequence of amino acids in PrP • Has role in activity of the brain but exaxt role still not known • Two stable tertiary structures of PrP • Normal functional structure with -helices called cellular PrP • Disease-causing form with -sheets called prion PrP • Prion PrP converts cellular PrP into prion PrP by inducing conformational change (acts enzymatically to do this) • Results in fatal neurological degeneration Other Parasitic Particles: Viroids and Prions

34. Characteristics of Prions • Normally, nearby proteins and polysaccharides force PrP into cellular shape • Excess PrP production or mutations in PrP gene result in initial formation of prion PrP • When prions are present, they cause newly synthesized cellular PrP to refold into prion PrP

35. Characteristics of Prions • All prion diseases involve fatal neurological degeneration, deposition of fibrils in brain, and loss of brain matter • Large vacuoles form in brain; characteristic spongy appearance • Spongiform encephalopathies – BSE, CJD, kuru • Prions only destroyed by incineration or autoclaving in 1N NaOH • Normal cooking and sterilization procedures do not destroy them Other Parasitic Particles: Viroids and Prions

36. [INSERT TABLE 13.5] Other Parasitic Particles: Viroids and Prions

37. Some scientists consider them complex pathogenic chemicals that lack the characteristics of life • Other scientists consider them to be the least complex living entities because they • Use sophisticated methods to invade cells • Have the ability to take control of their host cell • Are able to replicate themselves Are Viruses Alive?