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

2. Characteristics of Viruses
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. Characteristics of Viruses
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. Characteristics of Viruses
[INSERT FIGURE 13.1]
Characteristics of Viruses

5. Characteristics of Viruses
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 Viruses Based 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. Viral Replication of Bacteriophages
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. Viral Replication of Bacteriophages
[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. Viral Replication - Bacteriophages
[INSERT FIGURE 13.11]
Viral Replication - Bacteriophages

19. Animation: Temperate Bacteriophages
Viral Replication
Animation: Temperate Bacteriophages

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

22. Viral 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. Animation: Animal Viruses
Viral Replication
Animation: Animal Viruses

26. Viral 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. Viral Replication Comparison
[INSERT TABLE 13.4]
Viral Replication Comparison

28. The Role of Viruses In Cancer
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. Other Parasitic Particles: Viroids and Prions
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. Other Parasitic Particles: Viroids and Prions
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. Other Parasitic Particles: Viroids and Prions
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. Other Parasitic Particles: Viroids and Prions
[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?