1. Ch 13
Viruses and Prions

2. Student Learning Outcomes
Differentiate a virus from a bacterium. Explain the difference between enveloped and nonenveloped viruses. Define viral species. Describe how bacteriophages and animal viruses are cultured. Compare and contrast the lytic and lysogenic cycles of bacteriophages. Define oncogene and transformed cell. Discuss the relationship between viruses and cancer. Explain latent viral infections and give an example. Discuss how a proteins can be infectious.

3. The ability of a virus to infect an organism is regulated by
the host species.
the type of cells.
the availability of an attachment site.
cell factors necessary for viral replication.
all of the above

4. Foundations of Virology
Non-living agents that infect all life forms (phages vs. animal viruses) Viral cultivation differs from bacterial cultivation  1,500 known viruses (estimates:  400,000 exist) Advent of EM allowed for visualization of viruses

6. General Characteristics of Viruses
Obligatory intracellular parasites
Filterable
Virus = Latin for poison
Contain DNA or RNA
Contain a protein coat = capsid made up of capsomeres. Various shapes
Some are enclosed by an envelope (naked vs. enveloped)
Some viruses have spikes (COH/protein)
Most viruses are tissue specific
Host range is determined by specific host attachment sites and cellular factors

7. Host Range and Specificity
Usually narrow host range – due to?
Tissue tropism
Phage Therapy
Oncolytic viruses

8. Virus Shapes and Sizes
Fig 13.1

9. Which of the following statements about viruses is FALSE?
Viruses use their own catabolic enzymes
Viruses contain a protein coat
Viruses contain DNA or RNA but never both
Viruses use the anabolic machinery of the cell

10. Virion Structure Nucleic acid Capsid Envelope Spikes DNA or RNA
Capsomeres
Envelope
Spikes
Fig 13.2

11. Morphology of an enveloped helical virus
Example of a enveloped polyhedral virus: Hepes simplex

12. Polyhedral
Smallpox virus
Complex symmetry
Compare to Figs

13. Electron micrograph of Aeromonas virus 31, an unassigned virus in the family Myoviridae
photograph by Dr Hans Ackermann.

14. Taxonomy of Viruses No evidence for common viral ancestor.
Classification based on genomics and structure.
Family names end in –viridae
Genus and species names end in -virus.
Viral species: A group of viruses sharing the same genetic information and ecological niche (host). Common names are used for species.
Subspecies are designated by a number.

15. Examples of Naming Viruses
Family: Herpesviridae
Genus: Varicellovirus
Species and subspecies: Human herpes virus 3 (HHV-3
Briefly review Table 13.2
Family: Retroviridae
Genus: Lentivirus
Species and subspecies: Human immunodeficiency virus 1 and 2 (HIV-1, HIV-2)
Family: Picornaviridae
Genus: Hepatovirus
Species and subspecies: Hepatitis A virus

18. The viral envelope closely resembles the
Capsomere
Cytoplasm
Prokaryotic cell wall
Eukaryotic cell membrane
None of the above

19. Isolation, Cultivation, and Identification of Viruses
Fig 13.6
Viruses must be grown in living cells
Bacteriophages form plaques on a lawn of bacteria
Animal viruses may be grown in cell culture, embryonated eggs (Fig 13.7), or living animals
Fig 13.8

20. Virus Identification Serological tests Nucleic acids methods
Detect antibodies against viruses in a patient
Use antibodies to identify viruses (more after Immunology chapter discussion)
Nucleic acids methods
RFLPs
PCR

21. Viral Multiplication
Obligate intracellular parasites using host cell machinery
Very limited number of genes encode proteins for
Capsid formation
Viral nucleic acid replication
Movement of virus into and out of cell
Kill or live in harmony within the host cell – Outside the cell, viruses are inert

22. 2 Mechanisms of Bacteriophage Multiplication
Lytic cycle (by lytic or virulent phage)
Phage multiplies, eventually causing lysis and death of host cell
Lysogenic cycle (by lysogenic or temperate phage)
Phage DNA incorporated in host DNA  Prophage. No host cell lysis, cell lives. 3 results of lysogeny:
Lysogenic cell immune to reinfection by same phage
Phage conversion
Possibility for specialized transduction
Mastering: Viral Multiplication

23. T-Even Bacteriophage: The Lytic Cycle
Attachment to cell surface receptors (chance encounter – no active movement)
Penetration – only genome enters
Biosynthesis – Production of phage DNA and proteins
Maturation – assembly to form intact phage
Release due to phage induced lysozyme production
See Fig 13.11

24. Lytic Cycle of a T-Even Bacteriophage1 2 3
Fig 13.11

25. Some animal viruses exit the host cells via budding
HSV envelopment and release
Fig

26. Lytic and Lysogenic Cycles ( Phage)
Fig 13.12

27. Place the following in the order in which they are found in a host cell: (1) capsid proteins; (2) infective phage particles; (3) phage nucleic acid.
1, 2, 3
3, 2, 1
2, 1, 3
3, 1, 2
1, 3, 2

28. Multiplication of Animal DNA Viruses
Foundation Fig 13.15

29. Multiplication of a Retrovirus
Fig 13.19

30. Cancer - Oncology Cancer  uncontrolled mitotic divisions
Benign vs. malignant tumors
Carcinoma vs. Sarcoma
Adenocarcinoma
3 important characteristics of cancer cells:
Rapid cell division
Loss of anchoring junctions and contact inhibition  ______________
Dedifferentiation of cells

31. Viruses and Cancer Root of all cancers:
Chemicals and ___________ directly damage the genes through mutation rate
Viruses damage/alter genes by bringing new genes into the cell.  what kinds of genes?
Normal cell cycle ends in cell division. Necessary for normal growth & development and wound healing….

32. Viruses and Cancer Normal cell cycle regulator genes Proto-oncogenes
Tumor suppressor genes
Genetic material of oncogenic viruses becomes integrated into the host cell’s DNA  _____ virus.

33. Provirus leads to….
……conversion of proto-oncogenes to oncogenes or suppression of Tumor suppressor genes
Foot on accelerator model:
Proto-oncogenes turned ______
Foot off brake model:
Inhibitors of tumor suppressor proteins

34. Oncogenic Viruses are responsible for 10 % of human cancers DNA Viruses
RNA Viruses
Hepatitis C virus (HCV)  liver cancer
human T-cell leukemia virus (HTLV-1)
HPV  _________cancer
Epstein-Barr virus (EBV)  Burkitt’s lymphoma
HHV8  Kaposi’s sarcoma
HBV  _________cancer

35. carcinogens in cigarette smoke.
Proto-oncogenes can be activated to become oncogenes and cause cancer by
carcinogens in cigarette smoke.
overexposure to UV radiation in sunlight
spontaneous mutations.
virus infection.
all of the above.

36. Latent and Persistent Viral Infections
Latent: Virus remains in asymptomatic host cell for long periods
Persistent: Disease processes occurs over a long period; generally is fatal
Fig 13.21

37. Prions =
Inherited and transmissible by ingestion, transplant, and surgical instruments
Cause spongiform encephalopathies Human and 9 animal diseases, such as:
Scrapie,
Mad cow disease
CJD,
Kuru
PrPC: Normal cellular prion protein, on cell surface. Involved in cell death regulation.
PrPSc: Scrapie protein; accumulates in brain cells, forming plaques.
Review Fig 13.22

38. Spongiform Encephalopaties
Caused by altered protein:
Mutation in normal PrPc gene (sporadic CJD), or
contact with the abnormal PrPSc protein (Kuru)
Mastering: Prions

39. Fig 13.22 PrPc produced by cells is secreted to the cell surface.
PrPSc 1
PrPc produced by cells is secreted to the cell surface. 2
PrPSc may be acquired or produced by an
altered PrPc gene. 3
PrPSc reacts with PrPc
on the cell surface. 4
PrPSc converts the PrPc to PrPSc. 5
The new PrPSc converts more PrPc. 6
The new PrPSc is taken in, possibly by receptor-mediated endocytosis.
Lysosome 7 8
PrPSc continues to accumulate as the endosome contents are transferred to lysosomes. The result is cell death.
PrPSc accumulates in
endosomes.
Endosome
Fig 13.22

40. The End