1. Viral Structure and Life Cycles
Ch 5
Viral Structure and Life Cycles

2. SLOs Explain what it means when viruses are described as filterable.
Identify better terms for viruses than alive or dead.
Discuss the size of viruses relative to other microorganisms.
Describe the function and structure(s) of viral capsids.
Distinguish between enveloped and naked viruses.
Explain the importance of viral surface proteins, or spikes.
Diagram the possible configurations that nucleic acid viruses may possess.
Diagram the different steps in the cycle of animal viruses.
Discuss both persistent and transforming infections.
Provide thorough descriptions of both lysogenic and lytic bacteriophage infections.
List three principal purposes of cultivating viruses.
Describe three ways in which viruses are cultivated.
Name and summarize two noncellular infectious agents besides viruses.

3. Viruses as part of the Biological Spectrum
Infect every cell type (phages vs. animal viruses)
Pasteur: “living things” smaller than bacteria are causing diseases  “Filterable units”
Virus = Latin for poison
Obligatory intracellular parasites using host cell machinery
Dead or alive?
Better terms:___________________
Kill or live in harmony within the host cell. Outside of cell: Viruses are inert.

4. General Properties of Viruses
Nucleic acid core: DNA or RNA
Protein coat = capsid made up of capsomeres.
Some are enclosed by an envelope (naked vs. enveloped)
Viruses have spikes (COH/protein)
Lack enzymes for metabolism, incl. protein synthesis and energy production.
Host range is determined by specific host attachment sites and cellular factors
Most viruses are also tissue specific

5. Virus Shapes and Sizes
Advent of EM allowed for visualization of viruses
Compare to Fig 5.1

6. Naming of Viruses
Often based on hosts and diseases they cause. Clinicians usually use common vernacular names (e.g.: polio virus, chickenpox virus, measles virus, etc.) Most recent considerations: Structure and genomics

7. Examples of Naming Viruses
Family Names end in –viridae
Genera and species names end in -virus.
Subspecies are designated by a number.
Family: Herpesviridae
Genus: Varicellovirus
Species and subspecies: Human herpes virus 3 (HHV-3
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

8. Virion Structure Nucleic acid Capsid Envelope Spikes (on envolpes)
Capsomeres
Helical, icosahedral, or complex
Nucleic acid
DNA or RNA
Envelope
Spikes (on envolpes)

9. Fig 5.3

10. Table 5.2

11. Variety in Viral Nucleic Acid
DNA viruses: ds, ss, linear, circular
RNA viruses
Ds, but more often Ss
Positive-sense RNA: ready for immediate translation
Negative-sense RNA: must be converted before translation can occur
Segmented
Some carry their own enzymes, e.g.: Reverse transcriptase (Retroviruses)

12. Multiplication in Animal Viruses
Table 5.4
General phases of animal viral replication cycle:
Adsorption
Penetration
Uncoating
Synthesis
Assembly
Release
Length of replication cycle varies: 8 h in polioviruses; 36 h in herpesviruses
Kill or live in harmony within host cell (carrier relationship)

13. 2 types of penetration modes
Fig 5.5

14. Multiplication of Animal DNA Viruses
Naked animal viruses are predominantly released by host cell lysis!

15. Multiplication of a Retrovirus

16. Enveloped animal viruses may exit the host cells via budding
HSV envelopment and release

17. Damage to Host Cell Accumulated damage kills most cells.
Cytopathic Effects (CPEs): virus-induced cell damage visible microscopically
Examples of CPEs:
Inclusion bodies: compacted masses of viruses or damaged cell organelles in the nucleus and cytoplasm
Syncytia
Accumulated damage kills most cells.

18. Viruses and Cancer - Oncology
Expanded from book. Discard Fig 5.8
Cancer  def.?
Benign vs. malignant tumors
Carcinoma vs. Sarcoma vs. Adenocarcinoma
3 important characteristics of cancer cells:
Rapid cell division
Loss of anchoring junctions  ______________
Dedifferentiation of cells and changes in cell’s surface molecules (“cancer markers”)
Oncoviruses can transform cells  Tumors

19. Viruses and Cancer cont.
Root of all cancers:
Chemicals and ___________ directly damage the genes through mutation rate
Normal cell cycle ends in cell division. Necessary for normal growth & development and wound healing….

20. Viruses and Cancer cont.
Normal cell cycle regulator genes:
Proto-oncogenes
Tumor suppressor genes
Genetic material of oncogenic viruses becomes integrated into the host cell’s DNA  _____ virus.
Oncogenic Viruses are responsible for 20% of human cancers

21. Oncoviruses lead to….
addition of oncogene or 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

22. Oncogenic Viruses 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  _________ sarcoma
HBV  ______cancer

23. Bacteriophages Infect Bacteria
Mostly ds DNA viruses
Lytic or lysogenic cycles
2008: Discovery of virophages
Relevant for medical micro- biology because
easy to study, and
can make bacteria more pathogenic through lysogenic conversion. (See below) E.g: C. diphtheria, V. cholerae, C. botulinum)
Phage therapy!

24. T-Even Bacteriophage: The Lytic Cycle
Adsorption to cell surface receptors (chance encounter – no active movement)
Penetration – only genome enters
Biosynthesis and Assembly – Production and assembly of phage DNA and proteins
Maturation – assembly to form intact phage
Release due to lysis of host cell
Fig 5.9

25. 2 Mechanisms of Bacteriophage Multiplication
Lytic cycle (by lytic or virulent phages)
Phage multiplies, eventually causing lysis and death of host cell
Lysogenic cycle or Lysogeny (by lysogenic or temperate phages)
Phage DNA incorporated in host DNA  Prophage. No host cell lysis, cell lives. Allows virus to spread without killing host.
Induction: Activation of lysogenic prophage to go into lytic cycle

26. Lytic and Lysogenic Cycles ( Phage)
Compare to Fig 5.9

27. Cultivation and Identification of Animal Viruses
Viruses are obligate ……………………….
Culture methods:
In vivo: lab animals and embryonic bird tissues
In vitro: cell or tissue culture methods
Primary purposes of viral cultivation:
Isolate and identify viruses in clinical specimens.
Prepare viruses for vaccines.
Research

28. Other Noncellular Infectious Agents
Prions: Infectious Proteins
Cause chronic persistent spongiform encephalopathies
Long latency, progressive and universally fatal
Human and 9 animal diseases, such as:
CJD
Kuru
Scrapie
Mad cow disease = _________________
PrPC: Normal cellular prion protein, on cell surface. Involved in cell death regulation.
PrPSc: Scrapie protein; accumulates in brain cells, forming plaques.

29. Spongiform Encephalopathies
Caused by altered prion protein:
Mutation in normal PrPc gene (sporadic CJD), or
contact with the abnormal PrPSc protein (Kuru)
Spontaneous or transmissible by ingestion, transplant, and surgical instruments

30. Satellite Viruses Dependent on other viruses for replication
Adeno-associated virus (AAV):
Originally thought to only replicate in cells infected with adenovirus
Delta agent:
Naked circle of RNA
Expressed only in presence HBV
Worsens severity of liver damage

31. The End Inside the Clinic: Shingles Case File: The Domino Effect
Who will present?
The End