1. The Viruses and Virus-Like Agents
Chapter 14
The Viruses and Virus-Like Agents

2. 14.1 Filterable Infectious Agents Cause Disease
Many scientists contributed to the early understanding of viruses.
Adolf Mayer, Dimitri Ivanowsky and Martinus Beijerinck studied the tobacco mosaic virus.
The infectious particles “viruses” were found in the filtrate
Figure 14.03: Tobacco mosaic virus.
Figure 14.02A: Tobacco mosaic virus.
© Dennis Kunkel Microscopy, Inc./Phototake/Alamy Images
Figure 14.02B: Filter.
Courtesy of Clemson University - USDA Cooperative Extension Slide Series, Bugwood.org

3. Figure 14.04: Size relationships among cells and viruses.
Walter Reed studied yellow fever.
Frederick Twort and Felix d’Herelle studied bacteriophages.
In the 1930s, it was discovered that viruses are nonliving agents composed of nucleic acid and protein.
Alice M. Woodruff and Ernest W. Goodpasture developed a culture technique using chicken eggs.
Figure 14.04: Size relationships among cells and viruses.

4. 14.2 Viruses Have a Simple Structural Organization
Viruses are tiny infectious agents.
Viruses are small, obligate intracellular parasites.
They lack the machinery for generating energy and large molecules.
They need a host cell to replicate.
The viral genome contains either DNA or RNA, but not both.
The capsid is the protein coat, made up of capsomeres.
Some capsid proteins are spikes that help the virus attach to and penetrate the host cell.
Figure 14.05: Viral Replication Cycle.

5. The components of viruses.
Naked viruses are composed only of a nucleocapsid, a capsid with enclosed genome.
Viruses surrounded by an envelope are enveloped viruses.
A virion is a completely assembled, infectious virus outside its host cell.
The components of viruses.

6. Viruses are grouped by their shape.
Helical viruses have helical symmetry.
Isocahedral viruses have isocahedral symmetry.
Viruses that have both helical and isocahedral symmetry have complex symmetry.
Figure 14.07: Viral shapes.

7. Figure from Investigating the Microbial World 14 Experiment 1.
Viruses have a host range and tissue specificity.
A host range refers to what organisms the virus can infect.
Host range depends on capsid or envelope structure.
Many viruses infect certain cell or tissue types within the host (tissue tropism).
The virus needs a specific receptor in order to invade the host cell.
Figure from Investigating the Microbial World 14 Experiment 1.

8. 14.3 Viruses Can Ben Classified by Their Genome
A taxonomic scheme for all viruses has yet to be universally adopted
The International Committee on Taxonomy of Viruses (ICTV) is developing a classification system.
Figure 14.08: Classification fro the Human DNA and RNA Viruses.

9. Figure 14.09: Mutation Rate Versus Genome Size.
DNA viruses contain single- or double-stranded DNA genomes
Replicated in host cell DNA
RNA viruses contain single- or double-stranded RNA genomes.
Replicated at host cell ribosomes
Retroviruses are replicated indirectly through a DNA intermediate using an reverse transcriptase enzyme.
Figure 14.09: Mutation Rate Versus Genome Size.
Adapted from Gago et al. (2009) Science 323, 1308

10. 14.4 Viral Replication Follows a Set of Common Steps
Figure 14.10: Steps of Virus Replication.

11. Replication of Bacteriophages Can Follow One of Two Cycles
Lytic cycle: cells lyse to release new viruses
T-even bacteriophages are virulent viruses that carry out a lytic cycle of infection in prokaryotes.
Attachment by tail fibers
Penetration
Biosynthesis
Maturation
Release by lysis
Figure 14.11: Bacteriophage Structure and Genome Penetration.

12. Figure 14.12: Bacteriophage replication.
Temperate phages do not lyse the host.
They insert their DNA into the bacterial chromosome as a prophage (lysogenic cycle).
Figure 14.12: Bacteriophage replication.

13. Animal virus replication often results in a productive infection.
1. Attachment by receptors
2. Penetration
3. Biosynthesis
4. Maturation
5. Release by budding
Figure 14.13: The Entry of Animal Viruses into Their Host Cell.

14. Figure 14.14: Replication of a double-stranded DNA Virus.
Most DNA viruses replicate their genome inside the cell’s nucleus
protein capsids are made in the cytoplasm
proteins are transported to the nucleus and join with the viral genome for maturation
RNA viruses replicate in the cytoplasm
Figure 14.14: Replication of a double-stranded DNA Virus.

15. Figure 14.15: The formation of a provirus by HIV.
Some DNA viruses and retroviruses insert their genome into the host chromosome as a provirus.
Retroviruses use reverse transcriptase to transcribe their RNA to DNA.
The provirus encodes a repressor protein that prevents activation of the viral genes necessary for replication.
Latent proviruses are immune to the host body’s defenses.
They are propagated each time the cell’s chromosome is reproduced.
Figure 14.15: The formation of a provirus by HIV.

16. Figure 14.16: Potential Outcomes for Animal Virus Infection of a host cell.

17. 14.5 Viruses and Their Infections Can Be Detected in Various Ways
Detection of viruses is critical to disease identification.
Some diseases have specific symptoms, ex) mumps or measles
Light microscopes look for cytopathic effects, ex) syncytia (giant cells) in RSV
Electron microscopes examine cells
Serology looks for antibodies
Figure 14.17: Cells and Viruses.
© Dennis Kunkel Microscopy, Inc./Phototake/Alamy Images

18. Cultivation and detection of viruses uses eggs or cells in tissue culture.
In a primary cell culture, cells form a monolayer in a culture dish.
Viruses can be detected by the formation of plaques, clear zones within the monolayer of animal cells.
Figure 14.18C: Plaque formation in a cell culture.
Figure 14.18A: Viral Cultivation.
Courtesy of Giles Scientific Inc, CA,
Courtesy of Greg Knobloch/CDC

19. 14.6 Some Viruses Are Associated with Human Tumors and Cancers
Cancer is an uncontrolled growth and spread of cells.
A tumor is a clone of abnormal cells.
A benign tumor, normally, the body surrounds a tumor with a capsule of connective tissue.
A malignant tumor, Tumor cells can break free from the capsule and spread to other tissues of the body (metastasis).
60–90% of human cancers are associated with carcinogens.
Figure 14.15: The onset of cancer.

20. Viruses are responsible for about 20% of human tumors.
Oncogenic viruses transform infected cells.
Epstein-Barr virus is linked to Burkitt Lymphoma, a tumor of the jaw.
Human papilloma virus (HPV) is associated with cervical cancer.
There is now a vaccine against some HPV.
Figure 14.22: Retrovirus Stimulation of a Tumor and v-Oncogene Formation.

21. Figure 14.20: The oncogene theory.
Oncogenic Viruses Transform Infected Cells
Protooncogenes normally reside in the chromosomal DNA of a cell.
They can be transformed to oncogenes by:
radiation.
chemical
carcinogens.
DNA damage.
viruses.
Figure 14.20: The oncogene theory.

22. Figure 14.21: Viral oncogenes and Tumor Suppressor Gene Action.
RNA tumor viruses
If a provirus inserts near a tumor suppressor gene, it may inactivate it or if near a proto-oncogene it may activate it causing unlimited growth
DNA tumor viruses
Viral oncogenes are nuclear proteins that disrupt host DNA replication, inactivate tumor suppressor genes ex) hepatitis B and liver cancer
Figure 14.21: Viral oncogenes and Tumor Suppressor Gene Action.

23. 14.7 Emerging Viruses Arise from Genetic Recombination and Mutation
Emerging viruses usually arise through natural phenomena.
We’re at risk for zoonotic diseases, ex) influenza
Viruses may spread to new populations, or may expand host range, ex) west nile virus.
Genetic recombination can lead to “new” viruses.
Mutation can occasionally be advantageous and create a new virus or stain of virus.
Table 14.04: Examples of Emerging Viruses.

24. 14.8 Virus-Like Agents Include Viroids and Prions
Viroids are infectious RNA particles.
Viroids are tiny fragments of RNA that cause diseases in crop plants.
One hypothesis suggests they originated as introns.
Another hypothesis is the viroid RNA interacts with host cell RNA
Figure 14.23: Genome relationships.

25. Figure 14.24A: Brain tissue showing effects of a prion disease.
Prions are infectious proteins.
Transmissible spongiform ecephalopathies (TSEs) can occur in humans and other animals.
Ex), mad cow disease
TSEs are neurologic
degenerative diseases
that can be transmitted
within or between species.
Originally, scientists believed
TSEs were caused by a virus.
Stanley Prusiner discovered the proteinaceous infectious particle (prion).
Figure 14.24A: Brain tissue showing effects of a prion disease.
Courtesy of APHIS photo by DR. Al Jenny/CDC

26. Figure 14.24BC: Normal prion protein tertiary structure.
The protein-only hypothesis predicts that prions are composed only of protein and contain no nucleic acids.
Normal cellular prions have a different shape than abnormal prions, the latter of which cause TSEs.
TSEs may spread when infectious prions bind to normal prions.
This causes normal prions to change shape and become abnormal.
Abnormal prions do not trigger an immune response.
Figure 14.24BC: Normal prion protein tertiary structure.

27. Figure 14.25: Prion Formation and Propagation.
Death of the host occurs from nerve cell death leading to sponge-like holes in brain tissue.
Symptoms include:
dementia.
weakened muscles.
loss of balance.
This results from insoluble aggregates of abnormal prions in the brain.
The human form of TSE is called variant CJD (Creutzfeldt-Jakob disease).
Figure 14.25: Prion Formation and Propagation.