Material covered from 4/23 through 5/16: one-half of the
final. The other half will be comprehensive. Steps to success: Study exercises and questions: Note: These questions are not all inclusive of the
material to be covered on the final. They focus on the
material covered since the last midterm. Refer to the other
study guides to review the earlier material and to help
answer some of the questions here. 1. What is a viroid? How does it differ from a
virus? 2. It is hypothesized that many of the viroids
either co-descended with introns from some precursor or are
descended from introns. What evidence is there to support
this hypothesis? 3. Outline one apparent mechanism of replication
for viroids. Where in the host cell does this take
place? 4. Compare and contrast viroids, virusoids,
satellite viruses, satellite RNA, pseudovirions, and DI
particles. (A table is a good approach.) 5. Why is viroid RNA amazingly stable? 6. List three differences between hepatitis
delta-agent and other viroids. 7. OLD DOGMA: RNA are the primary communications network, the
gofers, and the manufacturing supervisors. (pink collar,
some training required) Proteins are the work force. (blue collar, rest breaks
allowed only when production inventory is high) REVISED OLD DOGMA: In these firms, RNA continue to perform traditional
RNA roles. (They also requisition additional support,
both in pink collar and blue collar positions from larger
host companies.) NEWEST REVISION: Give two examples of RNA acting as enzymes. 8. Define prions. How do they differ from true
"slow viruses"? 9. What evidence is there that supports nucleic
acid coding for prions? 10. What evidence is there that supports something
other than nucleic acids for the "coding" of prions? 11. Suppose that a few molecules of PrPsc, devoid
of any other contaminating substances, can really lead to
the development of disease. Construct a reasonable
hypothesis to explain how this could occur. How would you
test your hypothesis? 12. With regard to chemical agents and processing
protocols, compare the sensitivities and resistances of
prions to true viruses. 13. What is the difference between cis- and trans-
activation of genes? Give examples of each. 14. Compare and contrast the levels of control
found in prokaryotes with that found in eukaryotes. 15. Explain what genes, and how they are
expressed, are involved in lambda phage either completing a
lytic reproduction cycle or becoming lysogenized. 16. Suppose you want to construct a lambda phage
variant, which when combined with your custom target insert,
would result in lysogeny as a predictable event for all
recombinants, rather than some going through the lytic
cycle. Describe where and how you would modify the phage.
Describe any characteristics of your constructed insert
which would be necessary for your system to work. 17. Compare and contrast polycistronic expression
and monocistronic expression. Give examples of viruses which
use each of these strategies. 18. Give examples of two different strategies used
to control the quantity of mRNA produced. Cite examples of
viruses for each of the strategies you choose. 19. Give examples of two different strategies used
for temporal control of gene products during an infection
cycle. Cite examples of viruses for each of the strategies
you choose. 20. The understanding of the role of LTRs in
regulation of expression is still developing. Using
retroviruses as an example, discuss how LTRs are involved in
regulation. 21. Discuss two ways that nested sets of mRNA can
arise. How would you demonstrate which strategy a particular
virus used? 22. What characteristics of the host and of a
particular virus contribute to an infection becoming
established in the first place? Once an infection is
established, what characteristics of the host and the virus
affect whether the infection is cleared or becomes
persistent? 23. Discuss the different strategies which allow a
virus to continue infecting a host population. Compare the
advantages and disadvantages of these strategies. In your
opinion, which strategy would allow a virus to successfully
reproduce over many millions of years? Support your
answer. 24. What are the three types of interferon? How is
their production induced? 25. What are the primary effects of
interferon? 26. If interferon protects against viral
infection, why is it being used in cancer therapy as
well? 27. What is "viral interference"? Give an
example. 28. How do antibodies protect against viral
infection? 29. What is the difference between passive
immunity and active immunity? 30. What mechanisms do plants use to resist
viruses? How do these compare to animal responses? 31. Describe two defense mechanisms bacteria use
against phage infections. Describe how phage counteract
these mechanisms. [The old spy-versus-spy
routine.] 32. List three benefits phage can provide host
bacteria. Give an example of each type. What possible
benefits do viruses infecting eukaryotic cells provide to
their hosts? 33. Describe three methods animal viruses use to
enter host cells. Give an example of each. 34. List three methods of detecting active
infection by virus in cell culture. 35. Describe how you could detect a latent
infection in a cell culture. 36. What is the difference between reversible and
irreversible viral attachment? 37. What are the types of bonds involved in
receptor interaction between virus and host cell. 38. What is "capping" and what is its significance
in relation to viral attachment? How can capping be
demonstrated? 39. Some virus-infected cells aggregate. Why? 40. Describe the process of cell fusion. Give an
example of a virus which causes fusion. 41. Give an example of the use of cell fusion in
research. 42. What is the risk of using many of the current
anti-viral agents? 43. What are inclusion bodies? Describe three
different types of inclusion bodies and name a virus
responsible for each. 44. Viruses can affect protein synthesis, RNA
synthesis, and/or DNA synthesis. Give an example of a virus
for each class of effect, and state whether the affect is
stimulatory or inhibitory. 45. Name four mechanisms of viral modification.
Give an example for each. 46. Compare the significant properties of normal
cells and transformed cells. What are the differences
between benign and malignant tumors? 47. Compare the major characteristics between DNA
and RNA tumor viruses. Include mechanisms of
transformation. 48. Describe T antigens and their role in
transformation of cells. 49. Identify four major classes of oncogenes. Give
an example of each and its function. Describe the difference
between cellular and viral oncogenes, especially in terms of
function. 50. When a virus is newly discovered, how can it
be determined whether it is really a new virus or an old
virus newly emerging as a threat? 51. Your team of "disease detectives"
[epidemiologists] need to design a field survey to
track down the characteristics of what appears to be an
emerging virus. What factors are of most concern? How do you
acquire the information and collect the needed data? 52. What are the differences between horizontal
and vertical transmission? From the perspective of a virus,
compare the advantages and disadvantages between these two
general strategies. In your opinion, describe whether
horizontal or vertical transmission is easier to control.
Support your answer. 53. Which viruses are the best candidates for
elimination from the world via human intervention? Why? In
general terms, is it a good idea to eliminate specific
viruses from the world? Why [not]?
DNA are the brains of any company. (white collar
only need apply)
RNA can be the brains of some specialized small
firms. (therefore elevated to white collar)
RNA can act as part of the work force. (So not
only did they take over executive positions, they broke
into the workers' union as well!)
Updated 1/5/02 by thatcher@sonoma.edu