Material covered will be through 3/5, up through
[+] strand ssRNA viruses. Steps to success: Study exercises and questions: 1. Describe how it was first demonstrated that
nucleic acids carried genetic information rather than
protein. 2. Define "life" and compare the definition with
the actions and capabilities of viruses. 3. Define virus. Give at least four key
characteristics. 4. What are phage? What beneficial function do you
think they serve? 5. Draw three models of viruses and label the
parts: 1) A naked icosahedral virus with 60 capsid proteins.
2) An enveloped helical virus with peplomers. 3) A
bacteriophage which is bisymmetrical. What is the basic
function for each of the labeled parts? 6. You're working with a new strain of rubella
virus and are trying to build up a stock. Describe a scheme
for purifying the virus from tissue culture. The goal is a
pure preparation of virus without host cell contaminants,
yet still capable of infection. 7. Describe three basic methodologies of electron
microscopy in relation to studying viruses. State the
advantages of each method. 8. You only have a light microscope. (You have
repeatedly requested time on the EM, but you were told "Get
in line." When you submitted a request for purchase of a
second departmental EM scope, everyone laughed.) How can you
identify infected cells in tissue sections using only a
light microscope? 9. Briefly describe two methods which can be used
to demonstrate the presence of a specific virus without
actually trying to visualize the virion themselves. 10. What is an ORF? Give two ways ORFs are
regulated. 11. What are replicative forms (RF) and
replicative intermediates (RI)? What is the significance of
finding primarily RI during RNA phage replication? 12. What is a point mutation? Describe three
possible outcomes of a point mutation. 13. Why is the effect of a single-base or two-base
insertion or deletion generally more severe than a
three-base insertion or deletion? 14. Give three examples of phenotypic mutations.
Describe for each how they can arise genotypically. 15. How can the evolution of a virus be tracked?
What type of information is needed? 16. Describe a reasonable theory of the origins of
DNA viruses. What evidence is there to support it? 17. Describe a reasonable theory of the origins of
RNA viruses. What evidence is there to support it? 18. Why are RNA viruses thought to be more
primitive than DNA viruses? 19. What are the five phases of an infection
cycle? What occurs during each phase? 20. In general terms, compare the different
mechanisms viruses use to attach to potential host cells;
ei. phage, plant viruses, animal viruses. 21. How is a protein coat assembled? Give an
example of a helical virus. Give an example of an isometric
virus. 22. Why is the replication strategy an important
part of the classification of a virus? What are the basic
types of strategies observed? 23. You want to invent a new virus. While you are
designing the basic genomic content, you need to consider
controlling the release of progeny. Which method of release
would you choose? What are the advantages over some of the
other methods? 24. What is the ICTV? Why is their work
important? 25. What are the significant criteria used to
identify a virus? Why is pathogenesis not an important
factor taxonomically? 26. Why are RNA phage of leviviridae normally only
infectious for male strains of E. coli? How can you make
them infectious for female strains? Can the progeny virus
infect more female E. coli? Why (not)? 27. What function do hairpin folds in RNA viral
genomes play in regulating translation? 28. The genome of MS2 phage is apparently too
short to code for polymerase, adsorption protein, coat
protein, and lysis protein. How does MS2 solve this
problem? 29. Qb uses a different
conservative mechanism. Which two products are produced and
how is this accomplished? 30. Give an outline of RNA phage replication. 31. Describe two important mechanisms of
regulation of translation in RNA phage. 32. What is polycistronic RNA? What problems arise
in translating such RNA and how are these problems
overcome? 33. What is a polyprotein? How does it become
functional mature protein? Give an example of a virus which
does this. 34. Which group of picornaviruses are resistant to
acid? What is responsible for acid stability of these
viruses? 35. The fact that the host cell metabolism goes
awry following viral infection is well known; however, in
most cases what occurs is not understood. In the case of
polio, host translation is greatly reduced, if not halted
entirely. How? 36. Briefly outline, from translation to assembly,
the making of a progeny polio virion. 37. Describe the pathogenic progression of a polio
infection. At what point do the classic symptoms of
respiratory and motor paralysis appear? 38. What makes foot-and-mouth disease so difficult
to control, other than using outright
quarantine-and-slaughter? 39. Not all RNA carries poly(A) at the 3' end.
Give two examples of other 3' end sequences and which
viruses have them. What is their function? 40. In what ways are Caliciviridae different from
Picornaviridae? 41. What are dipartite and tripartite viruses?
Compare them to viruses with segmented genomes. What is
needed for infection? Name two possible advantages for di-
and tripartite viruses in plants. 42. Nodamura virus infects mosquitoes. It can also
infect mice and pigs. Although similar to picornaviruses in
several respects, it is bipartite. Give a hypothesis as to
why this virus is bipartite. How would you approach proving
your hypothesis? 43. Why are satellite viruses "parasites of
parasites"? 44. Tobacco mosaic virus(TMV) was pivotal in
proving that RNA could be genomic nucleic acids. Briefly
describe how this was proven. 45. Describe TMV's assembly mechanism, which is a
fine example of elegant efficiency. Does this assembly
require host energy? (Ignore replication step immediately
preceding assembly.) 46. Describe briefly how "copy choice" can account
for plant virus recombinants. 47. What is "host specificity"? What factors of
the host and what factors of the virus contribute to this
specificity? 48. Although plant viruses do not have host
specificity in terms of initiation of infection, there are
often considerable differences in pathogenicity depending on
the host infected. Briefly describe some possible reasons
for these differences. 49. Compare and contrast togaviruses with
coronaviruses, listing the major similarities and the major
differences. 50. What are "amphipathic" proteins? Where are
they found in a virion and what function(s) do they
serve? 51. Give an example of a virus which uses insects
as a vector and describe a complete "life cycle" (using
"life cycle" loosely, of course). 52. Why is rubella so devastating to fetuses, but
not to children or adults? Briefly outline what occurs. 53. Describe the structural features of
Coronaviridae. How can they be both spherical and
helical? 54. Compare and contrast Hepatitis A, Hepatitis C,
and Hepatitis E. Include family designation, structure, mode
of transmission, and pathogenicity.
Updated 1/5/02 by thatcher@sonoma.edu