Material covered will be from 3/7 through 4/18, up
through DNA viruses. Steps to success: Study exercises and questions: 1. Outline the general transcription and
replication strategy for minus-strand RNA viruses. What is
the significant difference from the general strategy of
plus-strand RNA viruses? 2. Briefly describe the assembly of a
rhabdovirus. 3. Although most rhabdoviruses are transmitted by
arthropod vectors, one significant member of this group is
not. Name this virus and describe the mode of transmission,
and outline its pathogenesis. 4. How do paramyxoviruses differ from
orthomyxoviruses? 5. How is translation frequency controlled in
minus-strand RNA viruses, such as rhabdoviruses and
paramyxoviruses? What is the mechanism for this control? 6. What is the function of paramyxoviral fusion
protein? What is the probable role of this protein in the
course of an infection? 7. Name the proteins which form peplomers in
paramyxo- and orthomyxoviruses. What are their
functions? 8. Describe how new serotypes of influenza viruses
arise quickly, often causing severe epidemics. 9. Outline the strategy of orthomyxoviruses for
transcription and replication. 10. Many viruses produce defective interfering
(DI) particles. In most cases, the means of interference is
not understood. How do influenza virus DI particles
interfere? 11. Describe the course of a mumps infection,
beginning with first exposure. 12. What are the major differences of morbilli
measles (a.k.a. rubeola, a.k.a. red measles) and rubella
measles (a.k.a. German measles)? 13. Vaccines vary in the level of protection and
the duration of protection. Natural infections vary in these
aspects as well. What are the major reasons for such
variation? (Include input from the host as well as the
virus.) 14. How do filoviruses differ from rhabdoviruses?
In what ways are they similar? 15. What is the current understanding of why
filovirus isolates from Africa are extremely pathogenic in
humans, while isolates from the Philippines are not? 16. What is "ambisense polarity" and which viruses
studied have it? Outline the scheme for translation and
replication. 17. Arenaviruses appear to have granules when seen
in electronmicrographs. What are they and what function do
they have? 18. Nearly all enveloped viruses acquire the
envelope lipids from the host cell. Outline a general scheme
of the process. What cell structures serve as source
material? Give examples of viruses which use these specific
sources. 19. How are progeny virus released from the cell?
Give examples of viruses for the mechanisms described. 20. California encephalitis virus group are
endemic to specific regions in the U.S. Why is this so and
why are they so persistent? 21. Describe conservative and semi-conservative
mechanisms of mRNA production by dsRNA viruses, noting the
significant differences. Provide an example of a virus for
each of these strategies. 22. Briefly outline the structure of a reovirus
and its replication cycle. 23. Give an example of a reovirus. Briefly
describe the disease it causes. How can it be
controlled? 24. What makes phage f6
unique from other phage? 25. Reverse transcriptase. What is it? How does it
work? Which groups of viruses use it? How does it contribute
to pathogenesis? 26. What makes an oncovirus an oncovirus? 27. Give an example of an oncovirus. Name the
proteins coded for by your selected virus and state their
functions. 28. Long terminal repeats are far from being
decorative sequences, yet they do not code for any proteins.
What function do they serve? 29. What is "latency" and how is it
accomplished? 30. Describe a mechanism whereby an unique
oncogene of an oncovirus with strict host specificity for
sheep, for example, suddenly appears in a population of
cattle. 31. What are retroelements? Describe one and its
significance. 33. Describe the structure of HIV. Describe how it
infects CD4+ cells. How does it infect other cell types?
What characteristics contribute to HIV being commonly known
as a "slow virus"? 34. Compare and contrast Hepadnaviridae and
Retroviridae in terms of structure and reproductive
strategies. 35. Compare and contrast Hepatitis A and Hepatitis
B with regards to viruses involved, transmission, and
pathogenesis. 36. What groups of phage have ssDNA genomes?
Describe their similarities and differences. 37. You are spending the summer as an intern at
Genescan. You are to design a project involving the
sequencing of a gene coding for a small protein secreted by
certain cancer cells. The estimated weight of the protein is
between 2000-2500 daltons. What phage-bacteria system would
you choose to use to create a recombinant first? What are
the reasons for your choice? 38. If instead, you were asked to create a
recombinant containing the gene for immunoglobulin heavy
chain, weighing in at 50 Kd, what system would you consider?
Why? 39. Outline the replication strategy used by ssDNA
phage. 40. fX 174 makes more
proteins than it apparently has genomic information to code
for. How is this accomplished? 41. What is the genomic structure of parvoviruses?
How does it differ from microviruses? 42. Outline the infection cycle of parvoviruses,
based on the phases of infection. (And you thought you'd
never hear about phases again!) 43. What are the significant differences between
polyoma viruses and retroviruses? 44. Compare and contrast papilloma viruses and
polyoma viruses. Give an example of a disease caused by each
and describe the reasons for the difference in
pathogenesis. 45. How do polyoma viruses replicate? How do they
transcribe and translate for the viral proteins? 46. Describe the general strategy of early versus
late transcription. Include the differences of products
produced and the effects on the host cell. Give an example
of a virus group which has this strategy. 47. Adenoviruses may cause transformation of host
cells. What conditions exist if transformation occurs? What
is the primary difference between an infection which causes
transformation versus one which does not? 48. Describe the basic differences between alpha,
beta, and gamma herpes viruses. 49. Outline the basic structures of a herpes
virus. 50. What is latency in relation to herpes virus?
How is latency established? 51. Give an example of re-expression of herpes
after latency is established. Outline the pattern of
disease. What causes expression after a primary infection of
herpes has passed? 52. How do baculoviruses infect larvae? Outline
the key events from transmission to entry of the cell. 53. What makes Iridoviruses iridescent? 54. Discuss the advantages and disadvantages of
using baculoviruses for biowarfare against some insect
pests? Why would baculoviruses be of interest to the biotech
industry? 55. Outline the basic structures of a pox
virus. 56. Describe the differences of DNA structure
between adeno, herpes, and pox viruses. 57. What are "factories" in relation to pox
viruses? Where are they found, and what occurs in the
factories? 58. What is vaccinia and why is it of interest to
the biotech industry? 59. How and why was smallpox successfully
eliminated from the world population? Will this scenario be
often repeated with other viruses in the future? Why
(not)? 60. How was Jenner able to demonstrate that cowpox
was protective against smallpox? 61. What are the basic similarities of
baculoviruses and poxviruses? 62. Outline the mechanism utilized by lambda phage
to lysogenize into the host genome. 63. What is circular permutation? What viruses
display this characteristic? 64. Describe the infection cycle of T-even
phage. 65. What are the significant differences of
replication between lambda and T-even phage? 66. You have a plate of E. coli with cloudy
plaques of lambda phage and a plate of E. coli with clear
plaques of T-4 phage. Explain why the plaques appear
different.
Updated 1/5/02 by thatcher@sonoma.edu