Ori Disclaimer The information represents my understanding only so errors and omissions are probably rampant It has not been vetted or reviewed by faculty The source is our class notes The document can mostly be used forward and backward I tried to mark questionable stuff with ID: 1006578
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1. Basic VirologySlackers Facts by Mike Ori
2. DisclaimerThe information represents my understanding only so errors and omissions are probably rampant. It has not been vetted or reviewed by faculty. The source is our class notes.The document can mostly be used forward and backward. I tried to mark questionable stuff with (?). If you want it to look pretty, steal some crayons and go to town. Finally…If you’re a gunner, buck up and do your own work.
3. Are viruses alive
4. It depends an who you ask. Dr. A says yes. They are obligate intracellular parasites that carry enough genes to reproduce themselves within the defined environment of their host.
5. How is genetic information encoded in viruses
6. Genetic information is encoded in either RNA or DNA depending on the virus. It is important to note that viruses do not contain both RNA and DNA.
7. What is a virion
8. A functioning virus particle. Distinguished from an defective particle.
9. Describe the range of size and complexity in the viraverse (viral-universe - a shiny new word)
10. Viruses range from the edge of detection with EM to about one-quarter the size of an E. coli.A,B,C,D Collie omitted for clarity E. CollieChickenpox virusPine cona virus
11. List the patterns of viral growth.
12. AcuteLatentChronicSlow chronicSet point escape
13. What is the expected growth pattern for an acute virus.
14. Initial rise and fall of viremia without resurgence. Done in one.
15. Describe the expected viremia pattern for a latent virus
16. Initial acute rise followed by virus free periods punctuated by less intense periods of viremia.
17. Describe the expected viremia pattern for chronic infection
18. Initial acute rise in viremia with a fall that does not reach zero. Viremia is detectable in blood or tissues
19. Describe the expected viremia pattern with slow chronic infection.
20. Viremia increases slowly over time.
21. Describe the viremia associated with set point escape
22. Really a combination of chronic viremia and rapidly rising slow chronic response. Initial acute infection followed by a drop in viremia that does not return to zero (aka set point). Eventually, the virus escapes the immune system in a chronic escalation. Set point (chronic)Slow chronic-like escape
23. List the prototypical virus for each pattern
24. Acute – influenzaLatent – HSV-1Chronic – Hep BSlow chronic - ??Set point escape - HIV
25. What is a viral envelope?
26. A lipid bilayer derived from host membranes. Most often the source is the plasma membrane but it may also be the ER/golgi or the nuclear membrane (herpes)
27. What is the a capsid?
28. A capsid is a protein structure that surrounds and protects the viral genome. The capsid organizes and provides shape to the virus.
29. What is nucleocapsid
30. Nucleocapsid proteins are proteins that organize the genome in enveloped viruses that do not have an icosohedral core.
31. What are viral spikes
32. Proteins that extend from the virus that allow it to interact with its environment.
33. What are matrix proteins
34. In enveloped viruses, matrix proteins link the nucleocapsid to the spikes and membrane
35. Will you take the blue or the red pill coppertop?
36.
37. What is a capsomere
38. A capsomere is an aggregation of proteins that forms a modular building component of naked capsid virus (cubic, icosahedral) and that of enveloped icosahedral virus..
39. Describe the structure of naked capsid virus.
40. A naked capsid virus consists of a genome packaged by core proteins surmounted repeating capsomeres organized into an icosahedral shell from which protein spike protrude.
41. What is the relative antigenicity of viral structural proteins?
42. Spikes are more apt to be exposed to the immune system and hence are more likely to be antigenic. Antibodies directed against spikes should be more efficacious.
43. What are the functions of spikes
44. Enzymatic (influenza neuroaminidase)Fusion with host cellsEliciting immune response
45. What is tropism
46. The propensity of a virus to infect specific tissues.
47. What is the basis for tropism
48. Access to the tissue and receptors on the tissue
49. If you were working in a bioweapons lab, what part of the virus would you change to alter its tropism
50. The spikes.
51. What is troopism
52. An actor’s propensity to form travelling groups.
53. What is the basis for virus classification. Consider old and new.
54. Old school: phenotypic and disease characteristics of the virus.New school: Genetic analysis
55. Is herpesviridae a fmily, genus, or species designation
56. A family.XXXviridae
57. Is simplexvirus a family, genus, or species
58. GenusXXXvirusGenius
59. Is herpes simplex 2 virus a family, genus, or species
60. A speciesXXX virus
61. What steps are required for viral infection
62. 1. Attachment2. Penetration3. Uncoating4. Replication5. Assembly6. Release
63. What are viral penetration mechanisms
64. Membrane fusion – only in enveloped virusesReceptor mediated endocytosis – naked capsid virus
65. Distringuish early and late replication
66. Classically early replication involves creation of regulatory elements while late replication involves creation of structural elements and duplication of the genome.
67. Where do RNA and DNA virus replicate as general rules.
68. RNA virus replicates in the cytoplasm except orthomyxovirusDNA replicates in nucleus except for poxvirusRetro viruses replicate in the nucleus.
69. What is the difference between sense (+) and antisense (-) genetic material
70. Antisense (-) strands are those whose 5’-3’ is opposite to the mRNA. Sense strands (+) are oriented in the same direction.
71. What sense are RNA viruses
72. RNA viruses can be either + or – depending on the species.
73. What is the advantage to + stranded RNA
74. The viral genome is expressed directly by cellular components on entry into the cell with minimal reliance on viral factors. In concept, + sense can be packed into a smaller suitcase.
75. What protein do all RNA viruses require for replication
76. RNA dependent RNA polymerase
77. Describe when + and – RNA will be present
78. Both + and – sense RNA is present during genome replication.
79. Why does pox virus bring an RNA polymerase
80. Even though pox is a DNA virus, it replicates in the cytoplasm and so has no access to cellular RNA trascription machinery.
81. Why would a DNA virus bring a DNA polymerase
82. To control replication without reliance on host replication machineryBecause it replicates in the cytoplasm (pox) where host machinery is unavailable
83. If DNA is normally double stranded, why doesn’t a ssDNA virus fail
84. Host repair machinery “fixes” the single strand
85. Describe how RNA viruses circumvent monocystronicity
86. SegmentationViral RNA polymerase stuttering (term?)Proteolysis
87. How do DNA viruses overcome monocistronicity
88. Alternative splicing
89. How are viruses released from the host cell
90. BuddingLysis – kill the cellCytocidal – wait for cell to die
91. Define productive cycle
92. Refers to the period of active virus replication
93. Define non-productive
94. A cell in which is infected based on the presence of viral genetic material but which produces no virus
95. Define temperate
96. A virus capable of entering a productive phase after a non-productive phase.
97. Define permissive
98. A cell that permits production of viral progeny or viral transformation
99. Define non-permissive
100. A cell that does not support replication but that may or may not support transformation
101. When a virus kills the cell before replication can occur, this is known as what?
102. Abortive replication
103. Define burst size
104. Define eclipse phase
105. The period in which virus particles are not present within cells in an infected cell culture
106. Define latent phase
107. The period in which virus particles are not present outside of cells in an infected cell culture.The phases are confluent at the beginning but latent phase is longer than eclipse and hence diverge
108. The number of virions produces per infected cells.
109. What is the role of interferon alpha and beta
110. Help to limit virus production by altering RNA persistence and translation.Acts to induce CTL and NK cell activity and proliferation(?)
111. Describe IFN action on RNA synthesis
112. The presence of dsRNA initiates interferon production. IFN induces the production of a protein kinase and an oligosynthetase which become active in the presence of dsRNA.The kinase inactivates ribosomes while the oligosynthetase actives production of an RNase. Thus IFN is a messenger that primes neighboring cells to halt RNA production should they become infected.
113. Human polymerases tend to be more tightly controlled than viral polymerases. Why?
114. Essentially each polymerase have different quality measures. Human polymerases foster genomic stability and slow mutation rates that prevent cellular derangement. Viral polymerases foster antigenic shift that allows viruses to keep ahead of the immune system at the expense of increased defective particles.
115. Describe recombination
116. When two similar viruses infect the same cell homologous recombination may occasionally occur that results in the transfer of genetic material between strains..
117. Describe reassortment
118. When two strains of a segmented virus infect the same cell, the resulting virus particles randomly incorporate segments from either virus.
119. Define antigenic drift
120. Point mutation in viral genomes that alters viral antigens as a result of point mutations made by viral polymerase.
121. Define antigenic shift
122. Large scale changes made to viral genomes as a result of recombination or reassortment.
123. Define virulence
124. The capacity of a virus to produce disease. Note this is dependent on both host and viral factors.
125. Which type of viruses are capable of causing transformation
126. DNA viruses and retroviruses
127. Define transformation
128. The conversion of a normal cell into a tumor cell as a result of virus activity.
129. Define vertical transmission
130. The spread of disease from mother to child in utero, during parturition, or by lactation