Immunology 200 Midterm 2

  1. What is the average size of viruses
  2. Are viruses living? Why?
    • Viruses lack the essentials of life
    • -They do not have the ability to take up energy and make use of it
    • -They do not transport molecules out of cell or into cell
    • -They do not reproduce themselves

    -However viruses can evolve by natural selection and have protecting contents from external environment
  3. What is the relationship of a virus with the host?
    Viruses are obligate parasites and they must have a host cell in order to reproduce
  4. What do viruses need to reproduce
    • -They need to be able to enter a host cell
    • -They have the host cell replicate the viral genetic material
    • -Have the host cell transcribe and translate the viral genese
  5. What is a virion
    A Virion is an infectious viral particle
  6. When was the first human virus identified and what is it called
    Yellow fever was identified in 1901
  7. What are River's postulates and what are they modified from
    • They are modified from Koch's postulates and they include:
    • -Isolation of virus from diseased hosts
    • -Cultivation of virus in host cell
    • -Proof of filterability
    • -Production of a comparable disease when used to infect experimental animals
    • -Re-isolation of the same virus from the infected host
    • -Detection of a specific immune response to the virus
  8. What is the general strategy all viruses follow
    -They package their genomes into a particle that mediates transmission from host to host

    -A virus genome contains the information for an infectious cycle within a susceptible permissive cell

    -All viruses are able to establish themselves in a host population so their survival is ensured
  9. Who proved that DNA is the genetic material
    Hershey and Chase
  10. How do viruses protect their genetic material
    -Genetic material is protected by the capsid  which makes them resistant to proteases, heat or temperature extremes

    -They use as few proteins as possible
  11. Describe the arrangement of nucleic acid and protein coat in tobacco mosaic virus
    -The RNA assumes a helical configuration surrounded by protein capsid

    -The information for assembly is contained within the protein structure itself (Self-assembly)
  12. Describe self-assembly or viruses coat
    Information for assembly of coat is contained within the protein structure itself forming the capsid
  13. What is a result of using as few proteins as possible in capsid synthesis
    • -Easier synthesis
    • -Repeating structure
  14. What are the five phases of the simplified viral life cycle
    • -Attachment using a variety of receptors
    • -Penetration of the membrane
    • -Utilization of host cell proteins/enzymes needed for replication, transcription and translation
    • -Biosynthesis of proteins
    • -Assembly of progeny particles
  15. What type of virus is measles
    An enveloped RNA virus
  16. What is the life cycle of an enveloped RNA virus, and what is an example of one such virus
    • Measles is an example of an enveloped RNA virus
    • -The viral envelope membrane fuses with the host cell membrane to allow entry
    • -RNA is transcribed and replicated using viral enzymes
    • -Virus can leave cell by budding off with host membrane
  17. What is the source of the envelope for enveloped viruses
    The host cell that is taken with virus budding
  18. How does the membrane help the virus hide from our immune system
    -The envelope, which is host membrane, is of host origin

    -It contains host proteins
  19. Why does exponential growth occur in viruses
    Viruses synthesize a large number of new progeny and release the progeny at once
  20. How is viral titre determined
    • -A dilution is mixed with bacteria and melted agar
    • -Agar is poured onto a plate and phage plaques make holes
    • -concentration is measured as plaque forming units
  21. What is the measurement of viral titre
    Plaque forming units per mL
  22. How are viruses classified
    • -The nature of the genetic material
    • -Symmetry of the capsid
    • -Presence of an envelope and the dimensions
  23. What is the genetic material of viruses
    Viruses can contain DNA or RNA, single or double stranded
  24. What are the three RNA viruses that will be focused on during the class
    • Polio
    • HIV
    • Influenza
  25. What are two DNA viruses that will focused on during the class
    • Herpes
    • Pox
  26. How are viral infections initiated
    • -Sufficient virus at site of entry
    • -Susceptible host cells that have
    • a.)receptors required for viral entry and
    • b.)they are permissive, containing factors needed for replication and dissemination
    • -Local antiviral defense must be breached
  27. What are some sites of viral entry into the host
    • Conjunctive
    • Respiratory tract
    • Elementary tract
    • Urogenital tract
    • Anus
    • Skin
    • Capillary
  28. What is an acute, rapidly spreading infection spread by aerosolized droplets?
  29. How is influenza commonly transmitted
    Through the air via aerosolized droplets
  30. What are the symptoms and subsequent consequences of Hepatitis B and how is it transmitted
    Fever, Loss of appetite, nausea, vomiting, abdominal pain, yellow colouring of eyes, dark urine

    It is transmitted in infected blood
  31. Why are some individuals chronic carriers
    They are unable to clear the virus
  32. Why is it an advantage for a virus to have a persistent lifestyle
    The virus can persist and overwhelm the immune system at a later date in time
  33. Name a virus that hides in the trigeminal ganglia and is reactivated with stress
    Herpes simplex 1
  34. Name an example of a persistent infection
    Hepatitis B
  35. Name an example of a latent, reactivating infection
    Herpes simplex I
  36. What are some symptoms of Measles
    Rash, Hypersensitivity reaction, fever, cough, conjunctivitis
  37. What is an example of an acute infection that may cause a rare latent disease.
    Measles can develop into SSPE: Measles subacute scelrosing panencephalitis
  38. How can viruses cause injury
    • -Cytopathic effects on cells directly
    •  o Cells may be lysed

    -Viruses can be oncogenic

    • -Immumopathology
    •  o Damage as a result of local inflammation
  39. Define oncogenic
    - Cells lose contact inhibition and their normal interactions (Anchorage - independence) become immortal

    - Can be transformed by virally encoded oncoproteins

    -Viral disruption of host genes
  40. Name a virus that can cause paralysis
    Poliomyelitis caused by poliovirus
  41. What is the cytopathic effect and what is a virus that causes this
    Cell rounding and lysis by a virus

    Poliovirus infections may cause this
  42. What is the significance of anchorage independence in viruses
    Cancer cells may lose their attachments and become mobile within the host
  43. What are the effects of Rous Sarcoma Virus on avian cells
    • Fusiform morphology
    • Anchorage independence
  44. What are oncogenes
    Genes that regulate cell cycle, replication or activation of cellular process

    Technically called proto-oncogenes until cancer is caused
  45. What is an SRC gene
    A signalling molecule that phosphorylates proteins involved in signal transduction
  46. when is cellular src tyrosine kinase usually activated
    When it binds to other proteins in the cell, causing conformational changes in the protein opening up the active site which becomes phosphorylated
  47. What does the entry process of viruses facilitate
  48. What act as many of the virus receptors on host cells
    Proteins, often glycoproteins
  49. What are the mechanisms for uptake of macromolecules from extracellular fluid
    • Phagocytosis
    • Endocytosis
    • -Pinocytosis
    • -Receptor mediated endocytosis
  50. Describe phagocyosis
    The particle is surrounded by plasma membrane by phagocytic cells.
  51. How molecules within phagosomes destroyed
    They fuse with lysosomes and the particles are destroyed
  52. What is pinocytosis
    • It is a type of endocytosis
    • molecules enter directly into the cell
  53. What is Receptor Mediated Endocytosis
    It is a type of endocytosis

    A ligand of molecule binds to the receptor of the host cell and is internalized.

    The most important mechanism of entry for viruses
  54. What is the most important mechanism of entry into host cells for viruses
    Receptor-mediated endocytosis
  55. What are the five steps of Receptor mediated endocytosis
    • -Ligand binds a cell surface receptor and diffuses into clathrin pit
    • -Clathrin pit pinches off forming a coated vesicle
    • -Clathrin uncoats the vesicle
    • -the vesicle fuses with the early endosome
    • -acidic environment of endosome releases ligand from receptor, and the receptor is returned to cell surface
  56. What is Clathrin
    Clathrin is a protein that plays a major role in the formation of coated vesicles
  57. How have viruses evolved
    Viruses have evolved to use proteins on the host cell as receptors
  58. Name two related picornaviruses
    Rhinovirus and poliovirus
  59. What is the poliovirus receptor
    PVR, or poliovirus receptor
  60. What is PVR
    PVR is the poliovirus receptor.

    It is involved in dendritic cell and Nkappa interactions in normal host interactions
  61. What is the receptor to rhinovirus
  62. What type of virus causes the common cold
  63. What is Icam-1
    Intercellular adhesion molecule-1 is the receptor for Rhinovirus

    It is involved in macrophage T-cell interactions in normal host interactions.
  64. What determines the specificity of the virus host range
    The presence of the receptor of which the ligand binds to
  65. What is the interaction between Icam-1 and the ligand of rhinovirus
    A direct interaction between the receptor and capsid
  66. Why do we not mutate our Icam-1 binding sites
    Because Icam-1 plays an essential role in macrophage t-cell interactions
  67. What are the phases of rhinovirus entry into host
    • -Virus attaches to Icam-1 and enters by endocytosis.
    • -Acidic environment of endosome causes uncoating
    • -RNA is released into the cytoplasm
  68. What does the Icam-1 facilitate when it interacts deep in the canyon of rhinovirus
    It facilitates destabilization of capsid
  69. Which picornavirus is more resistant to acid
    • Poliovirus is resistant to acid
    • Rhinovirus is not
  70. How do neutralizing antibodies effect rhinovirus
    They block the binding of the receptor to the canyon
  71. What causes major structural changes of poliovirus
    The interaction with PVR which causes the uncoating
  72. What is a difference in the uncoating between rhinovirus and poliovirus
    The acidic environment inside the endosome causes uncoating in rhinovirus

    In poliovirus, the interaction with PVR causes structural changes and release of RNA
  73. Describe the formation of the pore in the membrane by poliovirus
    Interaction with PVR causes structural change

    • N termini of VP1 protein extends into
    • membrane

    May form a pore in which RNA can enter
  74. How does RNA of poliovirus make its way across the membrane
    Structural changes allow for a pore to form and RNA to cross membrane.
  75. What are fusogens
    fusogen any agent, or set of conditions, that gives rise to fusion of membranes, including cell membranes
  76. What is the significance of fusogens with viruses
    enveloped viruses encode their own fusogens and allow the fusion of the two cell membranes to escape
  77. What is the cellular receptor for influenza
    Sialic acid
  78. What binds to terminal sialic acid
    Influenza virus hemagglutinin (HA)
  79. What does Influenza virus hemagglutinin bind to
    Terminal sialic acid
  80. What type of linkage exists between HA and sialic acid
    In birds, alpha (2,3)

    In human, alpha (2,6)
  81. How does influenza virus lyse cells
    Fusogenic peptide is exposed by an acid catalyzed structural change

    Virus acid is inside two membranes

    uses fusogen to escape
  82. What causes conformational changes in Hemaggluitin of influenza virus
    Acidic environment of endosome
  83. What is the adult prevalence of HIV
  84. What are the four phases of HIV
    Preliminary infection sometimes causing flu-like symptoms

    Asymptomatic phase around 10 years

    Symptomatic phase

  85. What causes AIDS
    The depletion of CD4 T cells
  86. Describe the surface of HIV
    • Carries envelope glycoproteins
    • Each capsid carries two RNAs and reverse transcriptase
  87. What is reverse transcriptase
    An enzyme that copies RNA into DNA
  88. What does HIV bind to
    CD4 and coreceptor on T cell
  89. Where does HIV undergo fusion
    At the cell membrane of the T cell
  90. How does HIV insert viral genome into host cell, which cell?
    • HIV particles bind to CD4 and coreceptor on T cell
    • Viral envelope fuses with cell membrane allowing viral genome to enter the cell
  91. What type of cells are infected by HIV
    HIV infect cells that have CD4 and Chemokine receptors
  92. What is the coreceptor for HIV entry

  93. What mutation aids in resistance to HIV infection
    A mutation in CCR5, a chemokine receptor.
  94. What is the HIV ligand
  95. What is the ligand of HIV and what does it bind to.  Describe the conformational changes
    HIV gp120 binds to CD4 and cause conformational changes that expose CCR5 receptor binding site.

    Binding to co-receptor induce second conformational changes exposing the fusion peptide
  96. What is the function of Reverse transcriptase in HIV
    It copies the ssRNA into double stranded cDNA
  97. What is the function of integrase of HIV
    • It inserts DNA into the genome
    • -Viral cDNA enters nucleus and is integrated into host DNA
  98. Describe the steps used to transfer Viral DNA into DNA
    • Reverse transcriptase
    • -tRNA serves as primer for first strand

    RNase H cleaves

    • DNA polymerase
    • -Polypurin tracts (PPTs) serve as primer for second strand
  99. What are the different types of errors with reverse transcriptase
    • Base substitutions
    • -Misincorporation mediated
    • -Dislocation mediated

    • Frameshifts
    • -Misincorporation initiated
    • -Slippage initiated
  100. What is required of infected cells with HIV for virus replication
    Infected cells must be activated
  101. Why must cells infected with HIV be activated for viral replication
    Transcription factor NFkB is turned on by activation of infected T cells or macrophages
  102. Describe the viral replication of HIV in an activated host cell
    • -T-cell activation induces low level transcription of provirus
    • -RNA transcripts are spliced allowing translation of early genes tat and rev
    • -tat amplifies transcription of viral RNA, Rev increases transport of singly or unsplised viral RNA to cytoplasm
    • -Proteins Gag, Pol and Env are translated and assembled into virus particles which bud from the cell
  103. What are the late proteins which are translated in HIV viral replication
    • Gag:group specific antigen
    • Pol: polymerase
    • Env: envelope
  104. How many HIV virons are produced a day and many infectious cycles occur per year
    • 1x10^10
    • Around 240 infectious cycles
  105. What is Baltimore classification of virus
    Based on how many steps to create mRNA
  106. Why don't + strand viruses not to package polymerases in their own RNA
    They can synthesize their own polymerases
  107. What is a + strand RNA
    5 prime to 3 prime
  108. Why does a positive strand virus make negative strands
    Because it replicates negative strand viruses
  109. What type of RNA is poliovirus
    Poliovirus is a +strand RNA virus
  110. How many proteins are within the capsid of poliovirus
    The capsid is made up of around 60 copies of four proteins
  111. What are the 13 steps in the reproductive life cycle of poliovirus
    • 1.Binding of virus to receptor and endocytosis
    • 2.RNA associate with ribosomes
    • 3.Translation
    • 4.Polyprotein is made
    • 5.Polyprotein cleavage
    • 6.RNA synthesis occurs on vessicle membranes
    • 7.+strand moves to vesicle
    • 8.-strand copies are made
    • 9.+strand copies are made
    • 10.+strands move to vesice
    • 11.Cleavage of the capsid precursors
    • 12.Assembly into new capsid
    • 13.Exit by lysis
  112. What can be seen on cells infected with poliovirus with ultrasound
    Vacuoles or vesicles
  113. What does the poliovirus +strand RNA encode
    • A polyprotein precursor
    • RNA is translated into a single polypeptide
    • -it is cleaved by two virally encoded proteases
    • o 2Apro and 3Cpro
  114. What are the proteases that cleaves single polypeptides translated from + strand RNA
    2Apro and 3Cpro
  115. What is the structure and significance of 3Dpol polymerase
    • RNA dependant RNA polymerase
    • unique to virus
    • specific for RNA template
    • copies viral RNA not host RNA
    • no proofreading activity so errors
    • error rate limits size of virus
  116. What is a poliovirus RNA dependent RNA polymerase
  117. What determines the secondary RNA structure
    The sequence of the base pair
  118. What does poliovirus use as a primer for replication
    RNA strand links to 3AB via a tyrosine

    -a protein
  119. Describe the polioviral replication using protein as a primer
    3AB takes RNA to membrane

    RNA strand links to 3AB via a tyrosine

    Primer starts synthesis on the tyrosine of 3AB


    Cleavage of VPg off 3AB
  120. Describe how genomic RNAs can server as mRNAs for the synthesis of new proteins
    • First step of translation is removal of VPg protein
    • When capsid proteins are abundant, RNA genomes are packaged
    • RNA recombination involves RNA polymerase template exchange
  121. What estimated percent of viral templates recombine
  122. How are attenuated viruses made
    Virus for humans may be attenuated by passage in non-human cell lines e.g. monkey
  123. What is the significance of virus reversion in vaccines
    If a reversion mutant occurs, the virus given in the vaccine may again become infectious to the human
  124. Name four DNA viruses
    • Parvo
    • Papova
    • Herpes
    • Pox
  125. What virus is required in DNA viruses to create mRNA
    • DNA dependent DNA polymerase (parvovirus)
    • DNA dependent RNA polymerase in all DNA viruses
  126. Where do large DNA viruses get required enzymes from
    They encode their own
  127. What are common mechanisms in exponential viral DNA replication
    • 1. Template directed
    • 2. Each strand is copied beginning at the origins
    • 3. Uses a DNA dependent DNA polymerase
  128. What are properties of replications in mammalian and viral DNA
    Bidirectional replication from an origin.
  129. What is the most common replication pattern of DNA of hosts and viral genomes
    Bidirectional replication from an orgin
  130. Which enzyme initiates RNA synthesis
  131. Describe how leading and lagging strands of RNA during DNA replication form okazaki fragments
    Synthesis of leading strand starts from replication origin on RNA primer

    Lagging strand proceeds in short pieces as template becomes open
  132. What are Okazaki fragments
    Open templates of RNA caused by the lagging strand of replication

    Removal of the primer from the 5 prime end creates a gap that cannot be filled
  133. Describe the rolling circle mechanism of DNA replication
    • 1. Nick one strand
    • 2. Replicate by continuous copying
    • 3.Displace a strand
    • 4. Complete the lagging strand
    • 5. Double strand DNA templates result
    • 7. Keep making more copies by continuing around again
  134. What do direct repeats do in DNA
    They help package one genome
  135. How do direct repeats at the ends of strands help package one genome
    • Proteins bind to specific sequences at ends of strands
    • Empty capsid binds to these proteins
    • DNA is stuffed in
    • A headful of DNA is stuffed in until proteins on other end are reaches
    • Cleavage of DNA
  136. What do the products of one replication cycle become
    Templates for the next replication cycle
  137. What is the difference between host DNA and viral DNA in regards to proof reading
    Viral DNA polymerases may not be proofread
  138. Describe the synthesis of proteins in the reproductive cycle of herpes simplex type 1
    First proteins synthesized are transcriptional activators of genes

    These transcripts make proteins needed later in synthesis

    Late proteins are required for Capsid assembly and membrane proteins
  139. Describe the assembly of a poliovirus
    • Virus attaches to PVR
    • Uncoating at cell membrane
    • Proteins are made as polyproteins
    • Initial cleavage is autocatalyzed bu then proteases are released
    • Capsid proteins autoassemble in a concerted assembly with RNA
  140. How is poliovirus transmitted
    fecal-oral transmission
  141. What type of virus is Westnile
    a flavi virus
  142. How does the 3Dpol polymerase tell which is viral and host DNA
    It can tell based on structural differences
  143. What is VPg
    It is the protein cap used for RNA stabilization
  144. What is the primer in rolling circle mechanisms of DNA replication
    OH 3`
  145. How does poliovirus assure that an RNA genome gets in every virion
    By making a capsid, the stabilization due to full capsid
  146. Do intramolecular interactions favour polyprotein precursors, polyproteins, or cleaved polyproteins
    Polyproteins are favoured
  147. What is another name for a complex retrovirus
  148. Where are integrase and reverse transcriptase packed in HIV-1
    In the virion
  149. Why are integrase and reverse transcriptase packed into the virion of HIV
    HIV integrates into the genome and then uses host transcription machinery to make more copies and therefore can allow alternate splicing of transcripts.
  150. How are viral proteins localized to the cellular membrane
    • -Rough ER buds off into Golgi, Golgi buds off into rough vesicles that fuse with the cell membrane
    • -Assembly of enveloped viruses frequently takes place at plasma membrane
    • -Secreted or TM proteins are made on the Rought ER and secreted into ER lumen or left in ER membrane
  151. What is the difference in NK cell mediated killing of infected cells and T cell mediated killing of infected cells
    T cell mediated killing of cells take effect later on in the infection and last longer
  152. Name three acute infections
    • Rhinovirus
    • Rotavirus
    • Influenza virus
  153. Describe pattern recognition
    • Antigens are recognized by innate immune system
    • TLRs recognize viral capsids, viral RNA or DNA
  154. What is the cytopathic effect of cell pathology
    Viruses that lyse the cell, or cause major disruptions to the morphology of the cell cause damage by direct cytopathic effect
  155. Name how viruses can cause tissue damage
    • Cytopathic effects
    • Inducing cell mediated immunity
    • inflammation
  156. What cells belonging to the innate immune cell respond to infection and what do they do
    • Neutrophils are the first to arrive at sites of infection
    • They are phagocytic
    • They are granules that contain antimicrobial peptides including defensins
  157. What anti viral effectors are made by neutrophils and how do they work
    Alpha defensins are potent antivirals

    • Some are directly lytic to virus infected cells
    • others bind to viral capsid and inhibit assembly
  158. What is the role of macrophages in viral defense
    • Receptors on macrophages recognize patterns on viral antigens
    • resident antigen presenting cells recognize the pathogen
  159. How are viruses recognized by macrophages
    Viruses are recognized by the presence of sugars on glycoproteins and surface TLR receptors recognize viral capsid or membrane proteins
  160. Describe the binding process of macrophages to antigens
    • Internalization of antigens
    • Detection by endosomal TLR receptors
    • Deliver signals into the cell to activate macrophages
    • Tells the macrophage what type of response to make
  161. How to macrophages initiate immune responses
    • They release cytokines to initiate immune respons
    • -TNF-alpha, interleukin-1, IL-6 and interferon
  162. What is interferon
    • Interferon is an effector made by cells
    • It is a warning protein made by leukocytes (especially dendritic cells) if they detect virus
    • It bind to receptors on other cells and turns on antiviral program
  163. What is the significance of type 1 interferons
    They have local effects on other immune cells

    -antiviral state is induced in neighboring cells
  164. What are three types of type one interferons
    • 2`-5` oligoadenylate synthetase
    • RNase L
    • dsRNA activated protein kinase (Pkr)
  165. What is 2`-5` oligoadenylate synthetase
    It is a type 1 interferon and is activated to make aoligoadenylate which in turn activates RNase L
  166. what is RNaseL
    It is a type of type 1 interferon and degrades cellular and viral mRNA
  167. What is dsRNA activated protein kinase (Pkr)
    It is a type of type 1 interferon and stops new protein synthesis in infected cells
  168. What do macrophages and natural killer cells each produce to amplify the cooperation of the immune system
    Macrophages produce TNF-alpha to activated natural killer cells which produce interferon gamma
  169. Describe how proinflammatory cells have systemic effects
    Proinflammatory cytokines act on hypothalamus

    Most viruses cause fever or increased body temperature
  170. How to proinflammatory cytokines affect virus
    They induce the liver to produce acute phase reactants which are effector proteins made in response to infection.  They bind directly to virus
  171. What are acute phase reactants
    They are effector proteins made from the liver in response to proinflammatory cytokines. They bind directly to virus particles in the host.
  172. What is mannan-binding lectin and what is its function
    It is an acute phase reactant.

    It binds to mannose of viral glycoproteins and acts as an opsonin.
  173. What is the significance of terminal galactose in viruses
    • It is on many viruses that are made in animal hosts
    • Primates to have this enzyme
    • The sugar is on many bacteria so we make antibodies to it
  174. What sugar is on many viruses that made in animal hosts but not on primates.
    Terminal galactose is found in viruses and we create antibodies to it.
  175. Why was the 1918 influenza so lethal
    It caused too much inflammation which caused pathology
  176. How long does cytotoxic T lymphocyte killing of cells take in the adaptive immune response
    Around one week
  177. How do cytotoxic T cells kill intracellular pathogens
    They kill the infected cell by the delivery of a signal inducing death or apoptosis
  178. How do CTLs recognize infected cells
    They recognize viral peptides presented on MHC class 1
  179. Where are peptides presented on MHC class 1 from derived from
    Newly synthesized proteins
  180. How does allelic variation of MHC class 1 impact individual viral immunity
    Resistance to a particular virus depends on the MHC of the individual
  181. What is the most important genetic variation that determines individual ability to fight a pathogen
    The allelic composition of MHC
  182. What are three steps required for cytotoxic T cell activation
    • Antigen presentation and costimulation
    • IL2
  183. How are helper T cells activated
    Antigen is internalized and presented on MHC class 2 of antigen presenting cell. Costimulation is also required
  184. How do helper T cells activate Cytotoxic T cells
    Helper T cells proliferate and produce IL-2 which activates Cytotoxic T cells.

    Activation of Naive CTL requires costimulation by APC
  185. How do dendritic cells activate CTL
    Infected dendritic cells can present the naive T cell costimulation to generate CTL effector cells
  186. What type of viruses can infect Dendritic cells
    Influenza, measles and HIV
  187. What is required for a CTL to become a memory cell
    Memory cells are made only if CTL is primed by IL-2 from a helper T cell
  188. How many times can CTL kill infected cells
    They are series killers

    They are not damaged in the killing process
  189. How do normal cells inhibit killing by natural killer cells
    The engagement of MHC class 1 by natural killer inhibitory receptor inhibits killing
  190. How do infected cells differ from normal cells? How does this cause for natural killer cells to kill
    Nk cell inhibitory receptor binds with MHC 1 on normal cell to prevent killing

    VIruses often down-regulate surface expression of MHC which makes them a target of NK cells
  191. What is the difference between monoclonal and polyclonal
    • Monoclonal antibodies recognize 1 epitope
    • Polyclonal antisera has many specificities
  192. What type of antibody recognized 1 epitope
    Monocolonal antibody
  193. What type of antibody recognizes many epitopes
    Polyclonal antisera
  194. Describe the specificity of antibodies in humans
    • Polyclonal antisera
    • they have many antibody specificity
  195. What is a neutralization assay
    An in vitro test in which antibodies bind to virus and prevent the infectious cycle
  196. Define virus neutralization
    Free virus particles are susceptible to neutralizing antibodes
  197. What are neutralizing antibodies and what are possible mechanisms for neutralization
    Neutralizing antibodies neutralize viruses

    • Possible mechanisms:
    • Steric interference with receptor
    • Fix capsid so pH dependent uncoating is blocked
    • Capsid stabilization so that uncoating is blocked
  198. How does HIV survive in the face of an active immune system
    many antibodies are useless, and HIV can mutate away from good neutralizing antibodies so they stop working.
  199. What are two slow virus infections
    • Measles
    • HIV
  200. What is often used as a diagnostic HIV test
    Western blot to detect anti-HIV antibodies in patient serum
  201. Why do most antibodies fail against HIV
    The structure of HIV-1 envelope glycoprotein contributes to evasion from the immune system

    Variable regions cover the conserved regions

    Important epitopes are hidden within the molecule such as the fusion peptide
  202. What is the structure of HIV -1
    Envelope glycoprotein
  203. What is the significance of the two receptor mechanism in HIV
    It is an evasion strategy

    Important epitopes of gp120 are hidden until fusion, where they are only exposed for a moment during fusion process
  204. What is molecular mimicry in HIV and what is its significance
    A loop structure on HIVs gp120 has the same shape as part of the chemokine RANTES which binds to CCR5 chemokine receptor

    This is an evasion strategy
  205. What provides an escape mechanism in HIV
    Changes in gp120 glycosylation

    mutations in the location of glyosylation sites means that HIV is making an evolving glycan shield
  206. Describe the weak antibody response to HIV infection
    Some neutralizing ab block fusion process

    Low affinity Ab binding to complement receptors can help HIV get in

    Regions of gp120 look like self, Ab are usually not made to self antigens

    Interfering Ab bind to HIv but do not block entry but block the action of neutralizing antibodies
  207. What happens when CTL declines in patients with HIV
    opportunistic infections and disease start
  208. What are first infected by HIV, why?
    Macrophages and responding T helper cells are the first infected. 

    Dendritic cells bring antigen in lymph node.  Dendritic cells can be infected by HIV
  209. How are infected dendritic cells and t helper cells killed in the lymph node
    Infected dendritic cells present antigens on MHC class 1.  The CD8 cytotoxic t cell kills them with signal and costimulation
  210. Where do CTL receive Il-2 from
    TH cells
  211. Where does MHC class 1 present peptides from
    Intracellular proteins
  212. How many types of MHC class 1 genes are codominantly expressed
  213. Describe the epitope bound by MHC class 1
    It is a linear 9 amino acid sequence from within the protein

    Viral peptides can be presented if they fit

    Each peptide varies except and anchor residues
  214. Describe Immunodominant epitopes
    CTL immune response tends to focus on a few epitopes originally seen
  215. Define zoonosis
    The transfer of a pathogen from non-human animals to humans and subsequent spread of the pathogen between humans
  216. Which animal does HIV-1 likely derive from
  217. What type of viruses that shuttle between human and birds are related
    + strand RNA viruses
  218. What are other names of severe west nile disease
    Neuroinvasive disease, west nile encephalitis, meningitis or west nile poliomyelitis
  219. What are humans in terms of West Nile Virus life cycle
    Humans are dead end hosts because viral titre is not high enough to transmit from us to other animals
  220. What is the incubation period and symptoms of SARS
    incubation period is 2-12 days, the symptoms include fever, muscle soreness, cough, hypoxemia and diarrhea
  221. What are super infective individuals
    Super spreaders, infected many people and hosted many strains of this RNA virus
  222. How do we prove which virus is infectious in an unknown infection
    We use Koch's postulates and infect a healthy animal to see if illness occurs
  223. Why are bats linked with emerging infectious diseases
    They can be infected with almost anything, RNA viruses, but they are often not harmed

    -They can host many things
  224. What happens if RNA dependent RNA polymerase is removed from influenza
    RNA dependent RNA polymerase does both transcription and replication, if removed replication can not occur
  225. How are influenza viruses names
    They are named for their HA (Hemagglutinin) and NA (Neuraminidase) types
  226. What is considered to be the mother of all pandemics?  What was so significant about it.
    The spanish flu

    Most people who died from the virus were young adults and otherwise healthy
  227. What is H5N1, and what does it do
    It is a bird flu

    It encodes an NS1 (Non structural gene 1) variant that shuts down the interferon response
  228. What is NS1 and what is its significance in host defense.
    NS1 is Non structural gene 1.

    It is an inhibitor of interferon, and if it is strong it shuts down the interferon response meaning the virus wins
Card Set
Immunology 200 Midterm 2
University of Alberta