Chapter 9 outcomes of infection Flashcards

1
Q
  1. What is the difference between innate and adaptive immunity?
A
  1. innate immunity involves immunity that is not specific to anything
    1. it can include Roels of compliment, interferons, Natural Killer cells, APOBEC3 and Tetherin
  2. these are cells and molecules that respond to specific epitopes of antigens
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2
Q
  1. What innate immune system components may be encountered by a virus after infecting a cell?
A
  1. innate immune system components include :
    1. complements
    2. interferons
    3. natural kills cells
    4. apobec3
    5. tethering
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3
Q
  1. outline complement system
  2. 3 ways it can interfere with viruses
  3. what cells are involved in the phagocytosis
  4. how does complement cause lysis
A

compliment protein complex are produced in the liver and circulate in the blood

  1. Process
    1. cell surface receptors and soluble factors detect and respond to foreign invaders
    2. results= modification to compliment proteins
  2. Ways
    1. complexes of modified compliment proteins can insert themselves into the membranes containing virus proteins this damages the enveloped virons and lysing infected cells.
    2. some compliment proteins can also coat virions and attach to phagocytes like neutrophils and macrophages via the compliment receptors on the phagocyte receptors
    3. compliment activation can also enhance adaptive immunity
  3. cells: neutrophil and macrophages
  4. cell lysis is caused because the enveloped virus becomes damaged ??
    1. membrane attacked = lysis
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4
Q
  1. how do interferons limit virion replication
  2. how is interferon alpha and beta synthesis induced
  3. outcomes of alpha and beta interferon synthesis/secretion
  4. what are the virus countermeasures to interferon production
A
  1. limit virion replication by: protect adjacent cells from infection and activate t-cell mediated immunity
    1. when virus protein bind to pattern recognition receptors synthesis of interferons occur
  2. a/b synthesis is induced hen VP and nucleic acid bind to pattern recognition receptors → the cell synthesize a/b interferons
  3. outcomes: interferons bind to receptors on other cells which activates a wide spectrum of genes
    1. these gene products may either block the virus replication or cause the infected cells to die (apoptosis)
  4. Countermeasures
    1. inhibit interferon gene expression (RNA viruses)
    2. proteins block interferon synthesis pathways (NS1 of influenza)
    3. break down of interferon system components
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5
Q
  1. What are natural killer NK cells
  2. are they innate or adaptive immunity
  3. how do they recognize infected cells
  4. how do they respond to infected cells
A
  1. NK cells, present in the blood, are lymphocyte like cells that can recognize changes in surface molecules of virus infected cells
  2. innate immunity
    1. do not recognize specific antigens
  3. recognize the change
  4. they bind and kill the infected cells
    1. they release gamma-interferon
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6
Q
  1. Peforins?
  2. their function?
  3. what interferon is released by NK cells
  4. what’s the outcomes of releasing this interferon?
A
  1. peforins= proteins that are inserted into the plasma membrane of the virus- infected cell
    1. they poke holes in the cell membrane which induces apoptosis
    2. release the interferon gamma
      1. causes recruitment and activation of more NK cells and phagocytes
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7
Q
  1. APOBEC3?
  2. what types of viruses does it relate to?
  3. Function in an infected cell
  4. how does it affect replication of viruses after exiting a cell and infecting another?
A
  1. apoliprotien B mRNA-editing enzyme, catalytic polypeptide-like 3 proteins
    1. enzyme
  2. interferes with the replication of reverse transcribing viruses (retroviruses and hepadna viruses)
    1. ex:HIV
  3. Function:
    1. they induce a lethal mutation by deaminating deoxycytidne to deoxyuridine during reverse transcription
  4. virion incorporation= the mutation is taken to the next cell where it can then wreak havoc during reverse transcription
  5. countermeasure
    1. protein Vif in HIV can trigger degradation so there is no more virion incorporation
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8
Q
  1. What is tetherin?
  2. how does it help combat virus infection ?
A
  1. Tethrin = interferon induced protein that is expressed at the cell surface as dimers anchored in the plasma membrane
  2. prevents the budding of enveloped viruses from the cell surface by forming a tether between the lipid membrane of the cell and the virion
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9
Q
  1. What is the structure of antibodies ?
  2. what part binds to antigens?
A

glycoprotein known as immunoglobulins

  1. structure
    1. has 2 heavy and 2 light chains
    2. has 2 antigen-binding sites
    3. region known as the Fc (Fragment Crystallizable region)
    4. 4 polypeptide chains held together by disulfide bonds
  2. the chains are arranged in such a way that forms two sites that can bind specific antigens
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10
Q
  1. what is an epitope?
A

epitope = specific part of the antigen that triggers a cascade of events that’s results in adaptive immune response

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11
Q
  1. What is the significance of the Fc regions of antibodies.
A

??

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12
Q
  1. How do different antibodies with different antigen affinities come about?
A
  1. Beta cell receptor genes are rearranged during lymphocyte development. → this generates millions of different binding specificities
  2. Antigen specific Ab are synthesized by plasma cells, which develop from B cells after having been stimulated by the antigen and a specific immunoglobulin receptor at the cell surface

Check this slide

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13
Q
  1. Explain how naïve B-cells are activated/stimulated to become mature B-cells and secrete their
    specific antibody.
  2. In what organ does this happen?
  3. What is the role of T-lymphocyte in this
  4. what type of T-lymphocyte is it?
  5. What is the role of MHC-II (Major Histocompatability Complex
    class II)?
  6. Where in the body do B-cells (plasma cells) reside and secrete their antibody?
  7. What is
    the role of T cell receptors?
A
  1. Picture
  2. bone marrow in mammal
  3. ?

Check this slide

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14
Q
  1. How do helper T-cells get activated?
  2. What is the role of antigen presenting cells (APC)
A
  1. look below
  2. APC role
    1. engulfs the antigen and starts to migrate toward the lymph node → on its way its way APC will process the Ag into peptide fragments that contain the epitope→ the fragments are presented on teh cell surface via MHC2 → its presented to a T helper cell which then biomes activated and goes on to activate a B-cell with the corresponding BCR
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15
Q
  1. What is the function of cytotoxic T-cells?
  2. how are they activated
  3. how do they perform their function
  4. what is the significance pf Major Histocompatibility Complex class 1
A
  1. kill virus infected cells at an early stage of infection
    1. have CD8 molecules on the cell surface
    2. destroy virus infected cells before any infectious virus is produced
  2. Activated:
    1. activated by having a TCR that recognizes an epitope displayed on an APC (antigen presenting cell)
  3. perform function by:
    1. TC migrates to the infection site where it recognizes virus infected cells→ it secrets perforin a molecule that perforates the cell membrane leading to the death of the cell
  4. MHC 1
    1. it virus infected cell displays a virus antigen fragments (epitope) on their surface which is bound to a MCH1 molecule.
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16
Q
  1. What is immunological memory
A
  1. formed from Natural infection or Vaccination
  2. B and T cells survive as memory cells long after the first or subsequent encounters with the virus antigens
  3. when present the signs and symptoms of the disease are likely to be less sever or absent
17
Q
  1. What are the most significant classes of Ab’s (Ig’s) in virus infection
  2. in what parts of the body are each type found predominantly?
  3. which type is a monomer, dimer, pentamer?
A
  1. Significant
    1. IgG
    2. IgM
    3. IgA
  2. found
    1. blood
    2. blood
    3. mucosal surfaces
  3. type
    1. monomer
    2. pentamer
    3. dimer
18
Q
  1. What are the functions of antibodies?
A
  1. neutralization of infectivity
    1. release of nucleic acid from virions
    2. prevention of virion attachment to cell receptors by masking the virus attachment sites
    3. release of virions that have attached to cell receptors
    4. inhibition of entry to the cell because the antibody coating fusion proteins
    5. inhibition of genome uncoating
19
Q
  1. What are the major factors affecting the outcomes of virus infection?
A
  1. A major factor affecting the outcomes of a virus infection is the efficacy of the hosts immune systems

Check this slide

20
Q
  1. What is RNA silencing (RNA interference) ?
  2. Describe the mechanism?
  3. What type of viruses does RNA silencing relate to?
A
  1. RNA silencing is also know as post-transcription gene silencing or RNA interference (RNAi).
    1. an intracellular process induced by dsRNA
    2. it results in the destruction of mRNA that have the same sequence as the inducing dsRNA
  2. Steps
    1. dsRNA is cleaved by the a protein complex contains an enzyme called dicer →they are cleaved into fragments with 3’ overhang of two or three nucleotides
    2. the siRNA join a complex of protein to form RISC → the ds siRNA is unwound and the minus strand RNA remains associated with the complex= activated RISC
    3. the minus strand RNA selects the target mRNA by complementary base pairing, then the mRNA is degraded in that region
21
Q
  1. What are the two types of non-productive infections
  2. what distinguishes them from each other?
  3. How is productive infection defined?
A
  1. latent and abortive
  2. latent
    1. unable to complete the replication cycle, but genome maintained in the cell
  3. abortive
    1. nothing persists and can kill cell
  4. Productive infection
    1. spread of infection within multicelular hosts
22
Q
  1. what is difference between signs an d symptoms
A

signs=objective, can be seen by others, rash, blood in feces

symptoms = subjective, reported by a patient, abdominal pain, fatigue