Chapter 9 outcomes of infection Flashcards
1
Q
- What is the difference between innate and adaptive immunity?
A
- innate immunity involves immunity that is not specific to anything
- it can include Roels of compliment, interferons, Natural Killer cells, APOBEC3 and Tetherin
- these are cells and molecules that respond to specific epitopes of antigens
2
Q
- What innate immune system components may be encountered by a virus after infecting a cell?
A
- innate immune system components include :
- complements
- interferons
- natural kills cells
- apobec3
- tethering
3
Q
- outline complement system
- 3 ways it can interfere with viruses
- what cells are involved in the phagocytosis
- how does complement cause lysis
A
compliment protein complex are produced in the liver and circulate in the blood
- Process
- cell surface receptors and soluble factors detect and respond to foreign invaders
- results= modification to compliment proteins
- Ways
- complexes of modified compliment proteins can insert themselves into the membranes containing virus proteins this damages the enveloped virons and lysing infected cells.
- some compliment proteins can also coat virions and attach to phagocytes like neutrophils and macrophages via the compliment receptors on the phagocyte receptors
- compliment activation can also enhance adaptive immunity
- cells: neutrophil and macrophages
- cell lysis is caused because the enveloped virus becomes damaged ??
- membrane attacked = lysis
4
Q
- how do interferons limit virion replication
- how is interferon alpha and beta synthesis induced
- outcomes of alpha and beta interferon synthesis/secretion
- what are the virus countermeasures to interferon production
A
- limit virion replication by: protect adjacent cells from infection and activate t-cell mediated immunity
- when virus protein bind to pattern recognition receptors synthesis of interferons occur
- a/b synthesis is induced hen VP and nucleic acid bind to pattern recognition receptors → the cell synthesize a/b interferons
- outcomes: interferons bind to receptors on other cells which activates a wide spectrum of genes
- these gene products may either block the virus replication or cause the infected cells to die (apoptosis)
- Countermeasures
- inhibit interferon gene expression (RNA viruses)
- proteins block interferon synthesis pathways (NS1 of influenza)
- break down of interferon system components
5
Q
- What are natural killer NK cells
- are they innate or adaptive immunity
- how do they recognize infected cells
- how do they respond to infected cells
A
- NK cells, present in the blood, are lymphocyte like cells that can recognize changes in surface molecules of virus infected cells
- innate immunity
- do not recognize specific antigens
- recognize the change
- they bind and kill the infected cells
- they release gamma-interferon
6
Q
- Peforins?
- their function?
- what interferon is released by NK cells
- what’s the outcomes of releasing this interferon?
A
- peforins= proteins that are inserted into the plasma membrane of the virus- infected cell
- they poke holes in the cell membrane which induces apoptosis
- release the interferon gamma
- causes recruitment and activation of more NK cells and phagocytes
7
Q
- APOBEC3?
- what types of viruses does it relate to?
- Function in an infected cell
- how does it affect replication of viruses after exiting a cell and infecting another?
A
- apoliprotien B mRNA-editing enzyme, catalytic polypeptide-like 3 proteins
- enzyme
- interferes with the replication of reverse transcribing viruses (retroviruses and hepadna viruses)
- ex:HIV
- Function:
- they induce a lethal mutation by deaminating deoxycytidne to deoxyuridine during reverse transcription
- virion incorporation= the mutation is taken to the next cell where it can then wreak havoc during reverse transcription
- countermeasure
- protein Vif in HIV can trigger degradation so there is no more virion incorporation
8
Q
- What is tetherin?
- how does it help combat virus infection ?
A
- Tethrin = interferon induced protein that is expressed at the cell surface as dimers anchored in the plasma membrane
- prevents the budding of enveloped viruses from the cell surface by forming a tether between the lipid membrane of the cell and the virion
9
Q
- What is the structure of antibodies ?
- what part binds to antigens?
A
glycoprotein known as immunoglobulins
- structure
- has 2 heavy and 2 light chains
- has 2 antigen-binding sites
- region known as the Fc (Fragment Crystallizable region)
- 4 polypeptide chains held together by disulfide bonds
- the chains are arranged in such a way that forms two sites that can bind specific antigens
10
Q
- what is an epitope?
A
epitope = specific part of the antigen that triggers a cascade of events that’s results in adaptive immune response
11
Q
- What is the significance of the Fc regions of antibodies.
A
??
12
Q
- How do different antibodies with different antigen affinities come about?
A
- Beta cell receptor genes are rearranged during lymphocyte development. → this generates millions of different binding specificities
- 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
13
Q
- Explain how naïve B-cells are activated/stimulated to become mature B-cells and secrete their
specific antibody. - In what organ does this happen?
- What is the role of T-lymphocyte in this
- what type of T-lymphocyte is it?
- What is the role of MHC-II (Major Histocompatability Complex
class II)? - Where in the body do B-cells (plasma cells) reside and secrete their antibody?
- What is
the role of T cell receptors?
A
- Picture
- bone marrow in mammal
- ?
Check this slide
14
Q
- How do helper T-cells get activated?
- What is the role of antigen presenting cells (APC)
A
- look below
- APC role
- 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
15
Q
- What is the function of cytotoxic T-cells?
- how are they activated
- how do they perform their function
- what is the significance pf Major Histocompatibility Complex class 1
A
- kill virus infected cells at an early stage of infection
- have CD8 molecules on the cell surface
- destroy virus infected cells before any infectious virus is produced
- Activated:
- activated by having a TCR that recognizes an epitope displayed on an APC (antigen presenting cell)
- perform function by:
- 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
- MHC 1
- it virus infected cell displays a virus antigen fragments (epitope) on their surface which is bound to a MCH1 molecule.
16
Q
- What is immunological memory
A
- formed from Natural infection or Vaccination
- B and T cells survive as memory cells long after the first or subsequent encounters with the virus antigens
- when present the signs and symptoms of the disease are likely to be less sever or absent
17
Q
- What are the most significant classes of Ab’s (Ig’s) in virus infection
- in what parts of the body are each type found predominantly?
- which type is a monomer, dimer, pentamer?
A
- Significant
- IgG
- IgM
- IgA
- found
- blood
- blood
- mucosal surfaces
- type
- monomer
- pentamer
- dimer
18
Q
- What are the functions of antibodies?
A
- neutralization of infectivity
- release of nucleic acid from virions
- prevention of virion attachment to cell receptors by masking the virus attachment sites
- release of virions that have attached to cell receptors
- inhibition of entry to the cell because the antibody coating fusion proteins
- inhibition of genome uncoating
19
Q
- What are the major factors affecting the outcomes of virus infection?
A
- A major factor affecting the outcomes of a virus infection is the efficacy of the hosts immune systems
Check this slide
20
Q
- What is RNA silencing (RNA interference) ?
- Describe the mechanism?
- What type of viruses does RNA silencing relate to?
A
- RNA silencing is also know as post-transcription gene silencing or RNA interference (RNAi).
- an intracellular process induced by dsRNA
- it results in the destruction of mRNA that have the same sequence as the inducing dsRNA
- Steps
- 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
- 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
- the minus strand RNA selects the target mRNA by complementary base pairing, then the mRNA is degraded in that region
21
Q
- What are the two types of non-productive infections
- what distinguishes them from each other?
- How is productive infection defined?
A
- latent and abortive
- latent
- unable to complete the replication cycle, but genome maintained in the cell
- abortive
- nothing persists and can kill cell
- Productive infection
- spread of infection within multicelular hosts
22
Q
- 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