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UofG Medicine Question Bank 2020 > Infection/Bacteria/Virus/Immune Response/Tropical Disease > Flashcards

Infection/Bacteria/Virus/Immune Response/Tropical Disease Flashcards

1
Q

What cells does the common myeloid progenitor cell give rise to?

A

Erythrocytes, Megakeryocytes (turn to platelets), Mast Cells, and Myeloblasts

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2
Q

What cell gives rise to a majority of our innate immune cells?

A

The Myeloblast Cell
Gives rise to basophils, neutrophils, eosinophils, and monocytes (which can give rise to macrophages and dendritic cells)

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3
Q

What are the different Antibodies?

A

Immunoglobulin: G, A, M, E, D

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4
Q

What immunoglobulin is largest, and what is it’s function?

A

M- form is a pentamer
First made in immune response
Complement activation

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5
Q

What is the difference between MHC Class 1 and 2?

A

Class 1 presents to Cytotoxic T Lymphocytes (CD8) which initiates perforin and granzyme release from T cell, resulting in apoptosis of Antigen Presenting Cell.
Class 1 is found on all nucleated cells, 2 is only on dendritic cells, macrophages, B cells (APC related cells)
Class 2 presents to Helper T Cells (CD4), and the T cell will activate the APC.

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6
Q

What are the steps in Extravacation?

A
  1. Rolling adhesion (E and P selectins on endothelial cell (expressed after histamine exposure) form weak bond with glycoprotein on leukocyte)
  2. Tight Binding (Integrins on leukocyte bind ICAMs 1 and 2 on endothelium with strength)
  3. Diapedesis (Leukocyte/Endothelium expresses PECAM (CD31), which binds leukocyte tightly and allows for diapedesis, leukocyte releases enzymes to break down basement membrane)
  4. Migration (leukocyte follows chemotaxis to site of infection)
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7
Q

Where is the primary residence of IgA?

A

Found in gut, respiratory tract, tears, saliva, urogenital tract.

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8
Q

Which Ig is most prevalent in the blood?

A

IgG mainly, and some IgM

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9
Q

What do antibodies do?

A

Opsonization- Bing pathogen and “draw attention” to it
Complement activation- bind pathogen, end of an Ig can bind first enzyme in complement cascade, initiating complement and lysis
Neutralization- bind pathogen, signal for macrophage ingestion (neutralization of target)

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10
Q

What receptors are found on B and T cells?

A

B Cell Receptor

T Cell Receptor

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11
Q

What response would an extracellular microbe cause in humeral immune response?

A

B lymphocyte will become activated after encountering microbe (and T cell activates it), release antibody that will either:

  1. Clump the bacteria together, causing macrophage to ingest the bacteria to kill it
  2. Initiate Complement (Classic Ab:Ag pathway)
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12
Q

What response would an extracellular microbe cause in Cell Mediated Immunity?

A

Dendritic/macrophages may take up the pathogen, and present to Helper T Cells
CD4 cell will activate Antigen Presenting Cell causing phagocytosis of microbe.

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13
Q

What response would an intracellular microbe cause in Cell Mediated Immunity?

A

Our CD8 cytotoxic T cells will kill the infected APC after presentation by injecting perforin and Granzymes into it, causing apoptosis.

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14
Q

Where does an adaptive immune response happen?

A

In the secondary lymph nodes

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15
Q

When does a T cell loose its naïve status?

A

Once encountering a pathogen

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16
Q

What is the difference between Humeral Immunity and Cell-Mediated Immunity?

A

Humeral involved antibodies and complement

Cell-mediated involves cytokines and T cell activation

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17
Q

What do the two classes of MHC bind to?

A

MHC1 on APC- Binds CD8 Cytotoxic T cells causing apoptosis of the antigen presenting cell it is on.
MHC2 on APC- Bind CD4 T Helper Cell causing activation of the cell that is presenting the antigen. Either presenting APC (macrophage, dendritic cell), or presenting B Cell is activated.

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18
Q

Give a summary of the adaptive immune response.

A

B and T Helper cells in lymph node interact with pathogen (APC presents to T cell)
B and T Helper cells migrate to each other (parafollicular cortex)
B and Th Cell bind, and clonal expansion begins,
B cell proliferate into plasma cell (or memory cells), and will begin to make Antibodies specific to pathogen.
Th cell will clonally expand and secrete large amounts of cytokines, helping to mount an immune response

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19
Q

Do B cells require antigen presentation?

A

No, they are regarded as APCs themselves.

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20
Q

Where are B and T cells found in the spleen?

A

Both found within “White Pulp”
T Cells- Paracortical area
B Cells- Lymphoid follicles

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21
Q

How many types of Helper T cells are there and their basic role?

A

Th1- Macrophage activation
Th2- Humoral Activation
Th17- Autoimmune disease pathogenesis
Treg- Modulates immune response

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22
Q

What are the types of complement pathways (give brief description of initiation)?

A

Lectin- Serum Lectin binds mannose on pathogen
Classical- Antigen/ Antibody complexes
Alternative- C3b binding to pathogens or apoptotic tissue

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23
Q

What are the goals of the Complement Pathway?

A

Kill Pathogen
Opsonize Pathogen
Recruit inflammatory cells

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24
Q

How does a macrophage initiate phagocytosis?

A

Pattern Recognition Receptors (PRRs), typically Toll-Like Receptors, recognize/bind DAMPs and PAMPs on pathogen or dying host cell, invagination of microbe begins, and is fused with lysosome.

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25
Q

What are the different ways phagocytes can kill pathogens once engulfing them?

A

Acidification (pH 3.5-4.5, bacteriostatic (prevent growth), bactericidal (kill)),
Toxic Oxygen-Derived components (hydrogen peroxide, hydroxyl radical),
Toxic Nitrogen Oxides (NO),
Antimicrobial Peptides (Macrophages: Cathelicidin, Neutrophils, a/beta Cathepsins)
Enzymes (lysozymes digest gram-positive bacterial walls, Acid hydrolases)
Competitors (only neutrophils- Lactoferrin, B12 binding protein)

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26
Q

What is the roll of Toll-Like Receptors?

A

Recognizing Pathogen Associated Molecular Proteins (PAMPs) on the pathogens and Damage-Associated Molecular Patterns (DAMPs) on host cells, initiating phagocytosis and inflammatory responses.

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27
Q

Where are Toll-Like Receptors typically found?

A

Sentinel Cells (macrophages, dendritic cells).

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28
Q

What is the goal of initiating inflammation?

A

Isolate damage, mobilize effector cells, promote healing and repair

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29
Q

How can inflammation be bad?

A

Autoimmune disease, allergies, chronic inflammatory conditions

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30
Q

Where does lymph drain back into blood circulation?

A

The lower limbs, left upper limb/ hemithorax/ neck/ head drain back via the THORACIC DUCT
Right upper limb/ hemithorax/ neck/ head drain back via RIGHT LYMPHATIC DUCT

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31
Q

How is lymph produced?

A

Hydrostatic pressure in arterioles push fluid out of capillaries, osmotic pressure draws fluid back into venule side of capillaries, although some fluid does not return, and enters into lymph system.

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32
Q

Where do B and T cells migrate to after activation?

A

B cells migrate to Paracortical area to bind with activated T cells

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33
Q

What white blood cells are involved in innate immunity?

A

Macrophages, Neutrophils, Basophils, Dendritic Cells, Eosinophils, Natural Killer Cells

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34
Q

What white blood cells are involved in adaptive immunity?

A

Antigen Presenting Cells, Lymphocytes (B cells, T Helper CD4 cells, Killer T CD8 cells),

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35
Q

What are the primary lymphoid organs and their function?

A

Bone Marrow- site of B and T cell production, and B cell maturation
Thymus- site of T cell maturation into Naive T cell

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36
Q

What are the secondary lymphoid organs, and their functions?

A

Spleen, Lymph Nodes, tonsils, Peyer’s Patches, Appendix

Antigen presentation, B and T cell activation/ migration (adaptive immune activation), Lymph filtration occurs,

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37
Q

Summarize Antibody Structure

A

Structure- light and heavy chain (heavy chain is base and inner side of Ab ‘arm’), contain hyper-variable region (tip of ‘arms’, where antigen is bound) and constant region (bottom half of ‘arm’ and base of Ab)

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38
Q

What is the function of antibodies?

A

Opsonization, neutralization, agglutination, and activation of compliment.
Function is to ‘tag’ invading pathogens/microbes, opsonizing pathogen and enhancing/quickening adaptive immune response.
Apart of humeral immunity.

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39
Q

How does complete B cell activation occur?

A

B cell interacts with pathogen in secondary lymphoid organ.
B cell migrates to paracortical area to bind with helper T cell (MHC2 of B cell will bind TCR, forming antigen presentation, CD4 of T cell will also bind the MHC2), causing activation of B cell.
B cell is completely activated, will undergo clonal expansion, and will differentiate into either plasma cells (producing antibodies) or memory B cells (life-long memory).

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40
Q

Where are Antibodies found?

A

Can be free floating in the blood, in tissue, or membrane bound (forming the B cell receptors)

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41
Q

How do T lymphocytes develop?

A

Produced from common lymphoid precursor -> small lymphocyte -> T cell -> either Helper T cell, Cytotoxic T cell, or Treg
Produced in bone marrow, travel to thymus for maturation into naïve T cell (develop into CD4/8/17/reg), will then travel to secondary lymphoid organs and await antigen presentation.

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42
Q

What role do CD4 Helper T cells play in cell activation?

A

Activation of B cell via B cell antigen presentation, binding of MHC2 on B cell to TCR and CD4, allowing for B cell to differentiate into Plasma/memory cells.
Activate CD8 Cytotoxic T cells using cytokines to initiate cytotoxicity

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43
Q

Do CD4 T cells require antigen presentation?

A

Yes, presentation occurs by APC or B cells on MHC2 receptor.

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44
Q

Do CD8 T cells require antigen presentation?

A

Yes, APC presents antigen on its MHC1 receptor to TCR/CD8.

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45
Q

How would a virally infected cell present to T cells?

A

Viral peptide will presented on MHC1 receptor to TCR and CD8 of cytotoxic T cell.
CD8 T cell will then use perforin to create channel in APC, and secrete granzymes into APC resulting in apoptosis.

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46
Q

What are the main differences in viruses and bacteria presentation to adaptive immune cells?

A

Virus- MHC1 presentation to CD8 T cell -> APC apoptosis
Bacteria- MHC2 presentation to CD4 T cell -> T cell clonal expansion -> CD4 activates APC/B cell (differentiates to mem. or plasma cell)

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47
Q

What is the difference between Gram-Positive and Gram-negative?

A

Gram-Positive contain large amounts of peptidoglycans in the cell wall.
This means when flooding with iodine and crystal violet and then decolouring the bacteria, gram-positive have enough peptidoglycans to retain the colour.

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48
Q

What may cause a gram staining result of Gram Variable/Uncertain?

A

Small bacteria
Don’t have normal complex cell wall
Atypical Life cycle / structure
Other methods of detection (serology, molecular (PCR)) can be used to determine

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49
Q

What are common Gram-Positive Bacteria (distinguish between rod and cocci)?

A

Rod- Listeria monocytogenes, Corynebacterium diphtheriae

Cocci-Staphylococcus aureus, Streptococcus Pneumoniae

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50
Q

What are common Gram-Negative Bacteria (distinguish between rod and cocci)?

A

Rod- Escherichia Coli, Salmonella species

Cocci- Neisseria meningitides

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51
Q

What does microbiology mean?

A

Study of living organisms that are too small to be seen with the naked eye

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52
Q

What are the classifications of microorganisms?

A

Bacteria, Fungi, Protozoa, Parasite, Virus, Algae, Archaea

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53
Q

Why is gram staining important?

A

It can help with diagnosis of infection, which will aid in treatment

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54
Q

What are the sterile body sites?

A 
Blood, tissues, organs
CNS
Lower Respiratory Tract
Sinuses, inner/middle ear
Renal system down until posterior Urethra
Female reproductive tract down to cervix
Eye (not the conjunctivas)
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55
Q

What is colonization?

A

When a species spreads to a new area.

In bacterial senses, colonisation would occur when bacteria are within the body, but don’t elicit an immune response

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56
Q

What are the stages of infection?

A

Entrance, Colonization, Multiplication, Penetration/Invasion, Signs/Symptoms, Resolution (or carrier state), Elimination

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57
Q

What molecule is found on gram-negative bacteria?

A 
Endotoxins (and less commonly exotoxins)
Lipopolysaccharide on bacterial surface 
Contains; Lipid-A (where endotoxin comes from),
Core Polysaccharide (antigenic diversity), 
O-antigens (which add to membrane integrity  and antigenic properties)
Endotoxins are released when the bacteria autolysis
Largely target Macrophages and Dendritic Cells
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58
Q

What toxin is released by gram-positive bacteria?

A

Exotoxins produced intracellularly
Secreted (or released during autolysis) by gram + (and less commonly -) bacteria causing serious local or systemic cell destruction or disrupting cellular metabolism.
Can lead to Toxic Shock Syndrome

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59
Q

When should antibiotics be prescribed?

A

After testing the patient sample (so you can tailor empirical antibiotic treatment to the patient), except in cases of emergency (i.e.. meningitis)

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60
Q

How does a blood culture work?

A

Blood is taken, and grown in a bottle in a machine for ~5 days.
If positive, culture will grow and produce CO2, which changes the sample’s pH, resulting in colour change of the pellets in the bottle.
Colour change is flagged as a positive result and further microscopy and cultures can be done.

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61
Q

How can Sepsis cause death?

A

Infection (exo/endotoxins) -> Vasodilation
Vasodilation -> reduced blood pressure
Reduced BP = Organ hypoperfusion
Hypoperfusion -> Tachycardia (increased heart rate)
Tachycardia is used to increase BP and restore perfusion so organs receive appropriate amounts of blood
Extended Tachycardia -> Heart failure/death

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62
Q

How do Bacterium reproduce?

A

Binary Fission

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63
Q

Where is bacterial DNA found?

A

In a circular chromosome, or excess is stored in plasmids

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64
Q

How do gram-positive bacteria evade breakdown in the intestines?

A

Thick peptidoglycan is hydrophilic and therefore resistant to activity of bile.

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65
Q

What is an example of antibiotic mechanism of action for gram-positive bacteria?

A

Preventing the synthesis of peptidoglycan
i.e. beta-lactam (penicillin) or glycopeptide (vancomycin) antibiotics.
OR
Inhibiting RNA polymerase using macrolides (erythromycin)

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66
Q

Are gram-negative bacteria hydrophobic or hydrophilic? Why?

A

Both
Hydrophilic- thin peptidoglycan layer
Hydrophobic- lipid components (LPS)

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67
Q

What are eosinophils typically recruited for?

A

Allergic Responses

Parasites

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68
Q

What are neutrophils recruited for?

A

Bacterial Infection

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69
Q

What are monocytes recruited for?

A

Inflammation

Viral, bacterial, parasitic infection.

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70
Q

What are 2 examples of a gram-positive cocci-shaped bacterium?

A

Staphylococcus aureus

Streptococcus pneumoniae

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71
Q

What is an examples of gram-negative cocci-shaped bacteria?

A

Neisseria meningitides

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72
Q

What are 2 examples of gram-positive rod-shaped bacterium?

A

Listeria monocytogenes

Corynebacterium diphtheria

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73
Q

What are 2 examples of gram-negative rod-shaped bacterium?

A

E. coli

Salmonella species

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74
Q

What colonisers are typically found within our intestines?

A

Bacteria: Escherichia coli, Enterococcus species, Streptococcus species,
Fungi: Candida albicans

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75
Q

What colonisers are typically found within the urethra?

A

Bacteria: E. coli, Streptococcus species

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76
Q

What colonisers are typically found within the throat?

A

Streptococcus species, Neisseria species, Corynebacterium species

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77
Q

What colonisers are typically found on the skin?

A

Staphylococcus epidermis, Propionibacterium acnes

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78
Q

What pathogen are natural killer cells typically used for?

A

Viral- they can detect changes in protein expression on a virally infected host cell

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79
Q

What cytokines do macrophages release to cause inflammation?

A

TNFa, IL-1, IL-6 (6 works more with chemotaxis)

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80
Q

What is the functional significance of clonal expansion?

A

It increases number of antigen-specific lymphocytes.

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81
Q

What is the functional significance of immune specialization?

A

Generates responses that are optimal for particular types of pathogens.

82
Q

What force holds B cells within the follicles of the secondary lymphoid organs?

A

Follicular Dendritic Cells release chemokine which attract B cells
When B cell activated by antigen, B cell receptor (CXCR5) expression changes allowing migration towards T cells

83
Q

What force holds T cells within the paracortex of lymphoid organs and periarteriolar lymphoid sheaths of the spleen?

A

Chemokines

When T cell activated by antigen, T cell receptor (CCR7) expression changes allowing migration towards B cells

84
Q

What are the two types of adaptive immunity, and what types of microbes do these adaptive immune responses combat?

A

Humeral- Antibody based- extracellular microbes

Cell-mediated- T cells- intracellular microbes (and extra)

85
Q

What are the principal classes of lymphocytes, and how do they differ in function?

A

B- Create Abs (plasma cells) for opsonization, neutralization, and complement activation, and memory B cells
T- Activate DCs/macrophages/B cells, induce apoptosis, release cytokines, express TCR (binds to MHC)

86
Q

What are the important differences among naïve, effector, and memory T lymphocytes?

A

Naïve- circulate through lymph/blood, haven’t encountered antigen, preferentially move towards lymph nodes, presentation most commonly done my dendritic cells
Effector- preferentially migrate to infected tissue to fight pathogens, have encountered Ag, can secrete cytokines
Memory T- Relatively inactive until interacting with same Ag that stimulated it’s development (more commonly presented by B cells, or other APCs)

87
Q

What are the differences among Ab secretion from naïve, effector, and memory B lymphocytes?

A

Naïve- secrete IgG and IgM (with low affinity)
Effector- IgA/D/E secretion increases
Memory- G/A/E

88
Q

How do naive and effector T lymphocytes differ in their patterns of migration?

A

Both found in lymph and blood
naïve preferentially migrate to lymph nodes
effector preferentially migrate to infected tissue

89
Q

If host cell death occurs within a sterile site in the body, how does the immune system respond to this to prevent necrosis?

A

Damage-associated molecular patterns (DAMPs) are released by cells when they die, and is recognized in a similar pathway to PAMPs, initiating recruitment of other immune cells

90
Q

How many types of receptors are found in the innate vs adaptive immune systems?

A

innate- ~100

adaptive- 2; membrane Ig (BCR- typically M/D isotypes) and TCR- they are just more diverse

91
Q

Autosomal mutations in Toll-Like Receptors can result in what?

A

Recurrent infection

Innate cells wont produce cytokine release as TLR fails to recognize a pathogen

92
Q

What cells are known for phagocytic function?

A

Neutrophils, Dendritic Cells, Macrophages

93
Q

What innate cells primarily reside in tissue?

A

Mast cells, Dendritic Cells, Macrophages

94
Q

What innate cells primarily reside in blood?

A

Neutrophils, Basophils, Eosinophils

95
Q

What innate cells release histamine?

A

Mast cells, Basophils, Eosinophils

96
Q

Which is the first leukocyte to respond to infection?

A

Neutrophils

97
Q

What role do Mast cells play in immunity (location of production and residence, activated by, primary target, cytokine/granule release, innate vs. adaptive)?

A

Produced in bone marrow
Reside in tissue and mucosal barriers
Activated by microbes (binding TLRs), complement, or antibodies.
Target helminths, snake/insect venom, allergic responses
Release cytokine TNFa (induce inflammation)
Granules release histamine (vasodilation/ ^ permeability) & proteolytic enzymes (kill microbes)
Innate

98
Q

What role do Dendritic cells play in immunity (location of production and residence, activated by, primary target, cytokine/granule release, innate vs. adaptive)?

A

Produced in bone marrow
Reside in tissue
Activated by microbes, complement, antibodies, T cells
Target invading microbes
Secrete IL-12 (T cell activation), TNFa (for inflammation)
Innate and Stimulate Adaptive

99
Q

What role do Natural Killer cells play in immunity (location of production and residence, activated by, primary target, cytokine/granule release, innate vs. adaptive)?

A

Located in blood and lymph
Produced in Bone Marrow
Bind APCs and induce apoptosis (virally infected APC), or activating APC (releasing interferon-γ)
Target viruses, bacteria, helminths, tumours
Release interferon-γ (activate APC), IL-12 (enhances NK killing function) and IL-15.
Innate lymphocyte

100
Q

Which pathways of complement are associated with innate vs. adaptive immunity?

A

Classical- Humeral arm of adaptive immunity (involves antibodies activating proteins)
Lectin- Innate (although activating same proteins as classical, they’re activated by binding mannose-binding lectin)
Alternative- Innate (complement proteins on microbes activate uncontrollably- have regulation proteins for this on host cells)

101
Q

How are cytokines TNFa and IL-1 utilized in immune responses?

A

Both activate endothelial cells
TNF recruits neutrophils
Both act on hypothalamus to induce FEVER
TNF released by Macrophages, T Cells, Mast Cells
IL-1 released by Macrophages, DCs, Mast Cells, endo/epi cells

102
Q

What cells produce IL-12 and why?

A

Macrophages and Dendritic cells

Activates Natural Killer Cells and T Cells differentiation (stimulates release of IFNγ, enhancing killing)

103
Q

How does interferon-γ enhance immune responses?

A

Released by NK cells and T cells
Increases macrophage activation/phagocytosis
Less often released by some Dendritic Cells to inhibit viral replication

104
Q

How can inflammation injure the host, in relation to neutrophils and their lysosomes?

A

Neutrophils die in response to phagocytosing microbes -> Neutrophil Extracellular Traps (NETs) are projected from dying Neutrophil to catch/kill more pathogens -> lysosome content (ROS and enzymes) released to external environment can injure host

105
Q

What are some examples of tropical infections spread by mosquitos?

A

Malaria, Zika Virus, Ebola, Lymphatic Filariases (Elephantiasis), Yellow Fever, Dengue Fever, Chikungunya, West Nile

106
Q

What are some examples of arthropod borne diseases?

A

Lyme Disease, Chagas’s Disease (aka American Trypanosomiasis, caused by kissing bug), Leishmania’s (sand-flies), plague (fleas), Relapsing Fever (ticks), African Trypanosomiasis (tsetse flies)

107
Q

What are some water-borne related diseases?

A

E. Coli, Shigella, Salmonella, Schistosomiasis, Cholera

108
Q

What part of a virus determines the tropism?

A

Viral proteins on the capsid or phospholipid envelope.

109
Q

What are the steps involved in the cycle of viral replication?

A
  1. Attachment
  2. Invasion
  3. Uncoating
  4. Replication (transcription, translation}
  5. Assembly
  6. Virion Release
110
Q

How do viruses penetrate into their targets?

A

After attachment, some viruses can induce endocytosis, or membrane can become fused following the attachment (attachment can cause conformational change to capsid/envelope)

111
Q

What is the de nova synthesis of viral genomes?

A

The transcription and translation of the viral genome and synthesis of viral proteins

112
Q

What occurs in the assembly phase of viral replication?

A

Viral proteins and genomes are packaged into new virions that are ready to be released from the host.
Also named maturation

113
Q

What are the two forms of virion release?

A

Lysis or budding

114
Q

What happens in lysis release of viruses?

A

Cytolytic viruses cause lysing of their host cell in order to release newly formed virions into the surrounding
Example: variola major also known as smallpox.

115
Q

What happens in the budding release of viruses?

A

Cytopathic viruses cause the formation of budding to escape the host cell through acquisition of the viral phospholipid envelope.
Doesn’t typically cause host cell death
Example: Influenza A

116
Q

How do T cells typically come into contact with viruses?

A

The remanence of virus proteins in host cell cytosols can be presented by MHC Class 1 molecules to CD8 T cells.
Antibodies can also target viral proteins left on the membrane of hosts, following virion release

117
Q

Where does viral replication typically take place within the host cell?

A

The cytoplasm (some RNA viruses) or Nucleus (some RNA viruses, DNA viruses transcribe viral mRNA, mRNA travels to cytoplasm for translation by ribosomes- although some viruses have their own polymerase enzymes which allow transcription to occur in the cytoplasm)

118
Q

What does a retrovirus contain, and how does it aid in virality?

A

Contains reverse transcriptase that transcribes the viral positive ssRNA into negative ssDNA, then its converted into dsDNA, then it enters nucleus, and becomes integrated in to the host cells genomes.
Host polymerase can then transcribe the viral DNA into mRNA.
Host daughter cells therefore carry the viral DNA.

119
Q

How do RNA viruses typically work within a host cell in terms of producing viral proteins?

A

Their RNA is injected into the cytoplasm, and translated by host cell organelles

120
Q

What is the difference between plus and minus RNA?

A

Minus RNA has to be transcribed into viral mRNA first in order to be used for viral protein synthesis, whereas plus can be directly used.

121
Q

What form (double vs single) do DNA and RNA viruses typically come in?

A

DNA- double, (single is more rare, i.e. inovirus)

RNA- single (double more rare)

122
Q

How do double stranded RNA viruses reproduce in hosts?

A

RNA is first transcribed by viral polymerase into viral mRNA.

123
Q

Can viral mRNA out-compete host mRNA?

A

YES! It can displace host mRNA so that monocistronic (single coding region) mRNA is preferentially synthesize.

124
Q

What’s an example of a positive sense ssRNA virus?

A

Poliovirus

125
Q

How does RNA replication of positive ssRNA viruses occur?

A

+ssRNA can be used directly as mRNA to create viral polymerase which will form new viral progeny
+ssRNA is also translated repeatedly to form viral proteins

126
Q

What is an example of a negative sense ssRNA virus?

A

Rabies virus

127
Q

How is the pox virus atypical from other DNA viruses?

A

Its replication occurs in the cytoplasm, typically DNA replication for viruses occurs in the nucleus

128
Q

What are some examples of viral glycoproteins found on the cell surface of HIV?

A

GP120 (binds CD 4 receptors, and CXCR5, CCR4)
GP41 (aids in fusion to host)
They are also inserted into the host membrane to allow for production and budding of a new virion.

129
Q

How do Nucleoside Analogs and Reverse Transcriptase Inhibitors work to treat HIV?

A

Help to prevent the formation of the ddDNA by reverse transcriptase from the initial + ssRNA HIV virus.

130
Q

How does Integrase work to aid in viral replication?

A

It inserts the viral DNA into the host genome, now it is called pro-viral DNA. It can remain dormant here, or host enzymes can produce viral genome RNA and mRNA.

131
Q

How does a protease enzyme aid in viral protein synthesis?

A

Viral mRNA is translated, and yields some proteins that need to be cleaved in order to work. Protease cleaves these proteins.

132
Q

How do protease inhibitors prevent viral protein formation?

A

They inhibit protease, so the long polypeptide viral protein cant be cleaved into functional proteins

133
Q

What role do matrix proteins play in viruses?

A

Some help form the viral envelope when budding

134
Q

How do viruses evade immune detection?

A

Develops variations in the antigens that aren’t recognized by the host, so it can evade detection

135
Q

What are the 3 types of variations in viruses?

A

Mutations, recombination and gene re-assortment

136
Q

What is an example of a virus that uses antigenic drift?

A

Influenza virus
This is why every year we need seasonal flu vaccines.
HIV (during infection), enterovirus, rhinovirus

137
Q

What is antigenic shift?

A

Large change in genome, extensive variation occurs which can allow for changes in the haemagglutinin and neuraminidase proteins on the viral surface.
More common during epidemics and pandemics.
Happen every 10 years typically

138
Q

What is the most crucial RNA re-assortment needed for antigenic shift?

A

Re-assortment of the RNA segments that transcribes the mRNA responsible for haemagglutinin and neuraminidase

139
Q

What type of antigen alterations typically causes the most severe pandemics?

A

Antigenic shift impacting both surface glycoproteins

140
Q

Define sterilising and non-sterilising immunity

A

Sterilising- you completely clear the pathogen

Non-sterilising- The pathogen is not completely cleared after initiating an immune response (I.e. HIV, tuberculosis)

141
Q

Discuss the human immune response to infection with tuberculosis and how the bacterium avoids immune clearance

A

Bacterium is inhaled, and not cleared from lungs properly.
Bacterium has evolved to survive in phagocytic cells by either;
-Pumping protons out of lysozymes, reducing ability of lysozyme to create acidic killing environment
-By causing host cell to encase bacterium in calcineurin, which prevents lysosomal fusion.

142
Q

Discuss the human immune response to infection with human immunodeficiency virus and how the virus avoids immune clearance

A

HIV contains GP120 surface proteins which cause it to bind and infect CD 4 T cells.
CD 8 Cells work to kill virus once it is first detected, however, virus elicits high ability to mutate, allowing it to evade CD 8 cells, and reaching a “set point” in which the CD8 cells are responding, but the virus is evading killing.

143
Q

Recall the concept of immune enhancement of infection and discuss infection with Dengue virus as an example

A

Large destruction of endothelial cell barrier in vessels
Inflammatory cytokines produced by infected macrophages causes this breakdown and leads to fluid loss into tissue, causing oedema.
This can lead to severe illness and death

144
Q

How do macrophages work to elicit an immune response in relation to T cells?

A

Macrophage releases IL12/18 which matures Th1 cells and stimulates NK cells
Increase Th1 secretion of IFNg and TNFa (cause formation of granuloma around macrophage).
IFNg enhances macrophage phagocytosis and killing

145
Q

What is severe dengue?

A

Caused by mosquito bite
High amounts of endothelial breakdown can result in;
Severe plasma leakage leading to serious levels of oedema
Severe haemorrhage
Organ impairment (especially liver)

146
Q

What may cause severe dengue?

A

There are different serotypes, so all the same virus, but some types are more severe

147
Q

What may cause severe dengue?

A

There are different serotypes, so all the same virus, but differ slightly in sequence, meaning some types are more severe.

148
Q

What immune responses are characteristic of dengue?

A

High IgG count after first 1.5 week of infection

High levels of inflammatory cytokines (TNF- α, IL-1β, IFN-γ, IL-4/6/7/13) released by virus infected macrophages.

149
Q

What may cause complications in dengue fever?

A

Secondary infection with a different serotype may lead to antibodies that can bind the virus, but don’t neutralize the virus, and rather leads to opsonization (uptake) of virus by macrophages leading to higher cytokine release and inflammation

150
Q

Why does the serotype of dengue impact vaccinations?

A

If given a vaccine for one serotype and you haven’t been exposed to dengue, it can lead to a severe response to infection, if you have been previously infected, a vaccine can enhance the immune response and act in the protective manner that it is meant to.

151
Q

In Type 1 Hypersensitivity, what percentage of population is impacted, what age group is largely impacted, and are rates increasing or decreasing?

A

2% of population (1 in 4 in UK)
>50% of children suffer
Increasing

152
Q

In the secondary hypersensitivity type 1 response, how do antibodies cause cytokine release from mast cells?

A

Antigen binds Ab which is already bound to mast cell ->Ab cross-links, signalling activation of phospholipase A2 -> phospholipase A2 signals cytokine gene activation which results in the formation and secretion of cytokines

153
Q

What is the primary type 1 hypersensitivity response in mast cells?

A

Antigen binds Ab -> tail of Ab binds IgE Fc receptor of mast cell -> signal for degranulation occurs -> histamine, proteases, and chemotactic factor (ECF, NCF) is released via degranulation

154
Q

What is the key mediator in a type 1 hypersensitivity response?

A

IgE

155
Q

What is the key mediator in a type 2 hypersensitivity response?

A

IgG and IgM

156
Q

What is the key mediator in a type 3 hypersensitivity response?

A

IgG and IgM

157
Q

What is the key mediator in a type 4 hypersensitivity response?

A

CD 4/8 T cells

158
Q

What are the systems that can be impacted within the body by autoimmune disease?

A

Organ-specific (i.e. type 1 diabetes) or systemic (non-organ specific, i.e. rheumatoid arthritis)

159
Q

What cells are responsible for causing type 1 diabetes?

A

CD8 T cells kills the pancreatic beta cells

160
Q

How is thyroid hormone produced and what is the negative feedback loop involved in this regulation?

A

Pituitary release TSH which binds TSHR on thyroid gland which stimulates thyroid cells to produce thyroid hormone.
Feedback loop feeds back to pituitary which reduces TSH production.

161
Q

What occurs in Grave’s Disease?

A

We have made antibodies for TSHR, so when antibody binds to the receptor, it mimics TSH binding, causing overproduction of thyroid hormone.
The feedback loop is still in tact, but antibodies continue to bind and cause production of thyroid hormone.
Symptoms: bulging eyes, weight loss, fast metabolism

162
Q

What happens in Rheumatoid arthritis?

A

Immune system tries to breakdown joints. It destroys cartilage and bone at joints.
Also impacts other body systems.

163
Q

What happens in the process of transplant rejection?

A

The macrophages and dendritic cells become activated by antigens on the transplanted tissue -> migrate to lymph node -> presentation to CD 4/8 -> CD4 activates B cells to create antibodies -> Antibodies can trigger complement activation -> Antibodies can activate NK Cells -> Rejection, immune response

164
Q

What are the types of rejection?

A

Hyper-acute , acute (humeral or cellular), and Chronic

165
Q

What is Hyper-acute rejection and when does it occur?

A

Happens minutes to hours, as soon as blood is flowing through, results of antibodies in transplant tissue- shouldn’t happen in clinical setting cause blood is matched.

166
Q

What is acute rejection, and when does it occur?

A

Happens days to month following transplant
T cells (cellular) and antibodies (humeral), no immunosuppressive therapy, so immune system mounts a response. We have immunosuppressants so it is not as common now.
Cellular- T cells destroy graft parenchyma (functional tissue) and vessels by cytotoxic and inflammatory response.
Humeral- Antibodies damage graft vasculature

167
Q

What is chronic rejection and when does it occur?

A

Months following transplant
Chronic deterioration, function slowly deteriorates
Predominantly arteriosclerosis, T cell reaction and secretion of cytokines causes proliferation of vascular smooth muscle cells in transplant.
Associated with parenchymal fibrosis (connective tissue replaces parenchymal tissue, building up scar tissue, leading to sclerosis)

168
Q

After Transplantation of a first organ the most likely type of rejection will be….?

A

Acute rejection.
This is mostly preventable with immunosuppressants, but this would occur weeks-months following transplantation, and would incur all components of the immune system that would typically be involved in fighting foreign antigens.

169
Q

What innate immune cells is typically responsible for true presentation of asthma?

A

Eosinophils (activated by T cells) typically drive the true asthmatic symptoms

170
Q

What is the pathophysiology of asthma?

A

Chronic inflammation of lower airway,
Thickening of basement membrane
Increased goblet cell activity (produce mucous)
Smooth muscle hypertrophy and thickening
Epithelial shedding
Airway occlusion
Mucous infiltration of T cells, eosinophils, and others

171
Q

How can presentation of asthma differ?

A

True presentation typically involves activation of T cells, other presentations have different immune cell involvement.

172
Q

What is the role of the mucosal plug in asthma?

A

Thick, sticky mucous forms by increased goblet activity and epithelial shedding leading to occlusion of the airway

173
Q

What are the names of the different presentations of asthma?

A

Allergic Eosinophilic Inflammation
Non-Allergic Eosinophilic Inflammation
Mixed Granulocyte Asthma
Type 1 and Type 17 Neutrophilic Inflammation
Non-Eosinophilic Asthma (Paucigranulocytic)

174
Q

How is COVID related to autoimmune responses?

A

The virus causes a hyperinflammatory state, and can lead to cytokine storm.
Cytokine storm impacts your clotting system, you can go into shock, have lung injury, ultimately go into renal and later systemic organ failure, and death.

175
Q

What is a cytokine storm?

A

When immune system works to hard.
There is too much activation of immune cells that then release a lot of cytokines, draw in more immune cells and continue to over-respond

176
Q

How can viral titter impact those with risk factors and survival of COVID?

A

Low titter means you are more likely to mount a response quickly, and less intensely, so less likely to go into cytokine storm

177
Q

What is primary immunodeficieny?

A

It is genetic, and inherited

It is typically recessively inherited although can be dominant

178
Q

What is secondary immunodeficiency?

A

Secondary to other causes, like malnutrition, treatment, HIV

179
Q

How is a primary immunodeficiency typically presented?

A

Typically a recurrent infection in the young, although depends on type of cell impacted

180
Q

How would an immunodeficiency impacting B cells typically present? Include histopathological and lab abnormalities.

A

Low B Cells- more likely to suffer from bacterial infections as Ab production is impacted
Reduced serum Ig and reduced or absent follicles at germinal centres in lymph node organs.

181
Q

How would an immunodeficiency impacting T cells typically present? Include histopathological and lab abnormalities.

A

Recurrent viral and fungal infections
May have reduced T cell zone in lymphoid organs
Reduced DTH reactions (i.e. low response to poison Ivy on skin) to common antigens
Defective T cell proliferative responses in vitro to mitogens.

182
Q

How would an immunodeficiency impacting innate immune cells typically present? Include histopathological and lab abnormalities.

A

More rare
Bacterial infections
Depends on which area of innate immunity is impacted.
Perhaps low visual representation of WBCs, neutropenia, low monocytes/basophils/eosinophils (low levels will depend on disorder)

183
Q

What are combined immunodeficiencies without syndromic features?

A

Affects both T and B cells

184
Q

What is X-Linked Severe Combined Immunodeficiency Disease?

A

Caused by mutations in cytokine receptors, IL-2R gamma which is needed to bind IL-2,4,7,9,15, 21.
Therefore, don’t respond to cytokines, you cant make T cells or NK cells, cant produce sufficient antibody responses, although you can make B cells

185
Q

What is Adenoside Deaminase Deficiency SCID?

A

Depletion of B, T, and NK cells.
Metabolic enzyme needed to produce energy needed for thymocytes to produce these immune cells. The deficiency is expressed in all cells, but the thymocytes rely heavily on the enzyme to provide energy, therefore production of these immune cells is not successful
Typically recessive

186
Q

How can we treat SCID caused by ADA deficiency?

A

Take bone marrow from individual
Virus is altered to express needed gene, and gene is inserted into human gene ex vivo using viral vector so cells are genetically modified to produce Adenoside Deaminase, the altered cell is then transplanted into conditioned human.
Conditioned with chemotherapy which will encourage proliferation of their new bone marrow.

187
Q

What is Hyper IgM Syndrome?

A 
Example of CD40L deficiency
High levels of IgM, but low levels of other Igs.
We typically switch from IgM to other Abs, but in this case, we are unable to switch, meaning we become susceptible to infection. 
Fault lies in CD40 ligand molecule on T cells. CD40L aids in communication between T and B cells, so activation of B cells doesn't occur properly, therefore class switching of IgM doesn't happen.
188
Q

What is and example of a combined immunodeficiency with syndromic features?

A

FoxN1 deficiency
FoxN1 encodes for thymic epithelium, therefore, individuals are athymic, so no T cells produced, B cells are produced normally, but are unable to be activated, and therefore combined.
The syndromic feature is alopecia, we need thymic epithelium for hair production.

189
Q

What is the most common cause primary immunodeficiency?

A

Humeral Defects

190
Q

What is Bruton’s Agammaglobulinemia?

A

Rare, X-linked mutation of Bruton’s Tyrosine Kinase Gene which prevents B cells development from pro-B cell to pre-B cell stage.
Results in few follicles in lymph nodes and low serum Ig.

191
Q

What is IgA deficiency?

A

Most common immunodeficiency
Genetic
Lack of interleukins mean B cells are unable to switch IgM to make IgA, they can make IgG though
Typically asymptomatic if living in area with stable GI bacterium, as IgG can make up for IgA.

192
Q

What is Chronic Granulomatous Disease?

A

Defects in enzymes needed to make superoxide, which macrophages use for killing ingested bacteria, leading to formation of granulomas (aggregation of macrophages) in many organs.
Inherited, recessive, 1 inherited copy may make you more susceptible.
Causes swollen lymph nodes, runny nose, recurrent infection, diarrhoea
AKA Bridges-Good Syndrome

193
Q

What is an example of an autoinflammatory disorder impacting imflammasomes?

A

Familial Mediterranean Fever
Inflammasome is needed to convert Pro-IL-1 to IL-1
Inflammasome regulators are mutated, causing increased conversion and presence of IL-1,
Have developed Anti-IL-1 Abs which can be used to control the condition.

194
Q

What are potential causes of secondary immunodeficiency?

A

HIV (CD 4 depletion),
Spleen removal (decreased microbe phagocytosis)
Cancer metastases to bone marrow (site of leukocyte production),
irradiation or chemotherapy (decreased bone marrow precursors),
protein-calorie malnutrition (metabolic derangements inhibit lymphocyte maturation/function)

195
Q

What is secondary immunodeficiency?

A

Immunodeficiency caused by something other than genetics.

196
Q

1 in 20 people carry a CCR5 mutation. How does this relate to HIV?

A 
CCR5 mutation (delta 32 mutation) of the bone marrow  which means specific molecule CCR5 is impacted.
The CCR5 cant be a receptor for some strains of HIV.
197
Q

What cells release IL-8 and what is the main purpose of this cytokine?

A

Macrophages, Dendritic Cells, Endothelial Cells, T cells, Fibroblasts.
Recruitment of Neutrophils

198
Q

What cells release IFNgamma and what is the main purpose of this cytokine?

A

NK Cells, T cells
Activation of macrophages
Stimulates some antibody release

199
Q

What cells release IL-6 and what is the main purpose of this cytokine?

A

Macrophages, Endothelial Cells, T cells
Liver synthesis of acute phase proteins (response to inflammation)
B cell proliferation and Ab release

200
Q

What cells release TNFalpha and what is the main purpose of this cytokine?

A 
Macrophages, T Cells, Mast Cells
Endothelial cell (inflammation/coagulation) and neutrophil activation, hypothalamus to induce fever, liver synthesis of acute phase proteins, fat catabolism, cellular apoptosis
201
Q

How does Haemagglutinin aid in infecting cells?

A

It binds the sialyl (sialic acid) receptor sites on target cells

202
Q

How does Neuraminidase aid in infecting cells?

A

It destroys the sialyl (sialic acid) receptors that the virus was bound to, allowing new viral progeny to disassociate, and to move on and infect more cells.

UofG Medicine Question Bank 2020 (42 decks)

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