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any final confusions Flashcards

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1
Q

dsDNA class 1 viral replication

A

replication in host nucleus, using DNA-dependent RNA polymerase to make viral mRNA
no other enzymes required

adenovirus, herpesvirus

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2
Q

ssDNA class 2 viral replication

A

replication in nucleus
host DNA polymerase converts ssDNA —> dsDNA
host RNA polymerase makes mRNA

no viral polymerase needed, only host enzymes

parvovirus

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3
Q

dsRNA class 3

A

host cells cannot read dsRNA directly

replication:
1. virus brings own RNA dependent RNA polymerase (RdRp)
2. RdRp copies negative strand into positive sense mRNA so can be translated now

virus must bring RdRp inside capsid when infecting

rotavirus

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4
Q

+ ssRNA class IV viral replication

A

postive sense RNA is same as mRNA so read directly

viral genome acts as mRNA so translated into viral proteins, making viral RdRp first to replicate the RNA genome from that

poliovirus and covid

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5
Q
  • ssRNA class V viral replication
A

negative sense is complementary to mRNA so cannot be read directly

virus brings own RdRp into host cell
RdRp copies -RNA into + mRNA for translation

influenza

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6
Q

+ssRNA class VI viral replication

A

viral reverse transcriptase copies RNA into DNA
DNA integrates into host genome via integrate enzyme
host RNA polymerase makes mRNA and new genomes

HIV

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7
Q

dsDNA gapped class VII viral replication

A

genome is partially double stranded DNA

host repairs gaps to make full dsDNA
host RNA polymerase transcribes

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8
Q

teichoic acid

A

gram positive bacteria

  • involved in adhesion/colonisation
  • inflammatory response
  • activation of complement and release of cytokines

detected by TLR2
highly antigenic - PAMP

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9
Q

LPS

A

gram negative bacteria

Lipid A - endotoxin, causes sepsis, high fever
O-antigen - highly antigenic, helps evade immune detection
immune activation, causes inflammation cytokines production like TNF-A IL-6
protect against antibiotics and host defences

detected by TLR4

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10
Q

IgM

A

lowest affinity as present on naive B cells, before affinity maturation (somatic hypermutation)
pentamer
activates complement system effectively
opsonisation

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11
Q

IgD

A

not fully understood
with IgM on naive B cells
monomer

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12
Q

IgG

A

most adundant antibody
monomer
can cross placenta to provide passive immune city to fetus
complement activation, opsonisation and ADCC

neutralisation of pathogens

FcyR on macrophages

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13
Q

IgE

A

allergic responses, defence against parasites
monomer
key role in mast cell and basophil activation to release histamines
opsonisation

FceR on mast cells

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14
Q

IgA

A

mucosal immunity
monomer in body and dimer in secretions
bad at opsonisation
least inflammatory causing
neutralisation effects - protect mucosal surfaces from infection

FcaR - macrophages

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15
Q

somatic hypermutation

A

this is affinity maturation
occurs in germinal centres of LN

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16
Q

somatic recombination

A

this is antigen specificity Fab region via VDJ recombinase

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17
Q

ADCC

A

antibodies bind to pathogens/ infected cells

the FC region binds to receptors on immune effect cells like NK, macrophages etc

this causes immune cell to activate and release toxic molecules that can induce cell death to target cell or phagocytosis

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18
Q

NK cells

A

innate
killing infected cells
recognise stressed or infected cells via an imbalance in activating and inhibitory receptors - like down regulation of MHC 1
kill target cells via perforin and granzymes to cause apoptosis
also use ADCC

secrete IFN-Y TNF-a
activated by type 1 interferons

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19
Q

neutrophils

A

innate cell
recognise pathogens via PRRs
kill pathogens through phagocytosis, ROS, lysomes, defensives
use NETosis to trap and kill pathogens outside cell

secrete - IL-1, TNF-A
activated by - IL-1 TFN-A IL-8

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20
Q

mast cells

A

innate , involved in allergy response
sweep and weep
release histamine, cytokines to cause inflammation
activated by IgE antibodies binding, cross linking activates mast cells to degranulate

secrete - histamine, TNF-A IL-4
activated by - IGE, C3A C5A IL-1

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21
Q

basophils

A

innate cells, allergies response
similar to mast cells, but less abundant and understood
IgE bind to degranulate

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22
Q

eosinophils

A

innate
involved in combating parasites and allergens
release toxic protein to damage parasites and cytokines

secrete - IL-4 IL-5 IL-13, MBP
activated - IL-5 IGE

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23
Q

macrophages

A

innate cells
phagocytosis and APC
recognise via PRRS
present antigens MHC2 to T cells

activated - IFN-Y IL-4 TNF-A C5A
SECRETE - IFN-Y TNF-A IL-1 IL-6 IL-10

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24
Q

CTLs

A

adaptive immune cells
CD8+ to kill infected cells and cause apoptosis
recognise via MHC 1
release perforin and granzymes to cause death
or FAS/FASL

ACTIVATED - IL-2 IL-12 IFN-Y
SECRETE - IFN-Y TNF-A

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25
Th cells
adaptive cells coordinating immune response and activating other cells Th1 activate macrophages and CTLs to fight intracellular pathogens Th2 help B cells product IgE to play role in allergy response and helminth infections Th17 produce IL-17 to contribute to inflammation in autoimmune and fungal infections Tfh help B cells product antibodies
26
Treg cells
adaptive cells maintaining immune tolerance and prevent autoimmune diseases suppress the immune system using IL-10 and TGF-B
27
efficacy formula
(attack rate unvaccinated - attack rate vaccinated) / (attack rate unvaccinated)
28
absolute risk reduction formula
antibiotic group % - placebo group %
29
CFU and PFU
number of colonies/ dilution factor x vol in ml or x 1/dilution
30
bacteria doubling time
(t2-t1) ÷ log2(N2/N1)
31
CRP
C-reactive protein produced by liver in response to inflammation - acute phase reactant infection and inflammation marker opsonisation complement activation elevated CRP levels indicate infection or injury, as high inflammation
32
live attenuated vaccine
live pathogens that are weak, still replicate in host cells strong immune response for humeral and cell mediated long lasting efficient risk for infection as can reverse storage issues, need cold chain storage
33
VLPs vaccines
mimic structure of virus but do not have genetic material, non infectious, do not replication non-infectious strong immune response- antibody response no risk of infection or disease limited to certain viruses multiple doses required
34
vector vaccines
deliver genetic material from pathogen to body strong immune response for both humeral and cell mediated versatile no live virus replication pre-existing immunity to vector side effects
35
subunit vaccines
contain specific pieces of pathogen rather than entire organisms safe targeted immune response no risk of infection need for adjuvants mutliple doses required
36
killed whole organisms vaccines
vaccines from whole pathogens that are killed or inactivated by heat, chemicals or radiation, cannot replicate safe simple to produce weaker immune response need boosters multiple doses adjuvants
37
units
nm = 10-9 x 1000 to next one um = 10-6 mm = 10-3 cm = 10-2 m = 10^1 km= 10^3
38
Th1
crucial against intracellular pathogens, can cause chronic inflammation cell mediated response activating macrophages secrets IFN-Y TNF-A differentiation drive by IL-12
39
Th2
crucial against extracellular pathogens lie helminths, parasitic and allergic response B cell activation, especially into IGE eosinophil recruitment secretes - IL-4 IL-5 IL-13 differentiation driven by IL-4
40
Th17
defend against extracellular bacteria and fungi, specifically at mucosal sites secrete IL-17 (recruit neutrophils) IL-21 IL-22 (tissue repair and barrier integrity differentiation driven by IL-6 TGF-B mucosal immunity
41
Tfh
help B cells during formation or germinal centres, needed for antibody production, class switching and activation forming memory cells humoral immunity secrete IL-21 IL-4 differentiation driven by IL-6 IL-21 BCL-6
42
entry of enveloped viruses
attachment with viral glycoproteins fusion with host membrane - changes in viral glycoproteins often due to pH changes - direct fusion or endocytosis in endosome
43
uncoating of enveloped viruses
direct fusion will release viral capsid into cytoplasm and lysosomes degrade eadosomal uncoating, virus undergoes acidification in endosome to release viral genome
44
entry of non enveloped viruses
attachment with capsid proteins to host membrane direct penetration into cell or endocytosis translocation of nucleocapsid into cytoplasm
45
uncoating of non enveloped viruses
direct penetration, capsid undergoes conformation change to release genome itself endocytosis, acidification occurs in endosome to do then
46
mRNA vaccines
mRNA is delivered in lipid nanoparticles LNPs, act as a template for host cell ribosomes to product antigen, in cytoplasm antigen is then presented onto surface and cause immune response of cell and humeral pros speedy development no live virus no risk of integration into DNA broad applicability cons storage and stability side effects potential unknown long term effects
47
antigen drift
small gradual changes - point mutations change in antigens over time - seasonal epidemics influenza does this
48
antigenic shift
sudden major change in viral genome to form a new virus train, often from reassortment of genetic material cause pandemics due to lack of any previous immunity in the population spanish flu
49
viral infections trigger cell-mediated immune response
increase in CTLs, NK, DC but also B cells for neutralisation
50
parasitic infections promote innate and adaptive immune responses, often Th2 (type 2)
increase in eosinophils, basophils, mast cells, macrophages, and Th2 cells
51
Bacterial infections trigger innate and adaptive immune response
increase in neutrophils, macrophages, DC, Th1, mast cells
52
fungal infections increase Th1 immune response
increase in macrophages, neutrophils , Th1 Th17 and DC
53
autoimmune infections or inflammatory conditions cause elevation in...
T cells - CD4+ B cells macrophages neutrophils
54
classical complement pathway
activated by antigen-antibody complexes - C1 binds to FC portion of antibodies that are bound to an antigen - cascade to activate C3 - cleavage of C3 = C3a C3b adaptive immune response
55
lectin complement pathway
activated by lectins (like MBL) binding to conserved sugar patterns on pathogen surface - lectures binds to sugar, activating it to activate C3 - cleavage of C3 to C3a and C3b innate
56
alternative complement pathway
continuously active at low levels, and can be rapidly activated when immune system detects a pathogen - C3b binds to a pathogen (amino acid or hydroxyls found on surface) to innate cascade of C3 cleavage and amplification - important for amplifying the complement response especially in absence of antibodies innate
57
complement opsonisation
C3b binds to surface of pathogens, marking for macrophages and neutrophils phagocytosis cells have C3b receptors enhances efficiency of phagocytosis, increasing it - especially helpful for encapsulated bacteria where phagocytosis is difficult
58
complement inflammation
C3a C5a trigger inflammations by binding to receptors on immune cells promote vasodilation, increased vascular permeability and chemotaxis - recruitment of cells to infection site
59
membrane attack complex complement
lysis of pathogens C5b binds to pathogens surface to create a pore disrupts cell membrane leading to osmotic lysis - particularly effective against gram negative bacteria
60
immune checkpoints
regulatory pathways that maintain self-tolerance and mediate the duration and amplitude of the immune response so it doesnt go on for too long and minimise damage these checkpoints have receptors on T cells that deliver inhibitory signals when engaged - CTLA-4 -PD-1
61
CTLA-4
expressed early in T cell activation cause down regulation to T cells and promote Tregs blocks co-stimulation
62
PD-1
expressed after activation, lead to T cell exhaustion, inhibits downstream TCR signalling
63
immune checkpoints and cancer
tutors can exploit these checkpoint pathways to suppress anti-timor immunity, expressing on timor cells PD-L1 which binds to PD-1 on T cells to inhibit function can have monoclonal antibodies that are inhibitors of this that block CTLA-4 and PD-1 to prevent this
64
Hard for the Innate Immune System to Detect: Needs Adaptive Help
pathogens that evade pattern recognition or overwhelm early defenses. Lack or masking of PAMPs - hiding or low Intracellular pathogens: High antigenic variation or mutation:
65
Hard for the Adaptive Immune System to Detect: Needs Innate Help
These pathogens prevent or subvert antigen presentation or suppress adaptive responses disruption of antigen presentation: T cell-independent antigens:don’t strongly activate T cell Rapid replication or overwhelming infection: adaptive is too slow

MII2 (30 decks)

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