Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MICI 2100 > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

The Immune System… (3)

A
  1. Defends the body agaist infectious agents
  2. Mostly non-self reactive (but sometimes will)
  3. Is tightly regulated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Spleen

A

Important organ full of blooc, lots of lymphatic tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Distributed lymphatic tissue ex

A

Gut. has more lymphatic tissue than the rest of the body put together because we get a lot of exposure to infection here and in the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Innate vs Adaptive immune response

A

Innate - there is a problem

Adaptive - specific response to the actual infection. Targeted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Complement?

C3a

C3b

A
  • Cascade of serum proteins.
  • C3a activated mast cells (C3aR)
  • C3b activated macrophages (C3R)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

LPS in immune response

A

The surface of bacteria has many polysaccharides.

LPS stimulate the immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Neuropeptides in the innate immune response

A

Pain is a neurological response of nerve stimulation via neuropeptides.

Neuropeptides activate the immune response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CPG motifs

A

Runs of C and G in bacteria DNA that are unsual in humans.

Stimulus for inflammatory cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DAMPS

define

PAMPS?

A
  • DAMPS = Damage associated molecular patterns
  • Inflammatory cells respond to molecules associated with tissue damage
  • eg. heat shock proteins
  • LPS and CpG motifs are PAMPS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

TLR

define

what do they do (3)

A
  • Toll-like receptors
  • Pattern recognition receptors
  • Recognize patters associated with infection and inflammation; NOT specific antigen.
  • Bind PAMPS (LPS and CpG) and DAMPS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mast Cell

A
  • Found only in issue
  • Look like basophils
  • Highly involved in allergic response
  • Also invovled in immunity and inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Monocyte/Macrophage

A
  • Monocytes are in blood
  • Macrophages in tissue - specializations throughout body
  • Phagocytic early responders to infection
    • Eat bateria - though, not as well as neutrophils
  • Involved in acute and chronic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mast Cells in innate immunity

A
  • Have TLR (bind PAMPS and DAMPS)
  • Release histamine imediately and and prostaglandins over time (take longer to produce, last longer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Histamine and prostaglandins

A
  • Produced by Mast Cells
  • Increase vascular permeability and vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Classic Characteristic of Acute Inflammation?

A

Vascular permeability and vasodilation

Vascular permeability allows fluid in - many soluble proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does vascular permeability lead to?

A
  • Leak in of soluble proteins inluding antibodies and complement
  • If you have seen the bug before antibody will bind
  • Complement will bind no matter what (more if it opsonized with a antibody)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Three ways to activate complement

A
  1. Classical (via antibody)
  2. Alternative => spontaneous cleavage of C3
  3. Lectins directly activate C (less important in this class)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Functions of Complement

4 functions

If you’ve seen the bug before

If you haven’t seen the bug before

A
  1. Target lysis (bacteria, virus)
  2. Target neutralization (prevent infectivity)
  3. Enhance phagocytosis
  4. Inflammation
    • C3a is a factor that attracts immune cells to the location
  • Complement binds directly & antibody will bind, activating killing pathways that include complement and phagocytosis
  • Complement will bind directly, but antibody now can’t bind
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Macrophage

what is it?

how is it activated?

Action?

A
  • Early first responder in inflammation/infection
  • Activated by CPG, DAMPS, PAMPS, Complement
  • Takes in bacteria and kills by phagocytosis => activated macrophage to a heightened state (angry macrophage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Macrophages can only take in 1 bacterium at a time? T/F

A

F. They can take in a number bacteria at once)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Phagocytic enhancers

Opsonization for phagocytosis

A
  1. Antibody
    • Macrophages hav fc receptors that bind to antibody on the bacteria
  2. Complement - macrophages have C3 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

bacterial phagocytosis (7 steps)

A
  1. Bacteria taken in
  2. Vesicle acidification
  3. Lysosome + phagosome => phagolysosome
  4. Lysosome contains digestive enzymes and nitrogen/oxygen intermediates etc
  5. Bacteria degraded
  6. Some material isn’t fully digested in residual body
  7. Garbage put out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

NO

A

Nitric oxide

Reactive nitrogen intermediate

Very potent therefore requires IFNy to be used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cytokines and chemokines

A

Cytokines are chemical messages from one sell to another

Chemokines are small molecules that are chemotatic - Chemotatic cytokines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

TNF, IL-1, IL-8

A

Cytokines and chemokines secreted Macrophages that are Neutrophil growth factors, make more CAMs and increase the whole cal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

CAMs and step process they are involved in

A
  • Cell adhesion molecules
  • Only present at site of inflammation because of chemokines secreted by macrophages
  • Selectin on neutrophil binds to Sialyl-Lewisx
  • Neutrophil rolling, sheds selectin
  • Integrin on Neutrophil binds E selectin
  • Adhesion, Neutrophil in.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Neutrophil

A
  • Most common white blood cell
  • Important early responder in bacterial infection
  • Highly phagocytic in tissue
  • Once they get into tissue they have a phenotypic change - live longer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Netosis

A

Large strands of DNA released into local environment by exploding neutrophils

Associated cellular proteins are sticky and they get all over bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do dendritic cells become active?

A
  • Cellular garbage put out by macrophages and neutrophils
  • Takes in garbage by phagocytosis and takes it to lymph node for presentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Uptake vs movement in dendritic cells?

A

High uptake = slow movement

low uptake = high direct movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Class 2 MHC

structure

In dendritic cells

A
  • Alpha side and beta side
  • Peptide fits into beta pleated sheet “like a hotdog in a bun”
  • In a vesicle that merges with phagolysosome and minds broken down x2 peptide. Goes to surface to present to T cell area in lymph node.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

T cells

process in adaptive immunity (up to producing effector cells)

A
  • Leaders of the immune response
  • Very specific. Random gene arrangement => diversity
  1. Many T cells speak to 1 dendritic cell at once
  2. T cell receptor and CD4 recognize peptide
  3. DC sends IL-12 (cytokine) to T cell and B7 on DC binds to CD28 on T cell = co-stimulation
  4. Co-stimulation leads to transcription of IL-2 and IL-2R
  5. IL-2 stimulates IL-2R, causing T cells to clone
  6. Some clones are memory cells, others are effector cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

T cell variety jobs

A

Memory

Helper - go to B cell area

Killer - make IFNy and that stimulates macrophages to be more angry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Activation of B cells - Process

A
  1. Helper T cells go to B cell area
  2. Dendritic cell spans T cell and B cell area, secreting some bacteria pieces
  3. B cells have IgG and IgM on surface that recognize antigens and bring it in by receptor mediated endocytosis
  4. B cell is now active
  5. B cell breaks down antigen and presents on Class 2 MHC
  6. When T cell clone finds a B cell with the same antigen it sends IL-4 and co-stimulation
  7. IL-4 = B cell growth factor; stimulates B cell cloning
  8. Some B cells become memory cells, most become plasma cells that produce antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Plasma cells

  • what they do
  • structure
  • Different stimulations
A

Clones B cells programmed to make antibodies

Lots of ER bc they are making lots of soluble protein

  • IL-4 Stimulation -> IgE
  • Naturally produce IgA
  • IFNy stimulation => IgG
    *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Basic antibody structure

A
  • 2 identicle havy chains and light chains
  • Fab region on the light chains and Fc region on the heavy chains
  • Fab regions are highly diverse
  • Fc region defines the class of the antibody
  • Fc or Fab can bind first
  • Fc binds to complement leading to MAC attack (lysis of pathogen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Fc variations

A

IgG

IgM

IgA

IgE

IgD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Monomer antibodies

A

IgG, IgE, IgD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Dimer Antibodies

linkage

A

IgA

linked at Fc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Pentamer Antibodies

A

IgM

J Chain a little up from Fc tips so antibodies can pivot and show Fc region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What do antibodies do?

the big thing

the 4 things

A

They help other things kill

  1. Opsonization for phagocytosis
  2. Fix complement
  3. Block attachment
  4. Neutralize toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Opsonization for Phagocytosis

A
  • Bacteria get coated w antibody
  • Fc regions on antibody find Fc gamma receptors on macrophages and neutrophils
  • Macrophages and neutrophils will take up bacteria regardless, but the candy coating opsonizes them
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Antibody function: Fix Complement

A
  • Antibodies on bacteria surfae need to be special distance apart so the 2 can bind complement
  • 2+ Clq fragments need to be bound by antibodies for complement cascade to incur
  • Complement binding (on own or with antibody) causes formation of membrane attack complex - MAC Attack
  • Makes pore in membrane and the cell will die
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Antibody function: Block attachment

A
  • Many viruses invade by brinding to receptors on cells
  • If antibodies are bound to the virus, the virus can’t bind to cell receptor
  • Also works with some bacteria + extracellular protozoa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Antibody Function: neutralize toxins

A
  • Antibody binds to toxins and created immune complexes of toxin
  • Prevents toxin from acting bc now it can’t bind
  • Toxin can then be taken out of circulation to the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

IgG

  • how much of Ig pool?
  • structure
  • what it’s good at
  • other goo things
A
  • 70-75% of total Ig pool
  • Monomer
  • Fixes complement well
  • Opsonization for phagosytosis
  • Blocks attachment well
  • Good at neutralizing toxins
  • Passes through placenta - early protection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

IgM

A
  • 10% of total Ig pool
  • Pentamer
  • Great at fixing complement bc the fc regions are the righ distance for complement
  • Not good at opsonization bc the 5 fc regions won’t fit into fc receptor
  • Good for neutralizing toxins
  • good at blocking attachment
  • Appears early in infection, wanes quickly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

IgA

A
  • 15% of total Ig pool
  • Dimer
  • In secretions (tears etc)
  • Protects mucous membranes in lungs and gut
  • Good a blocking attachment
  • Can’t fix complement (bc to available fc receptors)
  • Can’t opsonize for phagocytosis (bc fc regions aren’t available)
  • Okay at neutralizing toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

IgE

A
  • Low levels in circulation
  • Monomer
  • Binds to Fc on mast cells
  • Part of allergic rxn
  • Not good at anything
    *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

IgD

A
  • Surface Ig
  • Monomer
  • Unknown function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

agammaglobulinemia (ivlg)

A

You get no antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Monoclonal antibodies

(3)

A

produced in lab for experiments, diagnosis and treatment

Almost always IgG bc it has the longest lifespan

Some cancer are result of expansion of B cells and diagnosis by finding monoclonal antibodies in circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Immunity to intracellular infection

A
  • Baceria is inside cell so antibodies can’t be used
  • cell mediated immunity
54
Q

Imune response to extracellular infection

A

Innate and antibody

55
Q

Extracellular bacterial infection when you haven’t seen the bug before

A
  1. Antibody won’t bind
  2. Complement will bind directly and kill due to clotting factors breaking down C3
  3. Neutrophils and macrophages wil phagocytose and kill whether or not they have seen it before us
  4. Dendritic cells will take up bits for presentation at the lymph node
56
Q

Extracellular bacterial infection when you have seen the bug before

A
  1. Antibodies will bind and opsonize for phagocytosis
  2. Complement will bind directly and lyse, but will also be opsonized
  3. Neutrophils phagocytose and kill
  4. DCs still take up bits for presentation
57
Q

Post strep glomerulonephritis

A
  • Strep brings about antibodies
  • Immune complexes of antibody and antigen form
  • Complexes get deposited in kidney glomerulus and clogs it
  • Macrophages and neutrophils recognize the candy coated thing and try to eat it but it can’t eat the whole glomerulus => frustrated phagocytosis
  • Complement gets activated
  • Destruction of kidney tissue
58
Q

Post strep rheumatic fever

A
  • IgG responds to strep antigen
  • Strep antigen looks like an antigen on heart cells
  • Antibody tricked into thinking heart cells are foreign
  • Heart valves and myocardium damaged
59
Q

Tuberculosis

A
  • Lives in phagosome and prevents lysosome fusion
  • Resists killing. IFNy from T cells helps but IFN production is also shut down
  • No effective antibody response - only response is from effector T cells
  • Effector T cells create a granuloma (tubercule) of macrophages and T cells to starve it out
  • T effector cells produce IGNy to stimulate Macrophages ot creat TNF and IL-1
  • You get a tubercule with macrophages on inside and T effector cells producing IFNy to keep it up
60
Q

Tuberculosis and HIV

A

HIV => low T cell levels => can’t continue tuburcule => tuberculosis wins

61
Q

Listeria

A
  • Gets into phagosome, shuts down lysosome fusion and gets out
  • Motile so it can infect other cells
  • Presented on class 1 MHC to outside, so now listeria antigen is on cell surface
  • Cytotoxic T cell sees this and kills the cell
62
Q

Treetop disease

description

How is the mechanisms advantageous for the virus?

A
  • Catipillar feeds on contaminated foliage
  • Enhanced locomotor behaviour
  • Virus climbs to top of tree and liquifies
  • Enhances spread of the virus
63
Q

How does treetop disease virus cause the climbing phenotypes?

A

Virus disrupts hormones so catipillar climbs as it would during moulting

64
Q

Are viruses always harmful?

A

No. Many are beneficial. Only something result in disease (different than infection).

65
Q

Study of viruses has potential to (2)

A
  1. Aid disease prevention
  2. Help our understanding of the fundamentals of host biology
66
Q

Where are viruses?

A

Everywhere. Air, food, surfaces, genomes

67
Q

How many herpes viruses infect most people?

A
  1. Lifelong infection
68
Q

How do viruses become part of the human genome?

A

They must infect germ cells

69
Q

Integrated ancient viruses (2 examples)

A
  • Koala retrovirus, cause of koala AIDS is currently becoming endogenized
  • Virus on chromosome 7 essential for placenta development
    • Syncytin is a captured viral gene essential for the semipermeable layer
70
Q

Know: Viruses co-evolve with their host through an exchange of genetic information

A
71
Q

Ancient ________ and __________ infections in egyptian mummies

A

poliovirus and small pox

72
Q

Define virus

3 further defining factors

A

submicroscopic, obligate intracellular parisite

  • produced from preformed parts
  • Do not grow or undergo division themselves
  • lack genetic information for generation of metabolic energy and protein synthesis.
73
Q

Are viruses alive? 1 theory

A

Alive while inside and when outside they are just complex assemblages of metabolically inert chemicals

74
Q

Electron microscopy

A

(review diagram)

  1. pure populations of viruses or cells infected with viruses can be visualized
  2. ultrathin sample embedded on copper grid
  3. Chamber has a vacuum
  4. Electrons pass through sample and are detected with digit camera/phosphor screen
  5. Staining with heavy atoms necessary to diffract electrons and see structures
75
Q

Virus Particle

A

molecular structures that package viral genomes in infected cells and transmit them to new host cells

76
Q

Virion

define

must (5)

these explain:

A

A complete, infections virus particle (many defective particles are made)

  1. Correctly assembled
  2. Escape the cell for which they are made
  3. Withstand the EC environment
  4. Attach to and enter a host cell
  5. Releast the viral genome (into host cell)

Explains why there is such diversity in viruses

77
Q

bacteriophage t4 (musts for virus)

herpes simplex virus type 1 (action)

A
  • Bacteriophage = virus that infects bacteria. Bacteria are all thoughout our body. Has to infect, replicate, withstand EC env
  • Herpes infects oral epithelial cells => cold sores. Travels through neurons to tri. ganglia => achieves latency
78
Q

Capsid

traits - structure (3)

Job (3)

why are the jobs important? (1)

A
  • Rigid, symmetrical container for viral genomes
  • metastable
  • Protein subunits are multipily redundant - many copies called capsomers
  • Participate in infection
  • Protect genome from
    • physical damage (mechanical forces)
    • Chem damage (IV radiation)
    • Enzymatic damage (cell nucleases)
  • Damage to 1 or more capsomer may make virus dysfunctional or innoculous
79
Q

4 virus morphologies (2 most common)

A
  1. helical **
  2. icosahedral **
  3. enveloped
  4. complex
80
Q

Helical capsids

features

what kind of genome do they usually hold?

how do these bind to viral genome?

What governs length and diameter?

A
  • look like straws, simplest
  • not human
  • Single type of capsomer stacked around central axis to form a helical structure
  • Hollow centre of helix contains viral genome (usually ssRNA)
  • Electrostatic interactions. RNA -ve backbone, G, A, Hist +ve
  • Amount of RNA
81
Q

Icosahedral Capsids

shape

why do so many viruses take this shape?

A
  • 20 faces
  • animal and plant viruses, many enteric (gut) viruses
  • Strength - resistance to shear forces
  • Tight packaging of genome (sm SA for lg vol)
  • Genetic economy - can be built from a few repeating subunits
82
Q

How do we decontaminate surfaces with icosahedral capsids

A

Bleach. Will damage capsids.

83
Q

Enveloped Viruses

A
  • Host derived lipid envelopes protect viruses and contain both viral and host glycoproteins
    • viral glycoproteins are made by host
  • Space in between the membrane the capsid is the tegument
84
Q

Glycoproteins

A
  • Important for enveloped viruses that contain host and viral glycoproteins
  • Viral glycoproteins are made by host
  • Many host integral membrane proteins are glycosylated
    • N-Glyc - sugar added to N on asparagine
    • O-Glyc - sugar added to serine/threonine
85
Q

Influenza Envelope

A

Has host glycoproteins incorporated into its envelope

HA, a lectin that binds sialic acid receptor to get into cell

NA, enzyme that cleaves sialic acid allowing progeny viruses to be released from the host cell

86
Q

Can integration of host proteins confer an advantage to the virus?

A

Yes. Better invasion

87
Q

How does glycosylation of virus proteins affect immune regulation

A

Hides viral proteins because host membrane proteins are commonly glycosylated.

Sugar decorations block antibody binding sites.

88
Q

complex virus - bacteriophage t4

structure

genome

A
  • ocosahedral head containing dsDNA
  • helical tail (empty)
  • Hexagonal base plate
  • Protuding protein tail fibres
89
Q

Binding of bacteriophage t4 to e coli process

A
  1. long tails fibres recognize membrane protein OmpC or LPS of E. coli - REVERSIBLE
  2. 3+ long tail fibres bound => conformational change in baseplate; short tail fibres extend, bind IRREVERSIBLY to core region of host LPS
  3. Contraction of tail sheat + penetration of outer membrane
  4. T4 lysozyme degrates gram peptidoglycan layer
  5. Inner membrane degraded
  6. Phage DNA delivered to cytoplasm
90
Q

Viral infection of Eukaryotic cells

A
  1. Attachment
    • REVERSIBLE electrostatic interactions
    • IRREVERSIBLE tight interactions with receptors
  2. Penetration (pH dependend) by either
    • (enveloped) membrane fusion at the cell surface
    • receptor mediated endocytosis
  • specificity of these interactions defines the host range of the virus
91
Q

Bacteriophage capsid morphology

A

complex

92
Q

genome type of tobacco mosaic virus

A

ssRNA

93
Q

What type of genome can icosahedral capsids hold?

A

any kind

94
Q

How does influenza virus enter the cell?

A

Receptor mediated endocytosis with sialic acid receptor

95
Q

Sialic acid is ubiquitous on cell surfaces. What does this mean for influenza virus tropism?

A

By binding sialic acid, the virus is able to gain entry to a number of cell types

96
Q

HIV mechanism of entering the cell

A
  1. Initial attachment of HIV envelop gylcoprotein to cell surface glycoaminoglycans - REVERSIBLE
  2. Stable binding to protein receptor, CD4 - IRREVERSIBLE
  3. Binding co-receptor - IRREVERISBLE
  4. Conformational change causes exposure of fusion peptide (hydrophobic)
  5. Fusion. Viral and cell membranes mix
  6. Viral genome deliviered into host
97
Q

Ebola virus cell entry

A
  • Host cell takes in Ebola by macropinocytosis
  • Stable binding to intracellular receptor
  • Membrane fusion + RNA release
98
Q

Why do delilivered viral genomes travel to the nucleus?

exceptions?

A

That’s where the polymerases are - so virus can replicate using host machinery or integrate its genome into the host

It would need its own mRNA, own polymerases

99
Q

Lytic Replication

A

Fast growing viruses

100
Q

Latency

Lysogeny

A

When viruses establish a dormant state in a host cell\

Called lysogeny in temperate phages

101
Q

How do latent infections maintain long term persistence in their hosts?

A

The virus isn’t replicating so it is relatively invisible to the immune system. Isn’t producing any proteins to be recognized as antigens.

102
Q

What consequences does latency have for immune surveillance?

A

A passive mechanism for integrating genome into host

allows virus to pick an optimal time to replicate

103
Q

How is latency achieved?

A

Integration into host genome (retroviruses)

long term retention of viral episome - the virus can allow the genome to be associated with the host chormosome - can divide into daughter cells

104
Q

episome

A

a type of latency where the viral genome latches onto host chromosome and can be divided into daughter cells as such.

105
Q

How is latency advantageous?

A
  1. Carriage of the viral genome through many cycles of cell division (using host polymerases + nucleotides) => energetically favourable
  2. Evasion of immune surveillance
    1. few to no protens made (only ones made promote cell cycle, antigen presentation, and undermine antiviral response)
106
Q

Bacteriophage Infection

lytic?

Course

A

lytic infection

  1. Penetration => viral DNA delivered to cytoplasm
  2. Host gene expression arrested => host DNA/RNA degredation
  3. Viral enzyme synth (~5 mins)
  4. Viral DNA replication (~10 mins)
  5. Formation of new viral particles (~12)
  6. Lysis of host and release of viral particles (~30)
107
Q

Bacteria: Defense against viruses

explain

real life uses

A

Restriction endonuclease

  • Cuts DNA at restriction sites in foreign DNA
  • Makes 2 incisions on sugar phosphate backbone
  • Diff bacteria make diff restriction enzymes
  • Host DNA protected bc it is heavily methylated
  • useful for gene cloning and forensics (distinct digestion pattern for diff human DNA samples)
  • Can lead to recombinant DNA
108
Q

Central Dogma

how to viruses change it?

A

DNA dependent DNA polymerase uses dsDNA as template to make more dsDNA

RNA polymerase uses dsDNS as template to make + sense RNA

Ribosomes translate +RNA into amino acid chain

Viruses can to reverse transcription

109
Q

What sort of information is encoded in the viral genome?

A
  1. replication of viral genome
  2. assembly of packaging genome into viral particles
  3. Regulation and timing of replication cycle
  4. Modulation of host defenses
  5. Spread to other cells + hosts
110
Q

What kind of information isn’t encoded in viral genomes

info for.. (3)

A
  1. complete protein synthesis
  2. proteins incocled in energy production or biosynthesis
  3. Centromeres, telomeres
111
Q

+ssRNA virus translation location

how do they replicate their genome

generate

A
  1. Directly translated in the cytoplasm by hot ribosomes because they resemble mRNA
  2. viral RNA-dependent RNA polymerase
  3. polyproteins that get cleaved by viral or host proteases into viral proteins
112
Q

Why to proteases make good drug targets?

A

If they don’t work the polyproteins can’t be cleaved into viral proteins

113
Q

For the virus, are there any disadvantages to relying on host proteases?

A

The cell would have control over the genome

114
Q

Why would the genes for RNA dep RNA polymerase be transcribed at the 3’ end

A

There will be multiple rounds of protein synthesis. If it is at the 3’ end it is at the perfect position to lay down another strand right away

115
Q

Antiviral defense for Eukaryotes?

A

Immune system is triggered by Pattern Recognition Receptors that recognize foreign molecular patterns such as dsRNA and 5’-triphosphate RNA

116
Q

How do viruses replicate their genomes? (2)

A
  1. Confrom to host machinery (use host ribosomes)
  2. Alter host machinery for own use
117
Q

All roads of virus genomes lead to….

A

mRNA

118
Q

Poliovirus

  • method of spread

symptoms

structure

entry

A
  • water bourne - mostly fecal-oral spread
  • 95% infections asymptomatic, 5% lead to flu-like symptoms
  • 1% goes to CNS, replicates in motor neurons and leads to paralysis
  • Icosahedron - can survive gut acidity
  • Enters cells my receptor mediated endocytosis, +ssRNA
  • Normal function of receptor is epithelial cell-cell contact
119
Q

Poliovirus vaccines

A
  • Salk - Inactivated polio vaccine
    • formalin killed
    • injection
  • Sabin - oral polio vaccine
    • Attentuated by temp of growth
    • Gives mucosal immunity
120
Q

Polio genome replication

A
  • +ssRNA => dsRNS replicative intermediate => +ssRNA progeny genomes
  • co-translational - polyprotein cleavage and processing at same time
121
Q

Viral genome processing sequence

catalyzed by?

A

intial genome -> replicative intermediate -> progeny genome

RNA-dependent RNA polymerase

122
Q

Hep C intial genome

A

+ssRNA

123
Q

Flu initial genome

A

-ssRNA

124
Q

Ribavirin

A
  • Phosphorylated and activated in cells
  • Incorporated into viral RNA during genome replication
  • Base analog for A and G - can pair with U or C
  • Causes potentially lethal hypermutation
125
Q

Herpes Simplex Virus

genome

capsid

How does it express its genes?

How does it express its genes?

Where does this happen in the cell?

A
  1. dsDNA virus
  2. Enveloped icosahedron
  3. Host RNA polymerase
  4. Viral DNA-dep DNA polymerase
  5. Nucleus, bc it depends on host RNA polymerase
126
Q

Acyclovir

A
  • Herpes treatment
  • Relies on specific enymatic activity
  • Herpes phosphorylates drug 3000 times better than host
  • Acyclovir triphosphate incorporates into viral DNA terminating chain
  • Inhibits herpes DNA polymerase
  • Looks like G
  • Host cell hurt too - oh well
127
Q

HIV entry and mechanism inside

A
  1. Virus engages primary receptor and co-receptor => infection intialized
  2. Fusion => virion contents dumped
  3. RNA is virus reverse transcribed into dsDNA
128
Q

How to retroviruses express their genes and replicate their genomes?

A

Reverse transcription

dsDNA from reverese transcription is longer than the RNA that went in

129
Q

Zidovudine

why doesn’t it block host polymerase?

A

= AZT

  • An analog of T
  • Phosphorylated and incorporated into growing viral dsDNA
  • Chain terminator
  • It does, just has way higher affinity for HIV reverse transcriptase
130
Q

Viral evolution with reverse transcriptase

A
  • Reverse transcriptase is error prone
  • 1 mistake every 10 000 so one mistake every genome
  • Produces viral quasispecies
  • Quick evolution
  • Why vaccines don’t work
131
Q

Ebola route of transmission

A

body liquids exchange

132
Q

4 symptoms of acute inflammation and their causes (look these up)

A
  1. Redness
  2. swelling
  3. pain
  4. heat

MICI 2100 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions