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Immuno > Unit 3 > Flashcards

Unit 3 Flashcards

1
Q

Activation of the humoral immune system can cause changes in antibody structure. What are the changes and what is the purpose of them?

A

affinity maturation and heavy chain can change structure (isotype switching). Purpose is to produce higher affinity antibodies

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2
Q

What are the 4 ways antibodies help fight infections?

A

neutralization, opsonization, antibody-dependent cellular toxicity, and complement activation

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3
Q

What is neutralization?

A

blocks viral binding sites so viruses longer interact and infect other cells

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4
Q

How does opsonization work?

A

all phagocytes have many different types of receptors allowing them to recognize, bind, and phagocytose microbes

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5
Q

What is antibody-dependent cellular cytotoxicity (ADCC)?

A

Fc gamma receptor binds to constant region of IgG. IgG antibodies stuck on surface. NK cells has gamma receptors that bind to IgG antibodies and kills the IgG

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6
Q

What is phagocytosis and how is it involved in complement activation?

A
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7
Q

What is inflammation and how is it involved in complement activation?

A
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8
Q

What is microbe lysis and how is it involved in complement activation?

A
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9
Q

What is the classical pathway and how is it involved in complement??

A

starts with antibodies bound to an antigen

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10
Q

What is the alternative pathway and how is it involved in complement?

A

random separation of c3a and c3b. C3b sticks to microbial surface and get same pathway as classical

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11
Q

What is the lectin pathway and how is it involved in complement?

A

mannose-binding lectin binds to mannose (PAMP). Sticks to surface of microbes and activates complement pathway

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12
Q

What happens if we recognize self-antibodies?

A

causes autoimmune disease

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13
Q

How can we take advantage of ADCC for therapeutic approaches?

A

antibodies can be used to target and kill cancer cells

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14
Q

NK cells have what kinds of receptors

A

gamma receptors

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15
Q

How are NK cells different from CD8 T cells?

A

NK cells are innate and do not have a T cell receptor and instead bind to constant region of IgG antibodies and kills infected cells.

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16
Q

antibodies are good for what three purposes?

A

blocking microbes from getting through epithelial barrier, block binding of toxin to cellular receptors, and prevent infection of cells

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17
Q

What is the main function of antibodies?

A

coat proteins to make it easier for phagocytes to eat up

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18
Q

What are the two main differences between innate and adaptive immunity?

A
  • Innate: Nonspecific, responds quickly

- Adaptive: Specific, responds slowly the 1st time

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19
Q

What are the three ways complement activation is activated?

A

increases phagocytosis, recruitment of other cells, and osmotic lysis

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20
Q

What are the three ways of regulation of complement activation?

A

C3a and C3b, C5a and C5b, and membrane attack complex

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21
Q

What may happen if complement is dysregulated?

A

excessive inflammation

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22
Q

What pathway of complement requires antibody for activation?

A

classical pathway

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23
Q

What results in the activation of the classical pathway of complement?

A

antibody bound to antigen

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24
Q

What parts of complement are responsible for inflammation (recruiting immune cells to the site of infection)?

A

C3a and C5a

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25
Q

Is complement part of the innate or the adaptive humoral immune response?

A

innate

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26
Q

Complement activation results in inflammation, lysis of microbes and __________?

A

increased phagocytosis

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27
Q

What is the purpose of opsonization?

A

to make pathogens easier for phagocytes to recognize, bind and internalize

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28
Q

What cell type is responsible for antibody-dependent cellular cytotoxicity (ADCC)?

A

Natural Killer cells (NK)

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29
Q

How do phagocytes recognize antibody on microbes?

A

FcGamma receptors

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30
Q

Check yes or no for each of the following boxes from A to D (check - yes, x - no)

A
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31
Q

How (and why) do immune responses differ depending on the tissue involved?

A
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32
Q

How (and why) do immune responses differ depending on the tissue involved?

A
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33
Q

Mast cells play what role in mucosal immunity?

A
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34
Q

Macrophages and DCs play what role in mucosal immunity?

A
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35
Q

B cells (IgA secreting plasma cells) play what role in mucosal immunity?

A
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36
Q

What types of T cells are involved in mucosal immunity?

A

CD8 that live in epithelial barrier that can respond to virally infected cells and in the LP/PP, there are CD4 effector, memory, and regulatory T cells

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37
Q

What are the two main types of CD4 effector T cells that are involved and what role do they play in mucosal immunity?

A

Th17 cells which help to main epithelial barrier function and Th2 cells which enhance fluid and vomit out any parasites

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38
Q

What is the difference between innate and adaptive molecules?

A
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39
Q

How is mucosal immunity regulated?

A

TLRs and NLRs of intestinal epithelial cells detect PAMPs and allow commensal bacteria to not be stimulating the response. Regulatory T cells abundant in epithelial tissues control and dampen inflammatory response.

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40
Q

Why do we have regional immunity?

A

some areas are more vital to our survival than others

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41
Q

What is the general anatomical organization of epithelial barriers?

A
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42
Q

How does a regional immune system differ from the whole immune system?

A
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43
Q

Where are epithelial barriers found?

A
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44
Q

What are the three immunological properties of the GI tract?

A

mucus layer, antibiotic peptides, and secretory IgA

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45
Q

What is the structure of the gastrointestinal system?

A
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46
Q

How does the gut prevent infections?

A
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47
Q

Epithelial cells are joined by what?

A

tight junctions

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48
Q

Epithelial cells are joined by what?

A

tight junctions

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49
Q

What are the six chemical barriers to pathogens?

A

Fatty acids in skin, low pH, pulmonary surfactant, enzymes in tears and saliva, defensins, and normal microbiota

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50
Q

What is the function of defensins?

A

Prevent establishment of bacteria

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51
Q

What is the function of defensins?

A

Prevent establishment of bacteria

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52
Q

Secretory IgA is a _____?

A

dimer

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53
Q

How is IgA secreted?

A

After affinity maturation and isotype switching, constant region of IgA binds to Poly-Ig receptor. Poly-Ig receptor chaperones IgA molecule across epithelial barrier where it’s released into the lumen

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54
Q

What is the role of Peyer’s Patches in adaptive immunity?

A

provide a mini lymph node where B and T cells interact within the tissues. B cells are activated from IgM to IgA without T cell help

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55
Q

Commensal microbiome are necessary for what?

A

proper immune development

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56
Q

Commensal microbiome are required for what?

A

innate immune responses in the gut

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57
Q

Commensal microbiome influence _____ and ________ adaptive immune responses

A

local; systemic

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58
Q

How does the immune system balance immune defense against intestinal pathogens vs. tolerance to food and commensals?

A

Treg cells

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59
Q

What is the dominant secreted immunoglobulin in reproductive tract immunity?

A

IgG

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60
Q

Reproductive tract immunity is regulated by what?

A

sex hormones

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61
Q

What is immune privilege?

A
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62
Q

What four sites are immune privileged and why?

A

brain, eyes (visually oriented), spinal cord, and sex organs (pregnant uterus and testicles)

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63
Q

How is immune privilege maintained?

A
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64
Q

What happens if immune privilege is broken?

A
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65
Q

What are the benefits/risks of this immune privilege?

A
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66
Q

What three consistent strategies for immune tolerance?

A

physical barrier, Tregs, and regulatory cytokines

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67
Q

What are the three structural features of the eye in ocular immune privilege?

A

Retinal pigment epithelium, reduced MHC expression, and avascular and alymphatic cornea

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68
Q

What are the two reasons testicles need to be immune privileged?

A

limit inflammation that may impair male fertility and many self antigens in adult testis are first expressed at puberty

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69
Q

How does testicular immune privilege work?

A
  1. blood-tissue barrier to keep out immune cells
  2. hormones (androgens) –> low inflammation via macrophages
  3. Local regulatory cytokine production
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70
Q

What is the function of complement regulatory proteins?

A

to ensure complement cannot activate in specific localized areas

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71
Q

CTLA4 is a regulatory protein that binds to

A

B7

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72
Q

What prevents naive cells from becoming inflammatory T cells and activation of neighboring T cells?

A

IDO

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73
Q

What macrophages develop in the brain?

A

microglia

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74
Q

What are the consequences of losing immune privilege?

A

inflammation in immune privileged sites

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75
Q

What is sympathetic ophthalmia?

A

trauma hits the eye releasing some self antigens causing antibody production and blindness to both eyes

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76
Q

What is a situation when immune privilege is detrimental to health?

A

viral encephalitis

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77
Q

What is the tumor micro-enviornment (TME)?

A

tumor-associated macrophages produce regulatory cytokines inhibiting activation of NK cells and T cells to keep the immune system from responding to those macrophages

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78
Q

What is the metabolic pathway that leads to regulation of immune cells in pregnancy and cancer?

A

tryptophan

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79
Q

What are the tolerance-inducing receptors?

A

Fas-FasL, TRAIL-TRAILr, and PDL/PDL1

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80
Q

What are the basic mechanics of the immune response to SARS-CoV2?

A

virus particles infect mucosal epithelial cells via ACE 2 receptor. Innate response is activated through DAMPs and PAMPs released by infected cells. Innate response releases cytokines and leads to the adaptive immune response

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81
Q

What are the 3 main ways immune mechanisms interact with the CNS?

A

coagulopathies and thrombus formation, direct viral invasion of neurons and cerebrovascular endothelial cells, and overproduction of cytokines

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82
Q

What are the CNS related outcomes of the immune response to SARS-CoV2?

A

viral replication causing neuron injury, higher BBB permeability, increase in adhesion molecules, and decrease in tight junction proteins

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83
Q

What are some examples of recent treatment approaches?

A
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84
Q

Type I IFN is a key _______ response

A

antiviral

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85
Q

What is a cytokine storm?

A

overproduction of inflammatory cytokines

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86
Q

What is the adaptive response to SARS-CoV-2?

A

WBC with viral antigen displayed on surface. Antigen presented to helper T cells activating cytotoxic T cells and B cells to produce antibodies

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87
Q

How does coagulopathy work?

A

SARS-CoV-2 activates complement. C3a and C5a recruit neutrophils creating an inflammatory feedback loop leading to more complement activation producing cytokines causing blood to more likely coagulate and lead to stroke

88
Q

How do viruses infect the brain?

A

use hematogenous or retrograde axonal transport to get to CNS

89
Q

How do viruses infect the brain?

A

use hematogenous or retrograde axonal transport to get to CNS

90
Q

Based on the neuropathology symptoms associated with SARS-CoV2 (dizziness, brain f

A
91
Q

Immune system and CNS speak the same language, which is ________

A

cytokines

92
Q

What causes a cytokine storm?

A

immune system cannot turn off and causes toxins to be released in places where they shouldn’t be

93
Q

Systemic cytokines can cause what three symptoms?

A

loss of appetite, fever, and fatigue

94
Q

An over-response and cytokine storm can cause severe disease. So why not turn off the immune system to prevent damage?

A

risk of secondary infections would increase

95
Q

What is the difference between central tolerance and peripheral tolerance?

A

Central tolerance involves negative selection of antigens in the thymus and is the primary system while peripheral tolerance focuses on CD4 regulatory cells and is the backup system

96
Q

What gene is responsible for the development of central tolerance?

A
97
Q

How is peripheral tolerance maintained?

A

by using regulatory T cells that suppress immune responses and maintain self tolerance

98
Q

What cell types are involved in central tolerance? What cell types are involved in peripheral tolerance?

A
99
Q

What happens to autoreactive cells?

A
100
Q

What is an example of central tolerance?

A

self-reactive T cells are deleted during selection in the thymus

101
Q

What is central tolerance?

A

eliminate any cells that are self-reactive

102
Q

Immunological tolerance is _____ specific

A

antigen

103
Q

AIRE allows for ______ _______

A

central tolerance

104
Q

What is the function of AIRE?

A

it allows for cells in thymus to express all the self-antigens not normally found in the thymus

105
Q

What are the consequences for loss of function of AIRE?

A

autoimmune disease

106
Q

____-_ inhibits T cell activation

A

CTLA-4

107
Q

What are the two ways CTLA-4 inhibits T cell activation?

A

cell intrinsic mechanism and cell extrinsic mechanism

108
Q

What is the outcome of cell intrinsic mechanism?

A

termination of response

109
Q

What is the outcome of cell extrinsic mechanism?

A

Treg-mediated suppression of response to prevent immune response activation

110
Q

What is the cell extrinsic mechanism?

A

regulatory T cells express CTLA4 and regulates other cells binding to costimulatory molecules

111
Q

T cells sequester what cytokine?

A

IL-2

112
Q

What are the four functions of Treg cells?

A

Inhibitory cytokines, cytolysis, metabolic disruption, and targeting dendritic cells

113
Q

Mutation of what gene is associated with deficiency Tregs?

A

FOXP3, leading to autoimmunity

114
Q

What are three properties of B cell tolerance?

A

receptor editing, deletion, and anergy

115
Q

What is receptor editing?

A

B cells get to edit their gene one more time to try to bind to the self-antigen

116
Q

What are the three properties of peripheral tolerance?

A

anergy, deletion, and regulation by inhibitory receptors

117
Q

What can trigger autoimmune diseases?

A

Mutation in AIRE

118
Q

What is the difference between T cells and B cells in central tolerance?

A

T cells become Treg and B cells get one more chance to bind tightly to antigen

119
Q

What is cell intrinsic mechanism?

A

As antigens are eliminated and infection is being taken care of, there is less and less antigen. T cells upregulate CTLA-4 binding to B7 on APC giving T cell the signal to terminate its response

120
Q

What is autoimmunity?

A

failure of self-tolerance

121
Q

Production of IL-2 results in what?

A

T cell proliferation and differentiation

122
Q

How do Tregs maintain self-tolerance?

A

by removing the survival signals from T cells causing an inability of those T cells to respond

123
Q

Why do pro-apoptotic proteins far outnumber anti-apoptotic proteins?

A

Lack of survival signals like IL-2

124
Q

A lot of activated T cells will upregulate death receptors resulting in what?

A

receptor-ligand interaction between T cells leading to apoptosis

125
Q

What is autoimmunity?

A

failure of self-tolerance and results in immune reactions against self (autologous) antigens

126
Q

Name the two major pathways responsible for the deletion of T cells by apoptotic cell death

A

Mitochondrial (or intrinsic) pathway and death receptor (or extrinsic) pathway

127
Q

What are the three factors of autoimmunity?

A

genetic susceptibility, environmental triggers, and other factors

128
Q

Genetic susceptibility may lead to what?

A

failure of self-tolerance

129
Q

Why might genetic susceptibility lead to failure of self-tolerance?

A

MHC genes may not functional or affecting the selection in the thymus of T cells that can be activated

130
Q

Reaction to environmental stimuli can lead to what four steps?

A

tissue injury and inflammation → activation of tissue APCs → activation of self-reactive lymphocytes → full response to self-antigen

131
Q

Autoimmune disorders can be ________ or _____-_______

A

systemic; organ-specific

132
Q

What are the three immunological abnormalities leading to autoimmunity?

A

defective self-tolerance, abnormal display of self antigens, and inflammation or an initial innate immune response

133
Q

What is detective self-tolerance?

A

inadequate elimination or regulation of T and B cells, leading to an imbalance between lymphocyte activation and controls

134
Q

What is abnormal display of self-antigens?

A

increased expression and persistence of self-antigens that are normally cleared or structural changes in these antigens resulting from enzymatic modifications or from cellular stress or injury

135
Q

What is the innate immune response?

A

a strong stimulus for the subsequent activation of lymphocytes and the generation of adaptive immune responses

136
Q

What happens in self-tolerance?

A

A “resting” tissue DC presenting self-antigens binds to a T cell, the T cell will not activate because it has no costimulatory signal and become anergic (peripheral tolerance)

137
Q

What is bystander activation?

A

when a microbe triggers enough inflammation that it activates the cells around the inflammation presenting some self-antigen

138
Q

What two roles do infections have in autoimmunity?

A

bystander activation and molecular mimicry

139
Q

How does autoimmunity develop? How is tolerance broken via bystander activation?

A

self-reactive T cell that escapes central tolerance and breakdown of peripheral tolerance due to local inflammation, this APC is activated leading to activation of T cell response

140
Q

What is molecular mimicry?

A

some antigens of microbes cross-react with self-antigens initiating an immune response

141
Q

What happens in molecular mimicry?

A

microbial protein is presented on APC to create a response against microbe meets up with a self-reactive T cell that gets activated against microbe but microbe looks just like a self protein causing activation of immune response against self antigen

142
Q

What is multiple sclerosis?

A

an autoimmune disorder in an autoimmune response initiated against the myelin that keeps nerve signals running. Without myelin, nerve fiber is exposed and signals are lost so neurons must expend more energy

143
Q

What is multiple sclerosis caused by?

A

immune cell infiltration crossing the BBB

144
Q

True or False: Immune dysregulation in multiple sclerosis is not only in the brain

A

True

145
Q

People with multiple sclerosis have a suspected

A

molecular mimicry effect and genetic predisposition associated with reduced regulatory function resulting in loss of peripheral tolerance

146
Q

How do B cells contribute to multiple sclerosis?

A

increased resistance of effector B cells and can undergo affinity maturation to become more efficient at being self-reactive

147
Q

The blood brain barrier is an _____ _______ ____

A

immune privileged site

148
Q

What happens when immune cells infiltrate BBB from periphery?

A

increased permeability of BBB because body thinks that you are trying to fight an infection but the epitope is actually a self antigen calling in more immune cells as reinforcements to try to clear what it thinks is an infection

149
Q

What are the four functions of anti-B cell antibodies to treat MS?

A

target autoreactive B cells with antibodies killing off those B cells by attaching to those B cells and leading to antibody-dependent cellular cytotoxicity, cause signaling induced apoptosis, prevents production of autoantibodies, and prevents autoreactive T cells from activating the autoreactive B cells by binding to cell surface so other cells can no longer bind

150
Q

True or False: There is a cure for multiple sclerosis

A

False, there is currently no cure for multiple sclerosis

151
Q

What is an example of peripheral tolerance?

A

regulatory T cells inhibit activation of effector T cells

152
Q

How do regulatory T cells regulate other T cells?

A

produce regulatory cytokines, absorb the necessary survival signals to deplete them from activating T cells, act via regulatory receptors to inhibit T cell activation, and downregulate APCs ability to activate T cells

153
Q

T cells educated in the Thymus are selected so as not to respond to self antigen. This represents what kind of tolerance?

A

central tolerance

154
Q

Tissue-specific induction of regulatory molecules to induce tolerance (e.x. in the uterus during pregnancy) is what kind of tolerance?

A

peripheral tolerance

155
Q

What CD4+ T cell type is most important for maintaining tolerance?

A

Treg

156
Q

What gene is primarily responsible for central tolerance?

A

AIRE

157
Q

What 4 ways do regulatory T cells eliminate self-reactive cells?

A

inhibitory cytokines, cytolysis, metabolic disruption, and targeting DCs

158
Q

What is one way infections can lead to autoimmunity?

A

viral or bacterial antigens may just happen to share a similar structure with self-antigens

159
Q

What is the current strategy for treating multiple sclerosis?

A

antibody against B cells

160
Q

What is the innate response to intracellular bacteria?

A

Activate phagocytes and NK cells to kill the intracellular bacteria. A cell that is phagocytosed upregulates ligands that activates NK cells. ILCs produce cytokines to activate macrophages

161
Q

What are the three adaptive responses to intracellular bacteria?

A

CD4+ T cells activate phagocytes, CD8+ cytotoxic T lymphocytes kill infected cells, and cytokines

162
Q

What are the three immune evasion strategies for intracellular bacteria?

A

inhibition of phagolyosome formation, inactivation of reactive oxygen and nitrogen species, and disruption of phagosome membrane, escape into cytoplasm

163
Q

What is the innate response to extracellular bacteria?

A

complement activation, activation of phagocytes, inflammatory response, and innate lymphoid cells (ILCs)

164
Q

What is the adaptive response to extracellular bacteria?

A

Blocks/eliminates microbes and neutralizes microbial toxins (both are humoral immunity)

165
Q

What are the four immune evasion strategies for extracellular bacteria?

A

inhibition of complement activation, resistance to phagocytosis, scavenging of reactive oxygen species, and change surface antigens to avoid humoral immunity

166
Q

What is the innate response to fungi?

A

neutrophils release fungicidal substances and phagocytose fungi, macrophages and dendritic cells recruit and activate neutrophils, ILCs produce granulocyte-macrophage colony-stimulating factor (GM-CSF), and some fungi can inhibit macrophage activation and produce IL-10

167
Q

What is the adaptive response to fungi?

A

CD4+ and CD8+ T cells cooperate to eliminate infection, dendritic cells can stimulate Th17 differentiation, T17 stimulate inflammation, and elicit specific antibody responses

168
Q

What are the immune evasion strategies for fungi?

A
169
Q

What is the innate response to parasites (protozoa)?

A

PAMPs are recognized by TLRs, which triggers phagocytosis

170
Q

What is the innate response to parasites (helminths)?

A

Eosinophils release granule contents capable of destroying warm integuments, phagocytes can secrete microbicidal substances to kill the worm, and activate the alternative pathway of complement

171
Q

What is the adaptive response to parasites (protozoa)? - Ask Dr. Mills Ko

A

Th1 cells with proinflammatory responses good at targeting protozoa (cell-mediated immunity)

172
Q

What is the adaptive response to parasites (helminths)?

A

Activation of Th2 cells, production of IgE antibodies, and activation of eosinophils

173
Q

What are the four immune evasion strategies for parasites?

A

antigenic variation, acquired resistance to complement or CTLs, inhibition of host immune responses, and antigen shedding

174
Q

CD4+ helper T cells produce what?

A

cytokines

175
Q

Intracellular bacteria are shielded from many of the detection mechanisms of the immune system. What are the main receptors in which cell types that alert the immune system to the presence of intracellular bacteria?

A

in phagocytes, the TLR and NLR receptors detect PAMPs

176
Q

What is one way extracellular bacteria avoid detection by antibodies?

A

they vary the antigens expressed on their surface

177
Q

What is the primary innate cell responsible for responding to fungal infections?

A

neutrophils

178
Q

What adaptive response lads to clearance of protozoa infections?

A

Th1

179
Q

What adaptive immune responses target parasitic infections?

A

Th2, IgE, and Eosinophils

180
Q

What adaptive immune responses target parasitic infections?

A

Th2, IgE, and Eosinophils

181
Q

Virus genomes may consist of what?

A

double-stranded (ds) or single-stranded (ss) DNA or RNA

182
Q

Viruses replicate only in ____ _____

A

host cells

183
Q

Each virus can infect cells of only a limited number of host species, ____ _____

A

host range

184
Q

Viral replication happens where?

A

in the cytosol

185
Q

What are the two ways the body is able to fight viruses?

A

protection against infection and eradication of established infection

186
Q

In innate immunity, what cytokine do cells released when attacked by a virus?

A

Type I interferon

187
Q

What 2 cells are necessary to kill virally infected cells and remove the infection completely?

A

NK cells and CD8⁺ CTLs

188
Q

What three outcomes can happen that type I interferons have that put virally infected cells and cells around it into an antiviral state?

A

inhibition of viral protein synthesis, degradation of viral RNA, and inhibition of viral gene expression and virion assembly

189
Q

MHC I is an _________ _________

A

inhibitory receptor

190
Q

NK cell has a receptor that binds to what?

A

Class I MHC

191
Q

Why do many viruses inhibit class I MHC expression?

A

to avoid detection by cytotoxic T cells

192
Q

What happens when Class I MHC is downregulated?

A

NK cell binds to activating receptor and there is no inhibitory receptor there to bind to due to no Class I MHC activating the NK cell and killing the virally infected cell

193
Q

Antibodies are only effective against _____________ viruses

A

extracellular

194
Q

What is the adaptive immune response to viruses?

A

Antibodies bind to viruses, start the complement process, improve opsonization and phagocytosis, and antibody-dependent cytotoxicity

195
Q

What is the principal physiologic function of CTLs?

A

surveillance against viral infection

196
Q

What are virus-specific CTLs?

A

CD8⁺ T cells that recognize cytosolic viral peptides presented by MHC class I molecules

197
Q

When do latent infections occur?

A

viral DNA persists in host cells but the virus does not replicate or kill infected cells

198
Q

Viral particles are found to ________ at times when a host immune system is low

A

reactivate

199
Q

What happens when latent herpesvirus is stimulated?

A

reactivation of viral genome occurs and replication is turned on

200
Q

What are the three parts of immune response pathology for adaptive immunity to viruses?

A

tissue injury may be caused by CTLs, carriers of the virus, and circulating immune complexes can cause molecular mimicry leading to autoimmune disorder

201
Q

Some viruses inhibit ____ _ ___-associated presentation of cytosolic protein antigens

A

Class I MHC

202
Q

What are the two main ways viruses change their antigens?

A

point mutations and reassortment of RNA genomes

203
Q

What is reassortment of RNA genomes?

A

two different viruses can mix their genes and become a new mixed version

204
Q

Antigenic variation leads to what two outcomes?

A

antigenic drift and antigenic shift

205
Q

What is antigenic drift?

A

accumulation of point mutations

206
Q

What is antigenic shift?

A

multiple new viruses combining together to create new strains of different viruses

207
Q

What are the three main ways viruses can evade the immune system?

A

produce molecules that inhibit the immune response, cause T cell exhaustion, and may infect and either kill or inactivate immune cells

208
Q

What are the two main goals of the immune system when fighting a viral infection?

A

prevent the spread from one cell to another and eliminate virally infected cells

209
Q

Type I interferons induce an antiviral state in infected and nearby cells by:

A

inhibit protein synthesis, degrade viral RNA, and inhibit virion assembly

210
Q

The SARS-Cov2 virus has accumulated many point mutations in each new strain, this is an example of ______?

A

antigenic drift

211
Q

What is the general strategy of vaccines?

A
212
Q

How do we protect people from viruses?

A

a killed or attenuated form of an infectious agent or component of a microbe that does not cause disease but elicits an immune response that provides protection against

213
Q

What is passive immunity?

A

used clinically for rapid treatment of potentially fatal diseases caused by toxins and for protection from rabies and hepatitis

214
Q

What are the negatives of passive immunity?

A

short lived immunity and does not induce memory

215
Q

What is a live attenuated vaccine?

A
216
Q

What is a subunit vaccine?

A
217
Q

What is an adjuvant?

A

added to the vaccine that will trigger toll-like receptors and the immune response

Immuno (3 decks)

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