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Infection and Immunity > 16 Immunity - viral infections > Flashcards

16 Immunity - viral infections Flashcards

1
Q

what are the different types of outcomes for virus infections

A

Some virus infections are pathogenic and cause disease

Some viruses are persistent and cause long-term health problems

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2
Q

how are viruses broadly split

A

broadly split into DNA or RNA viruses

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3
Q

virus split imapct

A

impacts host recognition and immunity

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4
Q

what can DNA virus use

A

can use host polymerases and goes to the nucleus

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5
Q

what can RNA virus use

A

has its own RNA polymerase and replicates in cytoplasm

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6
Q

what is EBV

A

Epstein-barr virus

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7
Q

what is HCV

A

Hep C virus

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8
Q

DNA viruses replication

A
  1. Deliver viral DNA to the nucleus
  2. Replicate using viral or host DNA polymerases
  3. Generate DNA intermediates
    - DNA can accumulate in cytoplasm
  4. Can have very small genomes, or very large genomes
  5. Can result in cell lysis
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9
Q

RNA viruses replication

A
  1. Replicate in the cytoplasm
  2. Use viral polymerases
  3. Generate double-stranded RNA intermediates
    - RNA accumulates in cytoplasm
  4. Generally have very small genomes
  5. Can result in cell lysis
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10
Q

what can DNA virus replication cause directly

A

Can cause cancer directly

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11
Q

what can DNA virus replication cause indirectly

A

Can cause cancer indirectly

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12
Q

DNA virus direct cancer example

A

Viral oncogenes affect cell cycle

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13
Q

DNA virus indirect example

A

HBV

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14
Q

what can RNA virus replication cause directly

A

Can cause cancer directly

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15
Q

what can RNA virus replication cause indirectly

A

Cause cancer indirectly

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16
Q

RNA virus indirect example

A

HCV

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17
Q

RNA virus direct example

A

Retrovirus integration

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18
Q

what are chronic and acute infections controlled by

A

This is controlled by interplay between the virus and host immune system

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19
Q

what diseases are controlled by chronic and acute infections

A

HCV

HBV

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20
Q

what diseases are controlled by other viruses always establish chronic infection

A

HIV

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21
Q

Acute infections

A

Flu
RSV (important childhood infection)
Gastroenteritis
Infection of skin

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22
Q

Chronic infections

A

Infect immune system eg HIV,
Viruses can infect T cells
Chronic infection associated with small number of organs

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23
Q

acute virus infections equilibrium state

A

non-equilibrium state

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24
Q

what controls acute viral infections

A

Viral replication and host immunity control the dynamic

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25
Q

acute viral infections characteristics

A

rapid replication, generation of virions, and spread

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26
Q

Chronic virus infections equilibrium state

A

More equilibrium state than acute infections

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27
Q

chronic infection persistance

A

Virus is able to persist in the presence of host immunity

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28
Q

what is important about the chronic infection

A

Essential to evade the immune response, or become a latent infection

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29
Q

how is chronic infection characterised

A

progressive replication, suppression of immune responses

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30
Q

Types of chronic infections

A

latent
chronic
slow

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31
Q

example of latent

A

Herpes simplex virus

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32
Q

example of chronic

A

Hepatitis C virus

Hepatitis B virus

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33
Q

example of slow

A

Measles infection of the nervous system

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34
Q

what virus displays all three phenotypes of chronic infections

A

retroviruses

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35
Q

Latent

A

completely quiet, suppress themselves

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36
Q

Chronic persistent

A

constantly producing virus particles

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37
Q

Slow

A

replication so cause less immune response

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38
Q

Sites of chronic virus infections

A

Neuronal cells/CNS
Liver
Immune cells

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39
Q

Innate sensing

A

Virus-associated molecules recognised by the immune system:

  1. Viral proteins
  2. Viral nucleic acid (dsRNA; 5’triphosphate RNA)
  3. Infected cells
  4. Altered host proteins
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40
Q

Innate sensing PAMPs associated

A

Some are associated with the virion (particle itself)

Some are associated with viral replication

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41
Q

where is RNA genome in virion

A

RNA genome is contained in a nucleocapsid

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42
Q

Components of a virion examples

A

Not all viruses have all these, but examples

  • Reverse transcriptase
  • Protease
  • Integrase
  • Vpr
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43
Q

what is protease for

A

break down host cell proteins

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44
Q

what is integrase for

A

integrate into host cell genome

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45
Q

what is Vpr

A

accessory protein

46
Q

what encloses the nucleocapsid

A

capsid encloses it

47
Q

where is the matrix

A

matrix protein exists between the capsid and the envelope

48
Q

what is the virion lipid envelope populated with

A

virion lipid envelope is populated with viral attachment factor

49
Q

where are host cell proteins

A

Host cell proteins are also incorporated into the virion

50
Q

Sensing virus particles - detection

A

On infection with a virus particle, these viral proteins can be detected.
Virions are present in sites of infection, or systemically

51
Q

Sensing virus particles - recognition by lectins effects

A

Neutralization

Complement activation

52
Q

Sensing virus particles - recognition by antibodies

A

Neutralization

Complement activation

53
Q

Sensing virus particles - APC

A

Binding of B cells to viral antigens – B cell receptor

Binding of macrophages/dendritic cells to virus particles – lectin receptors; Fc receptors; TLRs

54
Q

T/B cell activation in virus infections

A 
APC activates T helper cells
Th2 activates the B cells
Get production of cytokines from Th1
Activates CTL’s which the recognise infected host cells
CTL’s then kill infected host cells
55
Q

Innate sensing of infections examples of important classes

A

Toll-like receptors (TLRs)
Rig-like receptors (RLRs) (associated with recognising RNA)
Cyclic dinucleotide receptors (CDRs) (associated with recognising DNA)

56
Q

Innate sensing of infections - detection

A

Virus infections are initially detected by different pattern recognition receptors

57
Q

Interferon-stimulated genes - major effector functions of ISGs

A
  1. Reduction in transcription of viral RNA
  2. Reduction of virus protein expression
  3. Degradation of dsRNA
  4. Editing of viral RNA
  5. Modification of viral proteins
58
Q

what do type I IFN make

A 
immature DC
macrophage
Th1 and NK
epithelial cells/fibroblasts
inflammatory cell
59
Q

immature DC effect - type I IFN

A

activation
migration
IL-12 production

60
Q

macrophage effect - type I IFN

A

induction of antiviral genes

death sensitization

61
Q

Th1 and NK cells effect - type I IFN

A

IFN-gamma expression

62
Q

epithelial cell or fibroblasts effect - type I IFN

A

inhibition of viral infection

63
Q

inflammatory cell effect - type I IFN

A

enhanced septic shock

64
Q

PKR

A

protein kinase receptor

65
Q

what induces PKR

A

PKR is induced by IFN

66
Q

what does PKR recognise

A

Recognises dsRNA associated with virus replication

67
Q

what does PKR do

A

Phosphorylates eIF2a, inhibiting protein expression

Recruits caspases, triggering apoptosis

68
Q

what does PKR activate

A

NFkB, promoting inflammation

69
Q

tetherin act against

A

against enveloped viruses
Binds to the surface glycoproteins
Act against a wide range of viruses (retroviruses; ebolaviruses)

70
Q

what does tetherin prevent

A

Prevents release of the virus while budding – stop being spread
Retained particles are targeted for degradation

71
Q

what does tetherin sense

A

senses enveloped viruses, triggering inflammation

72
Q

Innate immunity - viral infections

A
  1. Innate immunity is not sufficient for control of all virus infections
  2. Pathogens evolve quicker than complex hosts and can escape innate immunity
  3. Evolution of an adaptive immune response allows the host to rapidly react to different viruses
73
Q

Cellular recognition of infected cells

A
  • activate of APCs
  • induction of an antiviral state
  • killing of virus-infected cells
74
Q

Cross-presentation of viral antigens - direct presentation

A

Direct display of viral antigens on infected cells activates T cells

75
Q

Cross-presentation of viral antigens - cross-presentation

A

Dendritic cells can also display fragments of soluble antigens on MHC class I

76
Q

Cross-presentation of viral antigens - cross-dividing

A

Utilising trogocytosis, DCs can acquire MHC class I-loaded peptides for presentation to memory T cells

77
Q

CD8+ cells are activated by

A

MHC I expressed viral peptides

78
Q

what does CD8+ cells make

A

Perforins
Granzymes
Granulysin

79
Q

Antiviral effects of antibodies

A
  1. neutralisation
  2. complement lysis
  3. opsonization and phagocytosis
  4. ADCC
80
Q

NK cell effectors

A

Perforins
Granzyne
a-defensins

81
Q

what do NK cells secrete

82
Q

Viral mechanisms for evading host immunity

A
  1. Replication in privileged sites
  2. Protease cleavage of host innate immunity proteins
  3. Blocking ISGs
  4. Down-regulation of immune mediators
  5. Triggering immune tolerance
    - Host mimicry
    - Glycosylation
  6. Rapid mutation
  7. Latent infection
83
Q

Replication in immune privileged sites

A

Some tissues have blood-tissue barriers that prevent immune cells from transmitting

84
Q

Replication in immune privileged sites - examples

A

Replication in the retina
Replication in CNS
B cell follicles

85
Q

how can viruses ‘hide’

A

Viruses can also compartmentalise a cell to evade innate sensing
HCV replicates in ‘double-membrane vesicles’

86
Q

Viruses inactivate PKR

A

Many viruses block the signalling pathway that results in PKR blocking of eIF2a translation
Most block the dimerization or action of PKR directly

87
Q

Viruses evade Tetherin

A 
Tetherin has been co-opted for the entry pathway of CMV
Block tetherin
- HIV
- Dengue 
- Ebola
88
Q

HCV evasion of innate immunity - replication

A

Replicates in the liver

  • Tolerant site
  • Target cells are hepatocytes
89
Q

HCV evasion of innate immunity - virion and lipoproteins

A

Virion associates with lipoproteins

Enhance infection and prevent recognition by humoral immunity

90
Q

how does HCV evasion of innate immunity inactivate intracellular recognition

A

Has a range of mechanisms to inactivate intracellular recognition

91
Q

Protease cleavage of host innate proteins

A

Cleaving some of the host proteins
To get individual proteins it needs to function
have recognition sites in TRIF and MAVS

92
Q

Mutation rate

A

RNA-dependent RNA polymerase has no error checking

High viral turnover and error-prone replication leads to variation

93
Q

Latent infection – HSV1

A
  1. primary site of infection: productive infection of epithelial cells
  2. secondary site of infection and site of latent infection: sensory neuron
  3. site of recurrent infection: productive infection of epithelial cells
94
Q

‘Latency-associated transcript’ inhibit

A

cell death and establishes latent infection

95
Q

‘Latency-associated transcript’ alters

A

DNA binding to histones, preventing gene expression

96
Q

Tissue specificity is defined by

A

the surface haemagglutinin (HA) protein

97
Q

Influenza pathogenesis transmitted

A

Transmit in air droplets, penetrating the respiratory mucin layer and binding to airway epithelial cells

98
Q

Influenza haemagglutinin specificity

A

Specificity for different sialic acid types

99
Q

Influenza haemagglutinin

A

Allow the two membranes to fuse to allow them to invade

  • cell membrane
  • viral membrane
100
Q

Cleavage of HA - replication

A

Replication is usually restricted to epithelial cells of the upper and lower respiratory tract

101
Q

Variation is essential to continued spread of influenza virus

A

New variants are not recognised by host immunity
Immunity to specific strains prevents infection
This permits selective transmission of new variants

102
Q

Influenza possesses two different mechanisms for variation

A

Antigenic drift

Antigenic shift

103
Q

Antigenic drift cause

A

amino acid changes in immunogenic sites of HA/NA

104
Q

Antigenic shift cause

A

recombination of different HA/NA gene segments

105
Q

Antigenic drift responsible for

A

seasonal variations in the H1N1 and H3N2 strains

106
Q

Antigenic shift responsible for

A

emerging pandemics

107
Q

antibody-mediated immune control vaccine-induced adaptive immune examples

A

Influenza
(inactivated vaccines)
Hepatitis B virus
(recombinant vaccine)

108
Q

antibody-mediated and cell-mediated immune control vaccine-induced adaptive immune examples

A

Measles
(attenuated vaccine)
Rotavirus
(attenuated vaccine)

109
Q

why use antibody-mediated vaccine

A

antibody important for protection

110
Q

why use antibody-mediated and cell-mediated immune control

A

Combinations of cellular and antibody response contribute to clearing virus particles and infected cells

Infection and Immunity (29 decks)

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