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Virology > Lecture 17 - Viral Evasion of the Cellular Immune Response and its Products > Flashcards

Lecture 17 - Viral Evasion of the Cellular Immune Response and its Products Flashcards

1
Q 
Antiviral responses in a vertebrate host cell that a virus can stop
1)
2)
3)
4)
A

1) PRR function
2) Interferon signalling
3) Interferon-stimulated genes (ISG)
4) Host protein expression

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2
Q

Antiviral responses in a vertebrate host cell that a virus can up- or down-regulate

A

1) Autophagy
2) Apoptotic pathways
3) Cell cycle
4) Secretion of cytokines, MHC expression

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3
Q

Broad viral mechanisms to evade immune control
1)
2)

A

1) Avoid detection

2) Impair immune functions

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4
Q

Types of viruses that have acquired many strategies for immune evasion

A

Large DNA viruses. Particularly herpesviruses and poxviruses

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5
Q

Viral methods to avoid T cell and antibody response
1)
2)

A

1) Latency in host cells.
EG: EBV in B cells, HSV in neurons

2) Antigenic drift

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6
Q

Viral methods of impairing T cell priming by DC
1)
2)

A

1) Block TLR signalling in DCs (stops maturation)

2) Block mature DC interaction with naive T cells

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7
Q

Viral methods of impairing CD8+ T cell response
1)
2)
3)

A

1) Antigenic variation (HIV, influenza)
2) Inhibiting processing and presentation of viral peptides (many viruses)
3) Decreased MHCI production (HIV, RSV, adenovirus)

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8
Q

Viral methods of impairing NK cell recognition of infected cells
1)
2)
3)

A

1) Mutations in ligand for activating receptor (murine CMV)
2) Virus-encoded MHCI-like molecules (human CMV)
3) Upregulation of non-classical MHCI (HLA-E) (human CMV)

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9
Q

Viruses that decrease MHCI production

A

HIV, RSV, adenovirus

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10
Q

Difference in function between IFNa/b and IFNg

A

IFNg upregulates both MHCI and MHCII (increases presentation to CD4+ T cells)

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11
Q

Viruses that encode cytokine receptor homologues

A

Poxviruses: vaccinia, myxomavirus.

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12
Q 
Cytokine-based viral strategies for immune evasion
1)
2)
3)
4)
A

1) Encode cytokine receptor homologues
2) Misdirect T cell response
3) Block intracellular cytokine production
4) Interfere with intracellular cytokine function

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13
Q

Virus that redirects T cell response

A

EBV

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14
Q

Virus that blocks intracellular cytokine production

A

Vaccinia crmA protein blocks cleavage of pro-IL-1b into IL1-b

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15
Q 
Characteristics of latent infections
1)
2)
3)
4)
A

1) Infect a non-replicating cell (EBV in resting B cells, HSV in neurons) OR viral genome is replicated in conjunction with host genome, so that cell cycle is not disrupted (integrated HIV in T cells, EBV in proliferating B cells)
2) Viral genome persists intact so that virus can be produced at a later time for transmission
3) Expression of productive cycle virus genes is absent or inefficient.
4) Immune detection of latently-infected cell is reduced or eliminated

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16
Q

Evidence for herpesvirus proficiency at evading immune response

A

Latent immune evasion is in the context of a mature adaptive immune response, as virus needs to replicate in epithelial cells before establishing latency.

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17
Q 
Types of persistent viral infections
1)
2)
3)
4)
A

1) Latent infection
2) Chronic infection
3) Non-cytopathic infection of an inaccessible site
4) Acute infection with very-late complications

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18
Q

Examples of viruses leading to chronic infections

A

Hepatitis B and C

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19
Q

How does hep B establish a chronic infection?

A

Releases excess surface antigen proteins into the extracellular space. This mops up anti HCV antibodies

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20
Q

How does hep C establish a chronic infection?

A

All viruses have slightly different genomes.

This collection of mutants (quasispecies) presents a wide variety of different antigens, overloads T cells with antigen.

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21
Q

Example of a virus causing a non-cytopathic infection of an inaccessible site

A

HPV

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22
Q

Example of a virus causing acute infection with very-late complications

A

Measles subacute sclerosing panencephalitis.

Under immune pressure, measles mutant that expresses low levels of surface glycoproteins or matrix is selected, and can’t bud from cells.
Genome spreads from neuron to neuron in the brain by forming intercellular bridges.
Immune system can’t control infection, results in a progressive, fatal CNS infection.

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23
Q

Difference in antigenic drift between influenza and HIV

A

Antigenic drift of influenza occurs in a population.

Antigenic drift of HIV occurs within the one patient (because influenza is an acute infection and HIV is chronic)

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24
Q

Type of viruses that antigenic drift mostly occurs in

A

RNA viruses, because RDRP has no proofreading mechanism

25
Q

Essential steps for antigenic drift

A

First mutation, and then selection for mutation

26
Q

Mechanisms of drift in T cell epitopes
1)
2)
3)

A

1) Change anchor residues of epitope so that it no longer binds in MHC
2) Change flanking residues so that epitope is no longer processed from intact antigen
3) Change epitope where it contacts TCR, so that it is processed and presented on MHC, but can’t be recognised by TCR

27
Q

What is ‘hole in the repertoire’?

A

In chronic HCV patients, viral variants are reported with mutations in TCR contact residues that are recognised by no TCR in patient.

Might resemble a self protein or something.

28
Q 
How can viruses block DC priming of T cells?
1)
2)
3)
4)
A

1) TLR4 cytoplasmic tail homologue that inhibits signal transduction leading to DC maturation (vaccinia)
2) Block PRR signal transduction (HSV)
3) Block cytokine-induced maturation of DC (vaccinia, HCV)
4) Block T cell stimulation by mature DC (CMV, measles)
4)

29
Q

How are proteins marked for degradation by the proteosome?

A

They are ubiquitinated.

30
Q 
MHCI presentation pathway
1)
2)
3)
4)
A

1) Cytoplasmic protein ubiquitinated.
2) Ubiquitinated protein degraded by proteosome
3) Degraded antigen imported into ER by TAP
4) Peptide loaded into MHCI

31
Q 
Ways that viruses evade CD8+ T cell recognition of infected cells
1)
2)
3)
4)
5)
6)
7)
A

1) Antigenic variation
2) HIV nef induces endocytosis of MHCI
3) HSV ICP47 binds to and blocks cytosolic side of TAP
4) Murine CMV US6 binds to luminal side of TAP and blocks it
5) Adenovirus E3 binds MHC-peptide complex, retains it in ER. Also prevents recruitment of TAP to MHC loading complex.
6) Human CMV US3 binds to tapasin, prevents optimal peptide loading
7) EBV EBNA-1 can’t be adequately ubiquitinated to be sent to proteosome.

32
Q

HSV protein that binds TAP

A

ICP47 binds cytosolic side of TAP

33
Q

Murine CMV protein that binds TAP

A

US6 binds luminal side of TAP

34
Q

Viruses that interfere with TAP function

A

HSV, murine CMV

35
Q

Taspsin

A

Component of MHC loading complex. Selects protein to be loaded into MHC

36
Q

Viral protein that interferes with tapsin function

A

H-CMV US3

37
Q

How does EBV avoid CD8+ T cell destruction?

A

EBV EBNA-1 (Epstein-Barr Nuclear Antigen-1) can’t be adequately ubiquitinated to be degraded by proteosome. Therefore can’t be loaded into MHCI

38
Q

How does HIV avoid CD8+ T cell destruction?
1)
2)

A

1) HIV nef protein causes MHCI to be endocytosed.

2) Decreases MHCI gene transcription.

39
Q

How do adenoviruses avoid CD8+ T cell killing?
1)
2)

A

1) E3 protein binds to MHCI-protein complex, prevents it from leaving ER.
2) E3 protein also prevents recruitment of TAP to MHCI loading complex

40
Q

How does mCMV avoid NK cell killing?

A

Encodes a protein that retains NKG2D ligands in the ER

41
Q

How does hCMV avoid NK cell killing?
1)
2)

A

1) Encodes an MHCI-like molecule (UL18).
Delivers a negative signal to NK cells, but can’t express peptide
2) Upregulates expression of HLA-E, a non-classical MHC

42
Q

HLA-E

A

Non-classical MHC, which only binds and presents signal peptides of other MHCs

43
Q

Vaccinia and myxomavirus encode homologues of which cytokine receptors?

A

TNFaR
IFNa/bR
IFNgR

44
Q

How does EBV redirect T cell response?

A

Produces an IL-10 homologue, which suppresses a Th1 response

45
Q

Th response that is particularly effective against viruses

A

Th1

46
Q

Example of a virus that interferes with intracellular cytokine function

A

Adenovirus encodes proteins that interfere with TNFa killing of a cell

47
Q

Effect of TNFa on a virus-infected cell

A

Apoptosis

48
Q

Proteins involved in apoptosis

A

BCL-2 family proteins

49
Q

How can apoptosis be initiated?
1)
2)

A

1) Signalling through TNF or FAS

2) Permeabilisation of mitochondrial membrane

50
Q

FLICE

A

Caspase 8

51
Q

FLIP

A

FLICE inhibitory protein.
Inhibits conversion of pro-caspase 8 to caspase 8.
This stops apoptosis

52
Q

Viruses that encode FLIPs

A

Adenoviruses, herpesviruses

53
Q

Viruses that interact with BCL-2 to stop apoptosis

A

Adenoviruses, herpesviruses

54
Q

Autophagy

A

Process by which cells envelope bulk cytoplasm in a double-membraned vesicle, which is shuttled to lysosomes for degradation

55
Q

Xenophagy

A

Autophagy targeting viral particles

56
Q

Roles of autophagy
1)
2)
3)

A

1) Xenophagy
2) Initiation of innate and adaptive immune system
3) Can act as a scaffold for RNA virus genome replication

57
Q

Example of a virus that uses an autophagosome as a scaffold for genome synthesis

A

Denguevirus

58
Q

Example of viruses that encode C’ control protein homologues

A

Poxviruses, herpesviruses

Virology (29 decks)

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