Brainscape's Knowledge GenomeTM

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


See full index

MIIM30014 Virology > Immune Response (15,16) > Flashcards

Immune Response (15,16) Flashcards

1
Q

How do innate and adaptive immunity compare?

a. Natural killer cells are a second line of defence in innate immunity
b. Skin and lysozymes are a second line of defence in innate immunity
c. Cytokines are only produced during adaptive immunity
d. Antibodies are formed during the second line of defence in innate immunity

A

a. Natural killer cells are a second line of defence in innate immunity

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

Which endosomal receptor is critical during the innate response to viral infection?

a. TLR5
b. TLR1
c. TLR8
d. TLR11

A

c. TLR8

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

Which statement is correct?

a. PRRs are a major component of adaptive immunity
b. The innate response to repeat infections is much more rapid than the primary response
c. Innate immunes response are more diverse than adaptive immune responses in terms of specificity
d. Antibodies are a component of the adaptive immune response

A

d. Antibodies are a component of the adaptive immune response

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

Which is correctly matched?

a. TLR3 recognises flagellin
b. TLR8 recognises ssRNA
c. TLR7 recognises CpG unmethylated dinucleotides
d. TLR9 recognises dsRNA

A

b. TLR8 recognises ssRNA

a. TLR3 recognises flagellin (5)
b. TLR8 recognises ssRNA (7,8)
c. TLR7 recognises CpG unmethylated dinucleotides (9)
d. TLR9 recognises dsRNA (3)

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

What is special about viral specific TLRs?

a. All are embedded in the ER membrane
b. They are cytoplasmic
c. They are localised to the endosomal membrane
d. They can only be found on the cell membrane

A

c. They are localised to the endosomal membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is not involved in the activation of human TLRs?

a. There is ligand induced dimerization of TLR
b. MYD88 can repress NFKB and IRF7 activation
c. TLRs assemble with adaptor signalling molecules
d. MyD88 and TRIF activate transcription factors and MAP kinases

A

b. MYD88 can repress NFKB and IRF7 activation

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

What does IRF3 do?

a. It interacts with eIF3 to promote protein synthesis
b. It causes the production of IFN
c. It down regulates production of the antiviral ISG56 protein
d. It induces it’s effects from the cytoplasm

A

b. It causes the production of IFN

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

What is a feature of MDA5 and RIG-I?

a. MDA5 recognises long dsRNA such as that produced during picornavirus infection
b. RIG-I can only recognise RNA from a segmented viral genome
c. MDA5 recgonises short dsRNA such as that produced during paramyxovirus infection
d. RIG-I and MDA5 are TLRs embedded in the endosome membrane

A

a. MDA5 recognises long dsRNA such as that produced during picornavirus infection

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

What is MAVS?

a. An IRF that is activated via TRAF3 and TBK1
b. A mitochondrial membrane adaptor protein that is activated by RLR signalling
c. An IFN protein produced following NFKB signalling
d. A RLR that directly binds dsRNA before activated MDA5 or RIG-I

A

b. A mitochondrial membrane adaptor protein that is activated by RLR signalling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is involved in the early recognition of viral infection via RLRs?

a. dsRNA interacts with RIG-I or MDA5 which interact with MAVS on the ER
b. Interactions between RIG-I/MDA5 and MAVS are facilitated via the helicase domain
c. The NFKB signalling pathway is activated after RIG-I/MDA5 interact with MAVS
d. TRAF6, RIP1 and FADD facilitate the dimerization and activation of IRF3 and IRF7

A

c. The NFKB signalling pathway is activated after RIG-I/MDA5 interact with MAVS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is cGAS?

a. A viral protein that recognises foreign DNA in the cytoplasm
b. A host protein that can generate cGAMP when cytosolic DNA is detected
c. A monophosphate that binds STING in the ER
d. A ligand for TBK1, IRF3 and NFKB that leads to IFN production

A

b. A host protein that can generate cGAMP when cytosolic DNA is detected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which antiviral protein is cytosolic, sequesters nucleocapsids and is potent against influenza?

a. OAS
b. RNaseL
c. PKR
d. MxA

A

d. MxA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a feature of OAS and RNaseL?

a. OAS and RNaseL production is down regulated by IFN
b. They are antivirals against viral DNA species
c. OAS monomers form tetramers before making a nucleotide that activates RNaseL
d. OAS digests viral RNA when activated by RNaseL

A

c. OAS monomers form tetramers before making a nucleotide that activates RNaseL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a feature of Protein Kinase R (PKR)

a. It affects virus production without impacting the host
b. It can phosphorylate host EIF2a to halt host translation
c. It has a viral DNA binding domain
d. When it binds dsRNA, it forms a tetramer and up regulates host cell translation

A

b. It can phosphorylate host EIF2a to halt host translation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can a virus inhibit IFN signalling?

a. Measles virus can prevent phosphorylation of Tyk2
b. SARS CoV can degrade STAT proteins
c. Mumps can prevent the nuclear import of the STAT1/2 heterodimer
d. West Nile virus prevents the nuclear import of the STAT1 homodimer

A

c. Mumps can prevent the nuclear import of the STAT1/2 heterodimer

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

What is NOT an example of how viruses can counteract the innate immune response?

a. Upregulate TLR signalling and compromise host cells. i.e. Poxvirus
b. PKR can be inhibited as shown by poxvirus and reoviruses
c. IFN signalling can be inhibited, i.e West Nile Virus
d. RNA recognition and MAVs signalling can be interfered with. i.e. Influenza virus

A

a. Upregulate TLR signalling and compromise host cells. i.e. Poxvirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How can PKR be inhibited?

a. Poliovirus can phosphorylate EIF2a
b. Reovirus can cleave the inactive PKR monomer
c. Dimerization and phosphorylation can be prevented by poxvirus
d. HSV can produce fake RNAs that lead to PKR degradation

A

c. Dimerization and phosphorylation can be prevented by poxvirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

• NFKB and IRF are key TLRs involved in innate immunity.

A

F (TFs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

• RLRs are cytoplasmic helicases that recognise viral nucleic acid.

A

T

20
Q

• TLR3 activates IRF3.

A

T

21
Q

• MYD88 and TRIF are important transcription factors activated by TLR activation.

A

F (adaptor molecules)

22
Q

• Cytoplasmic DNA receptors can detect foreign, cytosolic DNA that results from some viral infections.

A

T

23
Q

• Interferons only demonstrate paracrine signalling action.

A

F (all 3)

24
Q

• Interferon can relieve sleepiness, muscle pain and nausea during viral infection.

A

F

25
Q

• STAT is a signal transducer and transcription factor with a key role in IFN signalling.

A

T

26
Q

• Type I IFN causes STAT1 and 2 to heterodimerise and Type II IFN causes STAT1 molecules to homodimerise.

A

T

27
Q

• RNaseL is always active and abundant in cells.

A

F

28
Q

• Influenza virus can interferes with RIG-I signalling via NS1.

A

T

29
Q

What would NOT be a way for a virus to interact with its host to avoid the immune response?

a. Stop the action of pattern recognition receptors
b. Up-regulate interferon signalling
c. Modulate apoptosis and autophagy
d. Stop host protein expression

A

b. Up-regulate interferon signalling

30
Q

What is NOT a feature of viral latency?

a. The viral genome can replicate in conjunction with the host DNA without disrupting the cell cycle
b. The viral genome can persist intact in the host nucleus
c. Expression of productive cycle viral genes is very efficient
d. Immune detection is greatly reduced

A

c. Expression of productive cycle viral genes is very efficient

31
Q

What is a correct example of viral persistence?

a. Influenza can cause a chronic infection due to producing decoy proteins
b. HPV causes a non-cytopathic infection of an inaccessible site
c. Measles demonstrates chronic infection due to immune exhaustion
d. HIV can avoid the immune response using antigenic shift

A

b. HPV causes a non-cytopathic infection of an inaccessible site

32
Q

Which virus can result in Subacute sclerosing panencephalitis due to persistence?

a. HBV
b. HPV
c. Vaccinia
d. Measles

A

d. Measles

33
Q

What is FALSE about Antigenic Drift of B cell epitopes?

a. In influenza, a diversity of strains usually arises in a single patient
b. The antigenic structure of the virus changes and is selected for
c. Changes can be spontaneous and due to errors in RNA replication
d. Drift occurs when changes are selected for and allow the virus to escape neutralisation by pre-existing antibodies

A

a. In influenza, a diversity of strains usually arises in a single patient

34
Q

What is a feature of Antigenic Drift of T cell epitopes?

a. It is commonly shown by HBV
b. The TCR contact residues can be changed so the epitope is not processed or presented
c. If the epitope anchor residues are altered, it can avoid binding MHC
d. Changing the flanking amino acids of the epitope allow for faster processing by T cells

A

c. If the epitope anchor residues are altered, it can avoid binding MHC

35
Q

What is not an example of how viruses can inhibt T cell priming by dendritic cells?

a. By blocking cytokine induced maturation
b. By blocking signal transduction in immature DCs
c. By blocking T cell stimulation at the receptors
d. By increasing signal transduction in mature DCs

A

d. By increasing signal transduction in mature DCs

36
Q

What is not part of CD8 T cell recognition of viral infected cells?

a. Viral proteins are degraded by the proteasome before the peptides are loaded to the ER through TAP
b. In the ER, Tapasin loads viral peptides into MHCI
c. Viral proteins are modified in the Golgi before being loaded into the ER through TAP
d. Once viral peptides are loaded into MHCI, the complex is transported to the cell surface

A

c. Viral proteins are modified in the Golgi before being loaded into the ER through TAP

37
Q

What is not a method used to evade CD8 T cell recognition?

a. Antigenic variation in the CTL epitope as shown by HIV
b. A HSV protein binds cytosolic side TAP to prevent ER translocation
c. A HCMV protein binds tapasin to inhibit peptide loading in ER
d. Adenovirus can increase the expression of MHCI genes

A

d. Adenovirus can increase the expression of MHCI genes

38
Q

What is not a viral evasion strategy shown by CMV (human or murine)?

a. Using a protein that sequesters NKC activation ligands in the ER
b. Up regulating cellular non classical HLA-E (MHCI) which only binds/presents signal peptides of other MHC molecules
c. Encode a soluble cytokine receptor homologue that binds and inhibits cytokine function
d. Encode a MHCI like molecule that is expressed on infected cells and activates “not kill” signals on NKCs

A

c. Encode a soluble cytokine receptor homologue that binds and inhibits cytokine function

39
Q

How does poxvirus interfere with cytokine function?

a. By encoding soluble cytokine receptor homologues that bind and inhibit IFN
b. By encoding a IL-10 homolog that suppresses the Th1 response and CTL activation
c. By encoding proteins that interfere with the TNFa mediated killing of a cell
d. By promoting the cleavage of IL-1B to decrease inflammation

A

a. By encoding soluble cytokine receptor homologues that bind and inhibit IFN

40
Q

What is not a feature of apoptosis?

a. The intrinsic pathway involves the permeabilisation of mitochondrial and release of cytochrome C
b. Dying cells release apoptotic bodies which contain viral proteins that can be taken up by APCs and presented on MHC molecules
c. The process is mediated by caspases
d. All virus infected cells eventually undergo apoptosis so viral particles can be released

A

d. All virus infected cells eventually undergo apoptosis so viral particles can be released

41
Q

What does a viral FLIP do?

a. It prevents pro-caspase 8 to caspase 8 cleavage
b. It binds to BCL2 to prevent the intrinsic apoptosis pathway
c. It promotes pro-caspase 3 to caspase 3 cleavage
d. It degrades cytC to prevent apoptosis

A

a. It prevents pro-caspase 8 to caspase 8 cleavage

42
Q

How do poxvirus and herpesvirus evade complement?

a. They encourage cells to undergo autophagy and degrade complement proteins
b. They encode control protein homologues which bind to C’ components and prevent the C’ cascade
c. They encode IgG ligand homologues that neutralise IgG antibodies
d. They undergo xenophagy and highjack the host cell lysosome so complement proteins are degraded

A

b. They encode control protein homologues which bind to C’ components and prevent the C’ cascade

43
Q

• Herpes virus grows productively in epithelial cells before becoming latent so evasion is in the context of an existing immune response.

A

T

44
Q

• Viruses that evade CD8 T cells by down regulating MHCI are also successful at evading natural killer cells.

A

F

45
Q

• EBV encodes an IL-10 homolog that suppresses the Th1 response and reduces CD8+ T cells.

A

T

46
Q

• Viruses always evade autophagy by blocking the process.

A

F

MIIM30014 Virology (23 decks)

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