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Microbiology Y2 > Viral Evasion of Host Community > Flashcards

Viral Evasion of Host Community Flashcards

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Biology 101 flashcards
1
Q
  • Cellular immunity clears viral infection via X but is YY
A

T cells (CD8) but is short lived

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2
Q
  • Humoral immunity is X with Y
A

is B cells with antibodies

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3
Q
  • Internal viral proteins can be targets of cellular immunity-> They tend to XX than surface antigens
A

vary less

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4
Q
  • Cells cut up pieces of viral and cellular peptides in the X
A

proteosome

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5
Q

viral and cellular peptides are loaded onto XXX for recognition via T cells

A

MHC class I

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6
Q

How are viral proteins presented on the surface? ( goes to X, then loaded on to W, then goes to Y then goes to Z)

A
  • These peptides are transported through the ER and get loaded into an MHC class I molecule
  • This is transported to Golgi and then the cell surface
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7
Q

What is the co stimulator for a T cell

A

CD8

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8
Q

What transports viral peptides to the ER

A

TAP

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9
Q

What is the purpose of tap

A

transports viral peptides to the ER

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10
Q

3 viruses that avoid antigen presentation onto cell surface (in a way that takes place before Tapasin)?

A
  • EBV
  • HSV
  • CMV
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11
Q

How does EBV avoid antigen presentation on cell surface?

A

EBNA1 cannot be processed by the proteasome

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12
Q

How does HSV avoid antigen presentation on cell surface?

A
  • HSV ICP47 blocks access of the processed peptide to TAP on the ER
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13
Q

How does CMV avoid antigen presentation on cell surface? (2)

A
  • CMV US6 prevents peptide travelling through TAP by blocking other side and stopping ATP binding and so has the same effect as HSV
  • CMV US3 protein binds tapasin and prevent peptides being loaded to MHC
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14
Q

Which virus prevents peptide travelling through TAP by blocking other side and stopping ATP binding and so has the same effect as HSV

A

CMV

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15
Q

Which virus blocks access of the processed peptide to TAP on the ER

A

HSV

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16
Q

Which virus blocks access of the processed peptide to TAP on the ER

A

EBV

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17
Q

What molecule places peptide fragments on to MHC class I for presentation on the cell surface

A

Tapasin

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18
Q

What does tapasin do

A

places peptide fragments on to MHC class I for presentation on the cell surface

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19
Q

Which 2 viruses avoid antigen loading onto MHC via tapasin?

A

CMV

Adenovirus

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20
Q

How does CMV interfere with tapasin?

A
  • CMV US3 protein binds tapasin and prevent peptides being loaded to MHC
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21
Q

How does adenovirus interfere with tapasin? (2)

A
  • Adenovirus E3-19K protein prevents recruitment of TAP to tapasin and also retains MHC in the endoplasmic reticulum
22
Q

Which virus has a protein that binds tapasin and prevent peptides being loaded to MHC

A

CMV

23
Q

Which virus has a protein that prevents recruitment of TAP to tapasin and also retains MHC in the endoplasmic reticulum

A

Adenovirus

24
Q

which virus interferes with antigen presentation at the cell surface?

A

KSHV

25
Q

How does KSHV interfere with antigen presentation at the cell surface?

A

kK3 protein induces polyubiquitinylation and internalization of MHC (it gets dragged back in from the cell surface) From the internalized endosome, MHC is passed to lysosomes where it is degraded

26
Q

Which virus induces polyubiquitinylation and internalization of MHC (it gets dragged back in from the cell surface) From the internalized endosome, MHC is passed to lysosomes where it is degraded?

A

KSHV

27
Q

Why is HPV an effective virus even with a short genome?

A
  • This short genome is feasible because the proteins they code for have multiple purposes.
28
Q

What do the virulence factors of HPV cause? (3)

A
  • E6 and E7 stop the IFNA signaling pathway, as well as the cGAS pathway
  • E5 then stops the presentation of its peptides on MHC by holding on to it
29
Q

How does CMV avoid missing-self being displayed on the cell surface

A

viruses encode MHC analogues (CMV gpUL40)

30
Q

2 ways viruses can evade the missing self mechanism?

A

viruses encode MHC analogues (CMV gpUL40) or upregulate MHC

31
Q

What cells detect missing self MHC molecules

A

NK cells

32
Q

What is antigenic variation?

A

Continued rapid evolution driven by antigenic pressure from host

33
Q

influenza antigenic shift is caused by…

A
  • Introduction of new subtypes from animal source
34
Q

what is the major spike protein/viral antigen in flu

A

Haemogglutinin

35
Q

Which part of haemogglutinin/any viral antigen is variable and which is fairly constant

A

Globular head domain (bit where antibodies bind and where receptors bind) is highly variable and the stalk is fairly constant

36
Q

Why is the stalk of a viral antigen fairly constant? (2)

A

Constant stalk may be because the structure is extremely important and viruses that have a mutation in the stalk probs just die, or because none of our antibodies really target that bit so there has been no evolutionary drive for that bit to change

37
Q

Target for a universal flu vaccine?

A

Constant stalk of the haemogglutinin

38
Q

What on antigenic cartography tells us how different the viruses are from each other

A

Distance between the dots

39
Q

How can we skew Ab response towards the HA stalk? (5)

A

Headless HA
Hyperglycosylating the antigen binding head
Peptides against fusion peptide and ectodomain
Ferritin based nanoparticles displaying HA
Sequential immunisation with chimeric HA

40
Q

Explain Ferritin based nanoparticles displaying HA

A

Ferritin nanoparticle core - This makes the HA’s a lot more separated than on the normal flu particle, giving access to the core easier.

41
Q

Explain Sequential immunisation with chimeric HA

A

When administering vaccine boosts, change the head but keep the stalk, rather than do the usual of giving the exact same antigen each time and gradually the immune system will adapt to fight what it sees the most often

42
Q

How does the HIV spike GP120 evade neutralisation? (4)

A
  • Large space between spikes prevents Ab crosslinking meaning efficiency of antibody binding is reduced
  • Extensive glycosylation masks antibody epitopes
  • Functionally important parts of the molecule are poorly accessible, CD4 binding site, redundant amino acids are visible to B cell receptor and antibodies
  • Huge variation in the redundant amino acids means most antibodies are highly clade specific
43
Q

What are broadly neutralising Abs in HIV therapy

A

Antibodies that can cross-react with HIV strains exist alongside the virus in people who control the infection

44
Q

why is it difficult to make a vaccine for rhinovirus

A

Big antigenic variation

  • Human rhinoviruses cause the common cold
  • They exist as more than 120 antigenically distinct serotypes that co-circulate
  • Impossible to make a vaccine against them all
45
Q

What does a vaccine against all three poliovirus’ at once result in

A

in virus interference (where one of the 3 serotypes survived better in people than the others and cause problems) and poor response to one component

46
Q

How is a dengue infection detected (2)

A
  • Detected by increase in red cell count and decrease in protein level in blood
47
Q

Treatment for dengue?

A
  • Treat with iv fluid replacement
48
Q

What is antibody dependent enhancement of dengue

A
  • Antibody generated against a previous infection can bind but not neutralize, and lead to ADE (ANTIBODY DEPENDENT ENHANCEMENT), causing Dengue Haemorrhagic Fever Basically, antibodies for one serotype of the virus actually end up helping the other serotypes to gain entry into cells, leads to cytokine storm
49
Q

why is measles vaccinations especially important (not just bc it prevents measles)

A

Measles vaccine helps maintain immunological memory and so protects against more than just measles
introduction of measles vaccine was associated with up to 90% reduction in childhood mortality in poorer settings

50
Q

How many serotypes of measles?

A

1

Microbiology Y2 (6 decks)

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