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Microbiology > Interferon invasion > Flashcards

Interferon invasion Flashcards

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Biology 101 flashcards
1
Q

Explain how viruses are processed and presented

A

Viruses are obligate intracellular parasites.
Their peptides can be cleaved by proteosomes.
Cleaved peptides enter ER via TAP for packaging with MHC 1.
MHC loaded with viral peptides presented are inserted on cell surface.
Recognition by cytotoxic T cells.

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2
Q

What is TAP and where is it found?

A

Transporter associated with antigen processing; presented on ER membranes

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3
Q

What does tapasin do?

A

Loads MHC with viral peptides

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4
Q

Name three viruses which evade TAP

A

EBV
HSV
CMV

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5
Q

How does EBV avoid TAP?

A

EBV has a viral protein called EBNA1 which can’t be chopped up by the proteasome, therefore can’t be loaded onto TAP

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6
Q

Name a product produced by Herpes Simplex virus which blocks TAP

A

ICP47

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7
Q

What does CMV produce which blocks TAP and how does it work?

A

US6; stops ATP binding to TAP, therefore prevents TAP translocation

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8
Q

Name two viruses which interfere with tapasin and MHC transport

A

Adenovirus

CMV

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9
Q

How does adenovirus interfere with tapasin and MHC transport?

A

E3-19K
Prevents recruitment of TAP towards tapasin
Keeps MHC in ER

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10
Q

How does CMV interfere with tapasin and MHC?

A

US3; binds to tapasin and prevents MHC loading

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11
Q

Name two products of CMV and state how they interfere with viral clearance

A

US3 - binds to tapasin and prevents MHC loading
US6 - prevents translocation of TAP by stopping ATP binding to it

NB: US = unique short region of a gene

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12
Q

Name two viruses which interfere with MHC presentation

A

Karposi sarcoma herpes virus KSHV

HPV

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13
Q

How does KSHV interefere with MHC presentation?

A

kK3 induces polyubiquitination and internalisation of MHC into endosomes.
MHC is then passed onto lysosomes for degradation.

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14
Q

How does HPV interfere with MHC presentation?

A

E5 - prevents insertion of MHC 1 and 2 into membranes
E6 - interfere with JAK and cGAS pathway (preventing IFNb production)
E7 - same as above, also prevents transcription of MHC-I

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15
Q

What should normally happen if there’s no MHC present on a cell?

A

NK-cell mediated apoptosis/cell destruction

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16
Q

What are the two ways in which viruses combat the NK-mediated missing MHC cell destruction?

A

Encode MHC analogues/mimics

Upregulate MHC?

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17
Q

Give an example of a virus and its MHC mimic

A

CMV - glycoprotein UL40 (gpUL40)

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18
Q

What is antigenic DRIFT and what it is driven by?

A

Continued rapid evolution of virus, driven by antigenic pressure from host e.g. B cells

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19
Q

What is antigenic SHIFT?

A

Introduction of new subtypes of a virus from an animal source (SHIFT to a new subtype)

20
Q

Which viruses undergo antigenic shift and drift and what do they avoid?

A

Acute viruses - to evade the humoural immune response

21
Q

How do viruses which don’t change their antigens cause harm?

A

They circulate together despite having genetically stable subtypes so it’s harder to tackle one specific subtype

22
Q

Name three viruses with genetically stable subtypes

A

Rhinovirus
Poliovirus
Dengue virus

23
Q

How many subtypes of rhinovirus are there?

A

120

24
Q

How many subtypes of poliovirus are there?

A

3

25
Q

How many subtypes of dengue are there?

A

4

26
Q

Name two viruses which undergo antigenic drift

A

HIV quasispecies

Influenza (also goes through antigenic shift)

27
Q

What is the major viral antigen?

A

Haemagglutinin

28
Q

What are two types of antibodies which can target a viral antigen and where do these act?

A

Specific Ab - acts at head

Broadly neutralising antibody - acts at stem

29
Q

What do you call the variable and constant region of an epitope (Ab binding region on an antigen)?

A

Variable - HA1

Constant - HA2

30
Q

Name the five antigenic sites of HA1 epitopes

A

Sa
Sb
Ca1, Ca2
Cb

31
Q

List some strategies to stimulate broadly neutralising antibody production
????????????????????????????????????????

A

Headless HA

Hyperglycosylating HA1 head forces Ab to see stem

32
Q

Explain how HIV evades antibodies

A

gp120 spike
has large spaces in between it, meaning that Ab can’t cross link
Extensive glycosylation masks the Ab epitopes
Functionally important parts of the molecule are poorly accessible
Ab are clade specific and can’t recognise the huge variation in other redundant amino acids present on virus

33
Q

What happens when broadly neutralising antibodies control HIV loads?

A

New mutant HIV strands appear

34
Q

What are the two types of polio vaccine?

A

Inactivated polio

Live attenuated polio

35
Q

What is the complication with live attentuated polio?

A

All three serotypes must be included at the same time, but this results in poor response to one component

36
Q

How can this complication be overcome?

A

By increasing the levels of that one serotype

37
Q

Describe the onset of symptoms with Dengue virus

A 
1st exposure - flu like symptoms 
2nd exposure (to a different serotype) - dengue hemorrhagic fever
38
Q

Why do patients get dengue hemorrhagic fever after exposure to a second serotype?

A

Ab mounted against the 1st serotype bind, but do not neutralise the second serotype, leading to immune complex formation.
Complexes ingested by monocytes via Fc receptors.
The virus continues to survive via monocytes.

39
Q

What do you call this type of enhancement of viral replication of the second serotype?

A

Antibody dependent enhancement

40
Q

What is viral tropism?

A

The ability of viruses to infect many different types of cells

41
Q

What does an increase in dengue viral load result in?

A

Even more interleukins
IFN
Cytokines

Leading to the haemorrhagic fever and leakage of blood plasma from capillaries

42
Q

What does measles infect?

A

CD150 positive cells

43
Q

What is another name for CD150?

A

SLAM

44
Q

Why is measles so deadly?

A

One of the CD150+ve cells it infects is memory T-cells

Therefore erases immunological memory

45
Q

What is the human consequence of antibody dependent enhancement (besides for the patient)?

A

Vaccinations could be dangerous as if the patient encounters a new serotype, it could cause severe shock.

Microbiology (8 decks)

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