Brainscape's Knowledge GenomeTM

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


See full index

Immunology and Infection > Antigenic Variation > Flashcards

Antigenic Variation Flashcards

1
Q

what is the antigen?

A
  • anything that an antibody will recognise

- antigens can vary, which can be evolutionary advantage

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

what are the two important proteins in influenza?

A

hemagglutinin (attaches to host receptors)

neuraminidase (breaks down sialic acid to allow budding)

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

what is antigenic drift?

A

minor mutations

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

what is antigenic shift?

A
  • major reassortment
  • virus infecting different species recombine leading to a major genomic change
  • leads to pandemics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the 3 subspecies of Trypanosoma brucei?

A
  1. T. brucei brucei
  2. T. brucei gamiense
  3. T brucei rhodesiense
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is T. brucei spread by?

A
  • the Tseste fly (infecting bile)

then you have haemo-lymphatic stage 1, meningo-encephalitic

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

what are the key points of how T. brucei achieves variation?

A

they switch surface coats - have variance surface glycoproteins (VSG surface coat)

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

what stages are VSG genes expressed by in T. brucei ?

A
  1. metacyclic

2. blood stream

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

how many VSG genes can the blood stream express?

A
  • around 1000 VSG genes
  • only one at a time
  • switch rate: every 100+ divisions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

where does T. brucei survive?

A

the bloodstream - extracellular

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

how does the VSG in T.brucei work?

A
  • tight protection coat
  • not accessing other proteins expressed
  • comes in waves
  • waves from the slender form to the stumpy form
  • stumpy forms dont divide
  • variant A will decline
  • variant B is produced and increases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe the process of VSG switching

A
  • entire VSG is internalised and recycled in 12.5min cycles
  • any antibody that lands on the antigen is digested
  • basis for evasion of the immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

where is the VSG most variable?

A

Ab binding region

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

what type of genes are VSGs?

A
  • pseudogenes or gene fragments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does T.brucei create new genes?

A

recombining fragments

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

where are expressed VSG genes located?

A
  • telomeric expression site (ES)

- only one expressed but multiple expression sites

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

how many expression genes are in the trypanosome nuclear genome?

A
  • around 20

- but only one is active at any given time

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

what does the telomere location of VSG expression sites suggest?

A

a role for position effect in their regulation

- specific structural features are associated with the DNA at ‘silent’ telomeres in blood stream trypanosomes

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

what are the mechanisms of activation for homologous recombination/gene conversion proposed in T.brucei?

A
  1. gene conversion
  2. segmental gene conversion
  3. telomere exchange
  4. transcriptional switch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is gene conversion in t.brucei?

A

VSG expressed is swapped for another

21
Q

what is segmental gene conversion in t.brucei?

A
  • multiple recombination

- made of multiple gene fragments

22
Q

what is telomere exchange in t.brucei?

A

from another expression

23
Q

what is transcriptional switch?

A
  • one expression site shut down another switched on
24
Q

what is the structure of a VSG expression site?

A
  • 50bp repeats upstream of promoter
  • 70bp, instrumental in recombination
  • ESAGS
  • VSG promoter ~50kb of VSG gene
25
Q

what are ESAGS in VSG?

A
  • expression site associated genes

- driven by polymerase 1

26
Q

what is the model for telomeric silencing in t.brucei?

A
  • silencing involves separate telomere binding and spreading factors
  • remove Rab repressor
  • T.brucei will express all 3 VSG coats
27
Q

how are enzymes used in the VSG of t.brucei?

A
  • mutants of enzymatic pathway show de-repressed VSG transcription
  • polymerase I expression limited through a kinase
28
Q

what causes antigenic variation in plasmodium?

A

Var genes

29
Q

what does plasmodium cause?

A

malaria

30
Q

why is plasmodium difficult to target for vaccines and treatments?

A

complex lifecycle

31
Q

give a brief overview of the human lifecyle of plasmodium

A
  • goes to the human liver first
  • merozoites then infect the RBCs
  • they are burst and destroyed
  • cause anemia and fever
  • produce gametes which are taken up by the mosquito
32
Q

when are the cycles of fever and chills in malaria?

A
  • every 48 hours
  • related to the bursting of RBC and the release of parasites
  • malaria is highly pathogenic
33
Q

how does the plasmodium transform the RBC?

A
  • has knobs and cytoadherence
  • infected RBCs develop suface knobs containing parasitic proteins
  • causes the RBC to stick in blood vessels and block capillaries (RBC not cleared)
  • forms clumps
  • results in liver and brain inflammation
34
Q

what is the main protein involved in the cytoadherence caused by plasmodium?

A

PfEMP1 - promotes parasite survival

- these proteins are transcribed throughout the genome

35
Q

what is PfEMP1 coded by in plasmodium?

A

Var genes

36
Q

what are the highly variable domains in PfEMP1?

A
  1. DBI domain

2. CIDR domain

37
Q

how do the DBI and CIDR domains cause variability in the plasmodium?

A
  • recombine and theres different categories

- can recombine with themselves and with each other

38
Q

where is PfEMP1 found?

A

on the surface of the host cell (rather than the parasite surface)

39
Q

how has T.cruzi been targeted?

A

targeting the vector rather than the parasite

40
Q

what strategy does t.cruzi use to evade the immune system?

A

the invisible cloak strategy

41
Q

what does the invisible cloak strategy entail in t.cruzi?

A
  • multiple copy families of surface antigens
  • lots of duplication
  • hard to classify because their surface proteins change
  • they can (theoretically) infect any nucleated cell
42
Q

how does t.cruzi overwhelm the immune system?

A

50% of genome is surface proteins and they are all expressed

43
Q

what are the main 3 highly heteregenous gene families in t.cruzi?

A
  1. trans sialidases
  2. mucins
  3. MASPs
44
Q

what are trans-sialidases in t.cruzi?

A
  • catalyses the transfer of silaic acid
  • bind to host cell receptors to invade
  • block complement/immune evasion
45
Q

what are mucins in t.cruzi?

A
  • major acceptors of sialic acid

- form a thick surface barrier of different lifecycle stages

46
Q

what are MASPs in t.cruzi?

A
  • highly polymorphic gene family
  • enable t.cruzi to invade and multiply in the cytoplasm of host cells
  • implicated in infertility; also reduce virulence
47
Q

how does t.cruzi fool the immune systeM/

A

fools T cells into thinking the parasites are self

48
Q

what does t.cruzi need sialic acid for?

A
  • host cell attachment
  • invasion of the cytosol
  • host mimicry
49
Q

how does t.cruzi obstruct CD8+ T cell immunity?

A
  • immune cell function dependent on sialic acid
  • activated when they lose sialic acid
  • puts them back on to the T cells to confuse the T cells
  • T cells are inactive and dont target the parasite

Immunology and Infection (13 decks)

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