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Basic Immunology- Module 1 > EBV > Flashcards

EBV Flashcards

1
Q

What is essential for virus genome replication and segregation of EBV?

A

EBNA1

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2
Q

What type of virus is EBV?

A

gamma-1 herpes virus (HHV4)

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3
Q

What is the virion of EBV?

A

dsDNA viruas

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4
Q

What is a virion?

A

complete infective form of a virus outside the host cell

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5
Q

What is the tropism of EBV?

A

infects B cell and sometimes epithelial cells and T cells

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6
Q

Where are latent EBV found?

A

memory B cells

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7
Q

Where is EBV found after lytic replication?

A

saliva

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8
Q

What malignant diseases is EBV implicated in?

A

B cell lymphomas; nasopharyngeal and gastric carcinomas

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9
Q

What type of B cell with EBV infect in vitro?

A

any resting B cell

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10
Q

what is the effect of EBV infection of a esting B cell?

A

drive out of resting state to become an activated proliferating lymphoblast

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11
Q

How many gene programmes does EBV have?

A

4

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12
Q

What are the 4 gene programmes that EBV has?

A

1- used to produce infectious virus; other 3 are associated with latent infection

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13
Q

What are hte 3 latent gene programmes in EBV?

A

growth programme- all 9 known latent proteins are expressed; default programme- restricted set of 3 latenet proteins; latency programme- few if any latent genes are expressed

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14
Q

What determines the gene programme used by EBV?

A

location and differentiation stateo f hte infected B cell

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15
Q

What is persistent infection by EBV characterised by?

A

stable numbers of latently infected B cells in the blood and steady shredding of infectious virus into the saliva

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16
Q

What immune response accompanies the persisten infection of EBV?

A

stable levels of CTLs and serum antibodies to lytic and latent-stage proteins

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17
Q

What does a simple mutation in SLAM-associated protein restul in?

A

diverts EBV from benign persistence to acutely aggressive X-linked lymphoproliferative disease

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18
Q

Which gene programme does EBV use to activate B cells?

A

growth programme

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19
Q

Which gene programme does EBV use to change activated B cell into memory cell?

A

default programme

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20
Q

What are the 3 viral proteins expressed in the default programme?

A

EBNA1; LMP1 and LMP2A

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21
Q

What are LMP1 and LMP2A?

A

multiple membrane-spanning molecules that lack significant extracellular domains which act as active ligand-independent receptors

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22
Q

What is the key function of LMP1 and LMP2A?

A

possess the signalling capability to rescue an activated B blast in to the memory B ecll pool

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23
Q

What receptor does LMP1 share functional homology with?

A

CD40- demonstrated by experiments showing that the signalling domains are interchangeable

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24
Q

What receptor does LMP2A share similatirty to?

A

same ITAMs found in the alpha and beta chains of the BCR, associates with Lyn

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25
Q

How do EBV-infected cells enter the memory pool?

A

shutting down expression of all viral latent proteins- latency transcipriont programme

26
Q

What is the result of signalling from both CD40 and LMP1?

A

rescue B cells from apoptosis and drive proliferation

27
Q

Where in the body is EBV active?

A

naeopharyngeal lymphoid system e.g tonsils

28
Q

Where in the body is EBV dormant?

A

peripheral circulation

29
Q

What protein is the master transcirption factor in the growth programme of EBV?

A

EBNA2

30
Q

How do es infectious virus arrive in the tonsils during active infeciton?

A

from saliva exchange with an infected individual enters the tonsillar crypts and crosses the epithelium

31
Q

Where is infectious virus produced by lytic replication produced in the tonsils?

A

follicular mantle

32
Q

What is foudn in the follicular mantle of the tonsil?

A

large concentration of naive B cells

33
Q

What phenotype does activation of naive B cells by antigen or infection with EBV result in?

A

fully activated lymphoblastoid phenotype

34
Q

What are the 2 fates of recirculating memory cells entering the tonsil?

A

re-express the default programme to ensure long-term survival and then elave to re-enter pool of recirculating memory cells or they initiate lytic replication

35
Q

What is the function of Myc?

A

widely acting driver of cell division

36
Q

What transcription factors does EBNA2 bind to?

A

RBPJ; EBF1 and Pu1

37
Q

Why is Myc a double-edged sword?

A

Myc induces cell proliferation, however excessive cell prolfieration induces DNA damage which then blocks cell proliferation

38
Q

How does EBV prevent cell cycle arrest?

A

EDNA3A and EBNA3C which block cyclin-dependent kinases

39
Q

What is function of EBNA3B?

A

transcriptional repressor- represses genes that are expressed at lower levels in GC cells

40
Q

What is the function of EBNA3C?

A

activates AID- elevated AID results in more Ig mutation

41
Q

What protein mimics Ig crosslinking in B cells in the GC?

A

LMP2A

42
Q

What protein mimics activated CD40 in the B cell?

A

LMP1

43
Q

What happens to B cells that detect self epitopes?

A

become anergic (exhausted)

44
Q

What pro-apoptotic rptein is important in establishing anergy?

A

Bim; RASGRP1

45
Q

How does EBV repress anergy in B cells?

A

EBNA3A and/or 3C can epigenetically repress Bim and RASGRP1

46
Q

How does EBNA3 repress Bim?

A

by DNA methylation of Bim promotor

47
Q

What proteins are important in B cells differentiating to beomce plasma cells?

A

BLIMP1 and p18

48
Q

What EBV proteins suppress BLIMP1 and p18?

A

EBNA3A and 3c by binding to BLIMP1 and p18 genes

49
Q

What is the function of BZLF1?

A

triggers virus production upon plasma cell differtiation

50
Q

What is the function of EBER1?

A

allows homing to lymphoid tissues

51
Q

What is the dunction of EBNA2?

A

drives resting–activated B cells (Myc)

52
Q

What are the functions of EBNA3A and EBNA3C?

A

prevents cyclin dependent kinase-induced arrest; 3C–increases AID–increased Ig mutation; blocks plasma cell differenitation; prevents anergy

53
Q

What is the function of EBNA3B?

A

helps repress genes to support B blast to GC differentation

54
Q

What AI diseases are strongly associated with EBV postiively?

A

MS and SLE

55
Q

Why might EBV increase autoimmunity?

A

genetic RFs for some SI diseases overlap with EBNA2 binding sites on the genome

56
Q

What is the function of SLAM?

A

signalling lymphocyte associated molecule enhances T cell proliferation and IFNy production

57
Q

What is the function of LMP2A?

A

as it is similar ITAMs found in the alpha and beta chains of the BCR it provies the tonic signal essential for the survival of all B cells

58
Q

What is the function of the viral default transcri[tion programme?

A

replaces the signals that B cells require from Th cells and antigen

59
Q

Which area of the body does EBV drive activation and proliferation vs residing quiescently?

A

nasopharyngeal lymphoid system is where the virus is active whereas in the peripehral circulation the virus is dormant

60
Q

What receptor does EBV bind to on B cells to gain entry?

A

CR2

61
Q

What parts of the virus envelope does EBV bind to CR2?

A

gp350/220

62
Q

What does fusion of EBV into normal B cells require?

A

endocytosis which is triggered by interaction ebtween gp350/220 and complement receptor 2

Basic Immunology- Module 1 (31 decks)

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