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Module 2 > Chapter 13 Part 2 > Flashcards

Chapter 13 Part 2 Flashcards

1
Q

What cells are specialised for type I interferon production early in viral infection?

A

plasmacytoid DCs

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2
Q

What is the benefit of a segmented genome?

A

the ability ot reassort during viral replication

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3
Q

What is the fucntion of hemagglutinin on influenza?

A

repsonseibl for viral binding to and entry into cells

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4
Q

What is antigenic drift?

A

emergence of point mutations to alter binding sites– can grow in cell immune to previous strain but as T cells and some antibodies can recognise epitopes that have not been altered will only get a mild disease

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5
Q

Waht is antigenic shift?

A

reassortment of the segmented RNA genomes of 2 different influenza viruses when they are able to infect the same cell reuslting in large changes in their haemagglutinin so T cells and antibodies to previous infections are not protective

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6
Q

What is a neutralising antibody?

A

prevent the virus from binding and infecting cells

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7
Q

What is dislocation?

A

when viruses catalyse the degradation of newly synthesised MHC-I molecules by initiating hte pathway normall used to degrade misfoleded ER proteins by directing them back into the cytosol and the ERAD pathway for disposal

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8
Q

How does CMV evade NK cytolysis?

A

produces a homolog of HLA class I - UL18 which binds LIR-1 on nk cells providing an inhibitory signal

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9
Q

What is the function of cytosolic ICP47 produced by herpes simplex?

A

prevents peptides from binding to TAP in the cytosol

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10
Q

What is hte function of US6 protein produced by CMV?

A

interferes with the ATP-dependent transfer of peptides through TAP

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11
Q

What is the function of E19 produced by adenovirus?

A

competes with tapasin and inhibits peptide loading onto nascent MHC-I molecules

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12
Q

What is the function of mK3 protein produced by murine herpes simplex virus?

A

directs the addition of ubiquitin subunits with K48 linkages resulting in degradation via proteasome

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13
Q

What cytokine homolog does CMV use to impair antiviral responses?

A

cmvIL-10 which downregulates pro-inflammatory cytokines

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14
Q

What do herpes viruses express in order to undergo a lysogenic phase?

A

express the latency associated transcript

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15
Q

What is the function of the latency associated transcript?

A

suppresses the transcription of the remaining viral genome and produces factors that interfere with host cell apoptosis

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16
Q

How does EBV enter B cells?

A

using CD21 (CR2) and MHC-II

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17
Q

What is the function of EBNA1 produced by EBV?

A

interacts with teh proteasome to prevents its own degradation into peptides that would otherwise elicit a T cell repsonse

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18
Q

What are the differences between HIV-1 and HIV-2?

A

HIV-2 is only really found in West Africa; HIV-1 replicates to higher viral loads in the blood and is more easily transmitted, HIV-2 is rarley vertically transmitted

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19
Q

what is the most common variant of HIV-1?

A

group M

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20
Q

What makes up the HIV viral spike?

A

gp120/gp41

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21
Q

What is the function of the RNA transcripts produced from the integrated viral DNA?

A

mRNAs to direct synthesis of viral proteins and the RNA genomes of new viral particles

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22
Q

What group of viruses does HIV belong to?

A

lentiviruses

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23
Q

What are the 3 cell targets of HIV?

A

CD4 T cells; macrophages and DCs

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24
Q

What is cellular tropism?

A

its ability to enter particular cell types

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25
Q

What determines HIV’s cellular tropism?

A

expression of specific receptors fro the virus on the surface of those cells

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26
Q

What are the major coreceptors for gp120 fusion and entry?

A

CCR5 and CXCR4

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27
Q

Which cells predominantly express CCR5?

A

subsets of effector memory CD4 T cells; DCs and macropahges

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28
Q

Which cells predominantly express CXCR4?

A

naive and central memory CD4 T cells

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29
Q

What happens when gp120 binds CD4?

A

undergoes a conformational change that exposes a high-affinity site that is bound by the coreceptor

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30
Q

What does binding of the coreceptor to gp120 cause?

A

gp41 unfolds and inserts a portion of its structure (fusion peptide) inot the plasma membrane of hte target cell

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31
Q

What is found in the viral nucleocaspid?

A

viral genome and associated viral proteins

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32
Q

How many genes does HIV have?

A

9

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33
Q

What is the form of DNA produced by reverse transcriptase?

A

cDNA

34
Q

What is used by integrase to integrate the cDNA into host DNA?

A

LTRs that reside at each end of the viral genome

35
Q

What is the integrated cDNA copy known as?

A

provirus

36
Q

What is the function of the gag gene?

A

encodes structural proteins of the viral nucleocapsid core

37
Q

What is the function of pol?

A

encodes enzymes involved in viral replication

38
Q

What is the function of env gene?

A

encodes viral envelope glycoprotein

39
Q

What 3 enzymes does pol encode?

A

reverse transcriptase; integrase; viral protease

40
Q

How are gag and pol translated?

A

as long polypeptide chains that are then cleaved by pol

41
Q

What is the product of the env gene?

A

gp160

42
Q

What is gp160 cleaved into?

A

gp120 and gp41

43
Q

What initiates transcription of hte provirus following integration?

A

host transcription factors which are induced during activation

44
Q

What is the function of Tat?

A

enhances transcription from hte provirus and binds to the RNA transcripts, stabilising them in a form that can be translated

45
Q

What is the function of Rev?

A

binds to singly spliced or unspliced transcripts and transports them to the cytosol

46
Q

What si the long-lived latency of HIV related to?

A

it is a consequence of the toprism of the virus for CD4 T cells

47
Q

What is the function of vif?

A

affects particle infectivity

48
Q

What is the function of viral protein R?

A

transport of DNA to nucleus, augments virion production, cell cycle arrest

49
Q

What is the function of viral protein U?

A

promotes intracellular degradation of CD4 and enhances release of virus from cell membrane

50
Q

What is the function of nef?

A

augments viral replication in vivo and in vitro. decreases Cd4, MHC-I and II expression

51
Q

What 2 transcription factors can initiate transcription of the viral genome?

A

NFkB and NFAT

52
Q

How may activation of NFkB take place independetly of antigen?

A

activation of effector-memory T cells can occur by cytokines

53
Q

How does Tat work?

A

binds to a transcriptional activation region in the LTR which recruits cellular cyclin T1 and its partner, CDK9 to form a complex which phosphoryaltes RNA polymerase and enchanes its ability to generate full-length transcripts of the vrial genome

54
Q

How does Rev work?

A

binds to Rev response element- a specific viral RNA sequences to prevent degradation of incompletely spliced mRNA transcripts by the host

55
Q

How does Nef augment viral replication?

A

lowers the threshold for TCR signalling and downregulates CTLA-4 which results in greater and more sustained T cell activation that promotes viral replication

56
Q

How does Vif work?

A

acts to overcome a cytidine deaminase called APOBEC which catalyzes the conversion od deoxycytidine to deoxyuridine in reverse transcribed viral cDNA thereby destroying its ability to encode protein

57
Q

How does Vpu work?

A

required to overcome tetherin which inserts into both the plasma membrane of the host cell and the envelope of hte mature virion to block its release

58
Q

How does Vpr work?

A

target restriction factor SAMHD1, which limits the intracellular pool of deoxynucleotides available for viral cDNA synthesis

59
Q

In what forms can the virus be transmitted?

A

free infectious particles or via infected cells for which the virus has tropism

60
Q

Why does inital viral replication favoured in Th1 and Th17 cells?

A

they express CCR5- naive T cells and Th2 don’t

61
Q

What strains of virus are typically required for transmission and why?

A

CCR5-tropic R5 strains as CCR5 dominates on CD4-expressing immune cells resident at the major sites of viral transmission;epithelial cells of the rectum and endocervix express CCR5 so R5 can translocate

62
Q

How can HIV bind to DCs?

A

binding of viral gp120 to CTLRs eg langerin; mannse receptor and DC SIGN– allows HIV to travel to lymph nodes

63
Q

Where do the highest number of CD4 T cells in the body reside?

A

GALT

64
Q

How may the depletion of immune cells in the gut coumpound rapid production of virus in the GALT?

A

result in barrier breakdown and translocation of constituents of the microbiota which increases immune cell activation

65
Q

What is the viral set point?

A

level of virus that persists in the blood plasma after development of CTL response and antibody production which occurs during the acute phase to control high viraemia

66
Q

What is the viral set point indicative of?

A

future disease progression

67
Q

What does the strong selectie pressure of hte antiviral immune response result in?

A

selection for HIV escape mutants that are no longer detected by the adaptive immune cells- many viral variants

68
Q

What happens to the dominanat viral type?

A

in about 50% it swithces from R5 to X4 variants which results in progression to AIDs

69
Q

What are the overall functions of the R5 and X4 variants?

A

R5 variants are critical for HIV transmission whereas X4 variants that emerge under selective pressure contribute to disease progression

70
Q

What is the correlation between the strength of CD4 T cell proliferative responses to HIV antigen and viral load?

A

inverse

71
Q

What are the 2 important aspects of hte antibody resposne to HIV?

A

generating neutralising antibody against gp120 and gp41 in order to block viral attachment or entry; generating nonneutralising antibodies that target infected cells for ADCC

72
Q

What are broadly neutralising antibodies?

A

antibodies able to block infection by multiple viral strains

73
Q

Why is homozygosity of HLA class I alleles associated with more rapid disease progression?

A

T cell response to infection is less diverse

74
Q

Give examples of HLA class I alleles associated with greater prognosis?

A

HLA-B57; HLA-b27; HLA-B13- delay HIV-1 escape

75
Q

Why do ARTs not prevent the release of virus?

A

cells that are already infected as provirus is already established so reverse transcriptase and integrase aren’t needed and inhibition of protease does not stop virus being released

76
Q

What causes the increase in cD4 T cells with HAART?

A

redistribution of CD4 T memory cells from lymphoid tissues into circulation as viral replication is controlled; reduction in immune activation so reduces killing of infected CD4 T cells by CD8 cells; emergence of naive T cells from the thymuc

77
Q

What is the function of APOBEC?>

A

causes extensive mutation of newly formed HIV cDNA to destroy its coding and replicative capacity

78
Q

What are quasi-species?

A

variants of HIV that develop from a single foudner virus

79
Q

Which viruses share the formation of quasi-species?

A

all lentiviruses

80
Q

which HIV gene is respondible for inhibiting the restriction factor SAMHD1?

A

Vpr

Module 2 (38 decks)

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