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BIOL 3155 > Chapter 29 > Flashcards

Chapter 29 Flashcards

HIV-1

1
Q

A retrovirus of HIV-1 was first isolated from

A

blood samples

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2
Q

HIV is considered a descendant of

A

SIV

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3
Q

the origin of HIV is

A

2 SIV -> SIVcpz -> HIV

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4
Q

HIV infects

A

CD4 helper T-cells

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5
Q

Lentivirus is

A

Genus of retroviridae that shows slow progression

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6
Q

Lentiviruses have

A

HIV-1 (1983), HIV-2, SIV, FIV

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7
Q

the progression of HIV-1 infection is typically followed as

A

decrease in CD4-T cells, immuno-compromised, susceptible to opportunistic infections

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8
Q

the three phases of the HIV progression are:

A

acute-infection, clinical latency, AIDS

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9
Q

acute infection comprises

A

entry of virus, localized replication at site of infection, release of virus into the circulation, seeding of lymph nodes throughout body, immune clearance of virus from peripheral circulation, continued replication in lymph nodes

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10
Q

clinical latency comprises

A

replication and destruction of lymph node architecture

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11
Q

AIDS comprises

A

release of virus into the circulation, loss of immune response, susceptibility to opportunistic infection

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12
Q

in AIDS, symptoms are

A

severe dehydration, diarrhea, bacterial infections, susceptible to skin cancer

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13
Q

the lower the virus load setpoint,

A

the slower the progression to AIDS

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14
Q

virus load setpoint is shown during

A

clinical latency after 12 weeks

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15
Q

HIV-1 is pandemic, where transmission is through

A

blood, sex, and breast milk

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16
Q

there are vaccine development with

A

30 candidates

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17
Q

antiviral treatments are done through

A

HAART, combination of at least three different drugs, inhibiting RT and PR

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18
Q

when virion protein R is packaged into the virion, tRNA of HIV is

A

lysine tRNA

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19
Q

general structure of HIV-1

A

conical capsid, VpR with tRNA lysine

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20
Q

genome structure of HIV-1

A

it has six additional ORFs of Vif, Vpr, Vpu, Tat, Rev, Nef

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21
Q

Vpr is structural, because

A

it is a part of the virion that has regulation roles

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22
Q

HIV produces over 25 mRNAs through

A

different splice sites

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23
Q

the 25 mRNAs are grouped in

A

three classes based on size

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24
Q

full length 9 Kb mRNA is used for

A

Gag and Pol (frameshift)

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25
Q

(single splice) 4 Kb mRNA is used for

A

Env, Vpr (frameshift), Vif, Vpu

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26
Q

(double splice) 2 Kb mRNA is used for

A

Tat, Rev, Nef

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27
Q

Vif is

A

viral infectivity factor

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28
Q

Vpu is

A

virion protein unique to HIV-1

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29
Q

Tat is

A

transactivator of transcripiton

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30
Q

Rev is

A

regulator of expression of virion proteins

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31
Q

Nef is

A

negative effector

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32
Q

HIV-1 targets

A

T cells and macrophages

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33
Q

T cells and macrophages have

A

CD4 receptor on surface

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34
Q

additional receptors of

A

CCR5 for macrophages and CXCR4 for T cells are needed

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35
Q

attachment protein is called

A

gp120 (SU) interacting with both primary and secondary receptors

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36
Q

gp41 (TM) is for

A

mediating fusion with PM

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37
Q

the capsid travels to

A

nucleus and enters via pores

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38
Q

the virus needs ds-DNA for

A

replication

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39
Q

Vpr is present in viral particle, carried into newly infected cell for two functions

A

1) helps virus enter nucleus through pores, required for HIV replication in non-diving cells
2) induces cell cycle arrest in the G2 phase, so viral transcription can be increased with HIV-1 LTR being most active in G2 phase

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40
Q

Core goes through RT, and travel through cytoplasm on

A

microtubule

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41
Q

in nucleus, pre-integration complex is composed of

A

IN, MA, and Vpr with the dsDNA

42
Q

viral latency is regulated by

A

transcriptional control elements in U3

43
Q

when foreign invader detected, immune response is

A

activated, along with T-cell activation

44
Q

T-cell activation leads to

A

activation of cellular TFs: NFkB and NFAT

45
Q

NFkB translocates into

A

nucleus, and interacts with U3 driving synthesis of the RNA

46
Q

T-cell activation activates

A

downstream TFs to translocate into nucleus where they bind to U3 to start transcription of proviral DNA

47
Q

NFkB and NFAT recruit

A

Pol II

48
Q

in the early gene expression, genes encoded in

A

the 2 kb class are expressed first

49
Q

CRS is

A

cis-acting repressive sequence of RNA in Gag/Pol and Env ORFs, causing viral mRNAs to be retained in the nucleus

50
Q

with CRS present, the full length 9 kb mRNA is

A

spliced twice to be transported to cytoplasm for translation

51
Q

the CRS present mRNAs are

A

retained in the nucleus

52
Q

Tat is

A

a highly basic protein of early gene that localizes to the nucleus to activate transcription

53
Q

Tat binds to

A

Tar in nascent viral RNA

54
Q

Tat recruits

A

Cyclin T and Cyclin-dependent kinase-9

55
Q

CdK9 is to

A

phosphorylate c-terminus of Pol II, enhancing processivity to increase full-length mRNA

56
Q

TAR is

A

a RNA element formed in the newly made transcript as a hairpin structure, bound to RNA pol II

57
Q

Rev is

A

a regulator of expression of virion protein of early gene that mediates nuclear export of LATE mRNAs in the 4 and 9 kb classes

58
Q

Rev binds to

A

RRE, rev response element in vRNAs, and Exportin1/RanGTP in Env ORF

59
Q

Exportin1/RanGTP is present only in

A

4 kb and 9 kb, involved in nuclear export pathways

60
Q

RRE located in

A

Env ORF

61
Q

Rev mRNA can exit from

A

nucleus to cytosol, to be translated as a protein

62
Q

Rev protein binds to

A

cellular protein Importin Beta, bringing it to the nuclear pore, and translocated into the nucleus

63
Q

Rev associating with

A

Exportin1/RanGTP, binding to RRE on mRNA, exits the nucleus

64
Q

Rev and Exportin1/RanGTP dissociates from RRE, and the mRNA is

A

now translated

65
Q

Nef is

A

a negative effect protein of early gene for determining pathology

66
Q

With Nef, there is

A

AIDS-like disease

67
Q

Without Nef, there is

A

no AIDS-like symptoms. It may be possible to develop an attenuated vaccine

68
Q

Nef’s known function is to

A

decrease surface expression of CD4 and MHC1, enhance virus infectivity, modify multiple parts of cell signalling

69
Q

Nef associates with

A

the cytoplasmic face of the PM

70
Q

Nef interacts with

A

the cytoplasmic tail of CD4, recruiting clathrin adpator protein 2

71
Q

Nef with clathrin AP2 undergoes

A

clathrin-mediated endocytosis of CD4, consequently decreasing CD4

72
Q

Nef interacts with MHC1 by blocking

A

Golgi to PM trafficing

73
Q

the absence of CD4 and MHC1 results

A

inhibition of immune response for the infected T-cell

74
Q

Nef associates with some proteins for cytoskeleton to enhance

A

releasing capsid into cytosol, leading to better infectivity

75
Q

Nef inhibits apoptosis through

A

associating with Pak2 kinase to increase anti-apoptosis signalling;
associating with Ask1 kinase to inhibit apoptosis signalling

76
Q

Vif is

A

a viral infectivity factor in late gene

77
Q

when Vif is absent, cellular protein Apobe gene gets incorporated into

A

budding virions from infected cell

78
Q

Once virion infects new cells, Apobe acts as

A

cytidine deaminase that converts cytosine to uracils in the (-)-strand DNA, resulting in G to A mutation in the (+)-strand during RT

79
Q

in absence of Vif, HIV goes through

A

hypermutation that inhibits farther viral spread

80
Q

Vif mediates in

A

degradation of host APOBEC3G through ubiquitination

81
Q

degrading APOBEC3G thorugh ubiquitin ligase protects

A

the virus from hypermutation

82
Q

mutant APOBEC3G with no deaminase activity retains

A

some inhibition of HIV

83
Q

A3G also directly inhibits

A

RT

84
Q

Vpu is

A

virion protein unique to HIV of late gene

85
Q

Vpu is

A

transmembrane protein that accumulates in Golgi and Endosomes

86
Q

Vpu has two functions of

A

degrading CD4 and enhancing virus release from PM

87
Q

Vpu interacts with

A

CD4 that normally would bind to gp160 in ER lumen, and recruiting beta-TrCP would ubiquitinate the CD4

88
Q

gp 160 is processed alone to be transported to PM, where it serves to

A

bud out new virions out of the cell

89
Q

Vpu enhances virus release from PM by

A

helping budding and releasing

90
Q

when mutated, Vpu allows

A

virions to accumulate on cell surface

91
Q

Vpu counteracts

A

anti-viral activity of a cellular protein Tetherin

92
Q

Tetherin interacting partially with

A

cellular PM and viral Env, forming a bridge for a cell to hold a virion for interferon regulation

93
Q

Vpu decreases

A

tetherin expression, possibly through Vpu-mediated degradation or sequestration

94
Q

immune system is evaded by

A

viral mutation to consequently alter viral proteins

95
Q

three vaccine types are

A

killed, attenuated or subunits

96
Q

phase two of vaccine test is on

A

small population

97
Q

phase three of vaccine test is on

A

large population

98
Q

first vaccine that went through phase three is

A

AIDSVAX

99
Q

AIDSVAX targets on

A

introduction of HIV surface protein gp120 to generate antibodies

100
Q

adenovirus 5 vector with Gag/Pol/Nef is

A

adeno5 vector used to deliver HIV-1 genes, ineffective

101
Q

recombinant viral vector with synthetic versions of Gag, Pr and Env genes + boosted with gp120

A

31% reduction in HIV acquisition

102
Q

Canadian HIV vaccine is

A

killed, no adverse effects, removed Nef and Vpr

BIOL 3155 (16 decks)

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