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MGY378 > HIV (Dr. Cochrane) > Flashcards

HIV (Dr. Cochrane) Flashcards

1
Q

Origin of HIV?

A

from SIVcpz of chimpanzees

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2
Q

What happens when old world monkeys have HIV-1?

A

High level of viremia
BUT not immune deficiency

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3
Q

Differences between SIV infection in human in natural host

A

I) Level of peripheral CD4+ T cells:
Healthy in host, low in humans
II) immune dysfunction: only found in human
III) chronic immune activation: only in human

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4
Q

Factors affecting transmission efficiency

A

I) inflammation due to other infections increase number of target cells in mucus, mucosal envrionment
II) viral load in inoculum

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5
Q

Types of HIV-1

A

R5, X4

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6
Q

Which form can transmit acroos mucosal membrane?

A

R5

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7
Q

Site of SIV-1 replication?

A

Gastrointestinal tract
Nasal cavity
Male genital tract
Lymph nodes
Lungs

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8
Q

Cells infected by HIV-1

A

I) CD4+ T cells
II) Monocytes/macrophages

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9
Q

What happens after CD4+ T cell infected by HIV-1?

A

Infected cells can induce death of neigbouring T cells by pyroptosis due to abortve infection

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10
Q

What happens after macrophages are infected by HIV-1?

A

Can enhance HIV-1 infection of surrounding cells

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11
Q

what decides the progression of HIV infection/

A

Viral load setpoint
—> the higher, the quicker it reaches end pt

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12
Q

Why current treatments unable to cure HIV-1

A

I) residual levels of viral replication (not fully suppressed)
II) small pool of cells with silent integrated genomes persist
III) persistent immune dysfunctions

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13
Q

What co-receptor do X4 bind for entry?

A

CXCR4

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14
Q

What co-receptor does R5 bind to?

A

CCR5

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15
Q

How does HIV-1 enter our cells?

A

I) bind to CD4 —> change in gp120 on virus
II) change in gp120 allow binding to secondary receptor (CXCR4/CCR5)

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16
Q

A genetic mutation that led to HIV-1 resistance

A

Lacking CCR5

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17
Q

What happens during clinical latency that complicates cure?

A

Lots of new virions formed per day (2 billion)—> kill equal number of T cells
—> lots of new mutation arise, huge variety in HIV-1

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18
Q

What is HIV-1/2 transcription dependent on?

A

Activation state of cell (must be activated)

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19
Q

Why is HIV-1 most active in T cells?

A

Active NFAT, NFkappaB, AP2 present only in activated T cells

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20
Q

How does HIV-1 exploit adaptive immune system?

A

Once T cells activated, HIV-1 can infect it
—> can integrate into memory T cells
—> oncre reactivated —> able to expand and replicate new virions

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21
Q

How does viral insertion into cell DNA + long living infected cells affect treatment?

A

I) no idea where the reservoir is + reservoir established 3 days after exposure
II) take long time for treatment as those with silent virus are not killed thru drugs (take 60 years)
III) withdrawal of drugs —> infection reappear rlly quick

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22
Q

Approaches suggested to kill HIV

A

I) Shock and kill
II) enhance function of immune system
III) Scorched earth
IV) Block and lockH

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23
Q

How does shock and kill work?

A

Use agents to force cells to express latent virus —> immune system can detect and kill

24
Q

How does scorched earth work?

A

Wipe out all immune cells and replace with new ones resistant to virus

25
Q

How does block and lock work?

A

Treat cells to prevent virus re-activation

26
Q

Features in HIV-1 RNA

A

I) encodes for 9 proteins
II) lots of splice donor (4) and acceptor sites (9)

27
Q

HIV non strucutral genes crucial in cells

A

Tat, Rev

28
Q

HIV non structural genes that are not essential in vitro (Needed for replication within host)

A

Nef, Vif, Vpr, Vpu

29
Q

Common features of HIV-1 non structural genes

A

I) lack enzymatic function
II) mediate new interactions between cellular factor

30
Q

What is the function of Tat?

A

Increase viral RNA synthesis by increasing elongation efficiency of RNA Pol II

31
Q

How does Tat increase RNA pol II’s elongation efficiency?

A

Bind to TAR at 5’ end of transcript
—> recruit Cdk9, cyclin T to phosphoryltae C term of RNApol2

32
Q

What is recruited after Tat binds to TAR on 5’ end?

A

Cdk9, cyclin T

33
Q

What genes are early expressed in HIV-1?

A

Tat, Rev, Nef

34
Q

Why are other genes expressed later?

A

Need Rev to induce export of incompletely spliced RNA

35
Q

Role of non structural genes in HIV-1 that is not essential in vitro

A

I) allow HIV-1 to overcome innate defenses of host cell
II) limit function of factors needed for adaptive immune response (MHC-I, II) + alter cell state to increase HIV-1 replication

36
Q

What happens when HIV/SIV cannot express nef?

A

No or slow progression to AIDS

37
Q

Function of Nef

A

I) remove CD4/MHC1 or II from cell surface
II) Arrest of apoptosis in infected cells
III) modulate T cell signalling
IV) enhance viral infection

38
Q

How does Nef remove CD4, MHCI or II from cell surface?

A

bridge CD4 with AP2, MHC with AP1
—> alter trafficking
—> removed from cell surface

39
Q

How does Nef enhance viral infection

A

Reduce surface expression of SERINC3, SERINC5

40
Q

What happens to HIV lacking Vif?

A
  • Reduced capacity to infect new cells
  • high levels of ApoBEC3F/G
41
Q

Function of Vif

A

Increase infectivity of HIV-1 by inhibiting APOBEC

42
Q

When does Vif act to help HIV-1?

A

During assembly of virus

43
Q

What is APOBEC3F/G?

A

cytidine deaminases

44
Q

What is the function of APOBEC3F/G?

A

selectively modify ssDNA

45
Q

How does APOBEC3G perform its function?

A

induce hypermutation in viral genome

46
Q

Function of Vpu?

A

I) Facilitate Gp120 release
II) enhance virus release from cell surface

47
Q

How does Vpu facilitate Gp120 release?

A

Induce degradation of CD4 in ER lumen

48
Q

How does Vpu promote virus release?

A

Stimulate uptake of tetherin into endosome
—> reduce expression of tetherin on membrane
—> less HIV-1 accumulated in vesicles

49
Q

Barriers to HIV-1 treatment and eradication

A

I) patient compliance (Need to maintain treatment)
II) drug resistance
III) viral latency (established early in infection + rebound is common after withdrawal from treatment)

50
Q

Which types of infected cells have long life span

A

T helper memory cells (hv latent virus)

51
Q

Which protein increase infectivity of HIV-1?

A

Vif-1

52
Q

Which protein degrades host CD4?

A

Vpu

53
Q

Which protein help with HIV-1 pathogenesis?

A

nef

54
Q

function of Vpr

A

cell cycle arrest, induce cell death

55
Q

Which protein is essential for expression of viral structural proteins?

A

Rev

56
Q

Which protein increase viral RNA synthesis?

A

Tat

MGY378 (13 decks)

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