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MIMM 324 > 32. Retroviruses 4 > Flashcards

32. Retroviruses 4 Flashcards

1
Q

what elements regulate splicing?

A

RNA cis-acting sequences bound by host factors

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2
Q

what are the 2 sizes of spliced mRNAs?

A

4kb and 2kb

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3
Q

2 types of RNA cis-acting elements

A
  1. exon splicing silencers
  2. exon splicing enhancers
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4
Q

locations of splice sites?

A

1 splice site on 5’ end, the rest are further downstream

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5
Q

4 examples of host TFs that bind transcription cis-acting elements in promoter region?

A
  1. TATA
  2. AP1
  3. NFkB
  4. Sp1
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6
Q

why do host TFs bind transcription cis-acting elements?

A

to enhance transcription

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7
Q

what is Tat and its 2 roles?

A

Tat = transactivating protein

  1. initiates transcription
  2. promotes elongation
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8
Q

how does Tat enhance transcription + elongation?

A

recruits CycT and Cdk9 TFs

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9
Q

what is the role of REV? how does it work?

A

REV promotes mRNA export from the nucleus by concatemerizing with RNA REV response element

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10
Q

where is the RNA REV response element found?

A

found in the envelope coding region, therefore found in 4kb mRNA but absent in 2kb mRNA

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11
Q

describe the 3 steps for rev and tat activity

A
  1. the spliced 2kb mRNAs for REV, TAT, and NEF are exported to cytoplasm to be translated
  2. REV goes back to nucleus to bind RRE and bring out 4kb mRNA
  3. TAT goes back to nucleus to increase transcription
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12
Q

what is the role of auxillary/accessory proteins?

A

for defense, enhance viral replication, etc.

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13
Q

what is Vif?

A

promotes degradation of APOBEC3 restriction factor to block APOBEC3 antiviral function

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14
Q

what is APOBEC3 antiviral function?

A

APOBEC3 associates with Gag and gets packaged –> creates errors in expression, leading to hypermutation

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15
Q

how does APOBEC3 create errors in expression?

A

deaminates cytidine to make uridine

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16
Q

what does APOBEC3 stand for?

A

APOlipoprotein B Editing Complex protein

17
Q

what are considered to be early events in retroviral replication cycle?

A

everything up to integration

18
Q

what are considered to be late events in retroviral replication cycle?

A

after integration, everything after transcription

19
Q

what does Vpu do in HIV1?

A

counteracts tetherin restriction factor

20
Q

what does tetherin do?

A

makes virions bind to PM or each other to prevent release of virions

21
Q

How is tetherin counteracted in SIV?

A

With Nef protein

22
Q

How is tetherin counteracted in HIV2?

A

With envelope protein

23
Q

what is required for tetherin to exert its function?

A

must function as a dimer

24
Q

how does Vpu target tetherin?

A

Vpu targets tetherin for degradation via proteasomal and lysosomal degradation pathways

25
Q

where is tetherin found?

A

golgi and PM

26
Q

3 mechanisms of HIV1 transmission

A
  1. free virus receptor-mediated entry
  2. entrapped virus in macrophages
  3. veritable cell-to-cell via virological synapse
27
Q

what is the issue with free virus receptor-mediated entry?

A

it is not efficient or beneficial for the virus

28
Q

what are the results when infected and uninfected T cells are mixed?

A

cells naturally contact and redistribute the CD4 receptor and envelop proteins –> uninfected cell becomes infected

29
Q

what is the virological synapse?

A

between infected and uninfected cells –> allows cell to cell transmission

30
Q

what 2 types of cells do T cells receive the virus from?

A
  1. macrophages
  2. T cells
31
Q

what is transferred btwn cells during cell to cell transmission?

A

Gag protein

32
Q

how do receptors on cell surface redistribute for cell to cell transmission?

A

the cytoskeleton changes

33
Q

steps for cell to cell transmission (6)

A
  1. recruitment of membrane receptors on infected cell
  2. cytoskeleton reorganizes
  3. viral protein and genome trafficking
  4. recruitment of membrane receptors on uninfected cell
  5. virological synapse forms
  6. virus transmission
34
Q

why is cell to cell transmission helpful?

A

evasion of host immune response + enhancement of viral propagation to enhance rate of infection by 1000x

35
Q

what is cell surfing?

A

virus surfs along extension on uninfected cell to enter uninfected cell

36
Q

2 requirements of cell surfing

A
  1. myosin and actin
  2. receptor:ligand/envelope anchoring
37
Q

why is cell surfing required?

A

allows viruses to travel to actin-poor and remodeling regions to facilitate entry

38
Q

2 types of extensions for cell surfing?

A
  1. filopodia
  2. nanotubes
39
Q

benefits of virus surfing?

A
  1. enhance efficiency and rate of transmission by 1000x
  2. immunological escape mechanism

MIMM 324 (37 decks)

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