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Virology > Lecture 5: DNA virus overview and polyomavirus > Flashcards

Lecture 5: DNA virus overview and polyomavirus Flashcards

1
Q

why don’t small DNA viruses encode entire replication systems

A

no DNA virus encodes everything they need

  • encodes proteins that orchestrate the host
  • papillomaviridae, polyomaviridae, parvoviridae
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2
Q

where does the polymerase come from

A

small DNA viruses

  • no DNA virus encodes everything they need
  • encodes proteins that orchestrate the host
  • papillomaviridae, polyomaviridae, parvoviridae

large DNA viruses

  • encode their own replication system
  • herpes, adenoviridae, poxviridae
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3
Q

basic rules of DNA replication in eukaryotic cells

A
  • DNA synthesized by template-directed incorporation of nucleotides into 3’-OH of DNA chain
  • always synthesized 5’ to 3’ (semiconservative)
  • replication origins
  • catalyzed by DNA dependent DNA polymerase and accessory proteins
  • always primer dependent
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4
Q

host cell nuclear functions

A
  • DNA replication (DNA polymerases, helicases, RNA primase, ligase, DNA binding proteins
  • RNA transcription (initiation factor, RNA polymerase II)
  • RNA processing (capping/splicing)
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5
Q

all DNA viruses encode an initiation protein that

A
  • bind to ORI region

- recruit host DNA replication proteins

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6
Q

all DNA viruses require ______ for DNA synthesis

A

RNA primer

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7
Q

replication fork vs strand displacement (primer)

A

replication fork

  • in both directions
  • papillomavirus, polyomavirus, herpesvirus, retroviral proviruses

strand displacement

  • one direction
  • adenoviruses (protein), parvoviruses (DNA hairpin), poxvirus (DNA hairpin)
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8
Q

describe the “end replication” problem

A

all linear DNA shortens when replicated

  • RNA primers added and removed during replication
  • primers located at 5’ end of linear DNA not replaced
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9
Q

what is the “solution” for DNA viruses

A
  • circular genomes
  • circularized linear genomes: inverted repeats
  • protei primers
  • hairpin loops
  • rolling circle
  • reverse transcription
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10
Q 
28 mn
no envelope
capsid: icosahedral (T=1)
baltimore class 2
linear, ssDNA (hairpin termini)
segments: 1
genes: 6 mRNAs
genome size: 5kb
members: B19, FPV, CPS
unique traits: integrate into host DNA
A

parvoviruses

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11
Q

replicate in cells that normally cycle and frequently enter S phase

A

autonomous parvoviruses

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12
Q

replicate in cells infected with a helper virus which indices entry of the cell into S phase
-may enter latent phase by integrating in host genome if helper virus is absent

A

dependent parvoviruses

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13
Q

gene products in viruses

A

multiple proteins from one open reading frame by staggering promoter

  • alternative splicing od mRNA
  • post-translational proteolytic cleavage
  • internal translation initiation
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14
Q

describe parvovirus replication

A

extremely host dependent

  • dependent on host cell DNA rep system
  • require actively dividing cells (s phase)
    • rbc precursors
    • cancer cells (lethal)

regulatory proteins (NS1 and Rep78/68

  • bind to viral DNA- powerful transcription activator for recruiting host polymerase
  • freeze cell cycle in s phase
  • helicase activity unwinds circular
  • endonuclease activity
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15
Q 
45 nm
no envelope
capsid: icosahedral (T=7)
baltimore class 1
circular, dsDNA; "minichromosome"
segments: 1
genes: 6-7 proteins
genome size: 5.3 kb
members: simian virus 40, BK and JC virus
unique traits: T antigens= oncogenes, tumorigenic in animals
A

polyomaviruses

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16
Q

polyomavirus structure

A 
72 pentomers (no hexamers)
inner: nucleosome with viral DNA wrapped around, VP2/VP3, VP1: outer
17
Q

describe the mouse polyomavirus: divergent transcription, early/late proteins, differential splicing

A

divergent transcription- complementary strands transcribed in opposite directions

early proteins: regulatory genes transcribed first

  • sm, middle, and lg T antigens
  • stimulate the cell cycle to enhance viral DNA replication

late proteins: transcription of structural genes is delayed
-capsid proteins

differential splicing of a common mRNA transcript maximizes coding capacity

all mRNAs are coded at the polyadenylation signal region

18
Q
  • functions by indirectly enhancing the transcription of cyclin D1
  • binds and inactivates protein phosphatase 2A
  • end result is binding of AP-1 to cyclin D1 transcription enhancer
A

small T antigen

19
Q

how do small T antigen function by indirectly enhancing the transcription of cyclin D1

A

activates the cell cycle and brings host cell into S phase

20
Q

why do small T antigen bind and inactivate protein phosphatase 2A

A

allows phosphorylation of MSP kinase pathway

21
Q
  • activates signaling pathways

- cell metabolism stimulated and initiates the cell cycle

A

middle T antigen

22
Q

how are middle T antigen pathway signals activated

A
  • middle T antigen anchored in cell membrane
  • associates with several protein tyrosine kinases
  • initiates cascade of signaling events
23
Q

tyrosine kinase protein that a potent oncogene, activator of cell cycle that has the ability to over stimulate cell growth but normally regulates the cell

A

C-Src

24
Q

tyrosine kinase proteins attached to middle T antigen

A

-C-Src, activated MAP kinase, phosphatidyl inositol 3 phosphate, inositol triphosphate (middle T antigen serves as dock for them)

25
Q
  • RB binding site and J domain dissociates the retinoblastoma protein (pRb) from E2F transcription factors
  • blocks protein p53, preventing activation of genes that black cell growth/induce cell death (apoptosis)
  • binds to viral DNA replication origin and recruits cellular DNA replication proteins
A

Large T antigen

26
Q

what happens if E2F transcription factors are bound to pRb

A

if pRb is bound then cell won’t divide

27
Q

what kind of cells can NOT survive without p53?

A

tumor cells

28
Q

describe the MAP kinase pathway

A

MAP kinase (inactive)

  • MAP kinase kinase + ATP = MAP kinase +P (activated)
  • phosphorylates and activates AP-1 (Fos/Jun)
  • AP-1 binds to cyclin D1 enhancer, stimulates transcription

OR

-small T antigen binds to protein phosphatase 2A and inactivates PP2A = inactivated MAP K

29
Q
  • identified in 1960
  • potent DNA tumor virus
  • natural host: rhesus monkey
  • persistent infections in kidneys
  • urine transmission
  • opportunistic pathogen
A

simian virus 40 (SV40)

30
Q

describe productive SV40 infections

A
  • completes infection cycle in permissive cells
  • requires actively dividing culture cells
  • cell lysis w/in 72 hrs
  • lg T antigen binds, allowing for replication
  • no cell transformation occurs (rhesus monkey to rhesus monkey)
31
Q

describe abortive SV40 infections

A
  • cells transform ONLY non permissive cells (non natural host and injections of high titers into post-natal animals)
  • early genes expressed, DNA replication is aborted and not late proteins expressed (no virus production)
  • small portion of cell transformed (~10/10^5)
    • increases cellular DNA replication/ cell division
  • early gene region of viral genome integrated into host genome
  • purely lab phenomenon
32
Q

first polio vaccine

A

Salk vaccine

33
Q

what happened with the SV40 in polio vaccine

A

SV40 in polio vaccine, made it more resistant to activation

vaccinated people with polio killing AND SV40 virus, not knowing SV40 can cause cancer
-10-30 millions exposed to SV40

34
Q

significant risk of SV40 and cancer

A

risk/benefit of vaccines

-theres always a risk when producing vaccines so you weigh risks and benefits

Virology (15 decks)

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