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MICR3320 > 16 - Oncogenic Viruses > Flashcards

16 - Oncogenic Viruses Flashcards

1
Q

Transformed cells

A
  • Are immortal, grow indefinitely (e.g. Vero; HeLa)
  • Loss of contact inhibition
  • Loss of anchorage dependence
  • Forms colonies in semi solid media
  • Altered requirement for growth factors and nutrients
  • Not necessarily oncogenic
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2
Q

Carcinogenesis

A

Complex multistage process by which cancer develops

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3
Q

Carcinoma

A

A malignancy that begins in skin or in tissues that line or cover internal organs

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4
Q

Sarcoma

A

Begins in bone, cartilage, fat, muscle or other connective tissue

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5
Q

% of human cancers that virla cancers account for

A

20%

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6
Q

T/F: Malignancy is required for viral replication

A

FALSE

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7
Q

T/F: Cancer is a side effect of host response or host-viral interaction

A

TRUE

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8
Q

RNA tumour viruses and their oncogenes

A

Can activate cellular growth signalling pathways

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9
Q

DNA tumour viruses and their tumour suppressor proteins

A

Can disrupt pathways that prevent cell proliferations

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10
Q

Proto-oncogenes

A

Normal cellular proteins involved in promoting regulation and proliferation of normal cells

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11
Q

Oncogenes

A

DNA sequence that has been altered via mutation from its original form (proto-oncogene), causing formation of cancerous tumour

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12
Q

Oncogene single gain of function mutation

A

Single activating mutation enables oncogene to stimulate cell proliferation

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13
Q

Tumour suppressor loss of function mutation

A

Two inactivating mutations eliminating the tumour suppressor gene, stimulating cell proliferation

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14
Q

Retroviral insertion into proto-oncogenes

A

Can convert proto-oncogene (integral to control of cell division), into an oncogene

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15
Q

Acutely transforming virus

A
  • Produces tumours within weeks of infection
  • Incorporates genetic material from a host cell into its own genome upon infection, forming a viral oncogene
  • When the viral oncogene infects another cell vDNA which includes the oncogene is then integrated into the cellular genome
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16
Q

Slowly transforming virus

A
  • Requires months to elicit tumour growth
  • Does not disrupt cellular function through the insertion of a viral oncogene
  • Rather, it carries a promoter gene that is integrated into the cellular genome of the host cell next to or within a proto-oncogene, allowing conversion of the proto-oncogene to an oncogene
17
Q

Rous sarcoma virus

A
  • Virus of chickens that contain oncogene viral(v)-src (an incorporated proto-oncogene cellular(c)-src)
  • Altered form of avian leukosis virus that common infects chicken flocks
18
Q

Src

A

Tyrosine kinase that is involved in regulation of cell growth and differentiation

19
Q

c-Src

A
  • Cytoplasmic signaling protein that can be phosphorylated at different sites.
  • Responds to extracellular growth factors by binding to an activated growth factor receptor, becoming phosphorylated at certain positions, and subsequently sending a proliferation signal.
20
Q

c-Src C terminal regulatory region

A

Can also be phosphorylated, but in that case phosphorylation is inhibitory event that turns signalling off when extracellular stimulus is withdrawn

21
Q

RSV v-Src protein

A

Lacks C-terminal phosphorylation site so that v-Src is constitutively active, sending a constant proproliferation signal irrespective of the presence or absence of growth factors

22
Q

Two groups oncogenic retroviruses are classified into

A
  • Oncogene transducing retrovirus
  • Oncogene deficient retrovirus
23
Q

Oncogene transducing retrovirus

A
  • Carry oncogene as part of their genome
  • Rapidly leads to cancer in nearly 100% of susceptible animals
24
Q

Oncogene deficient retrovirus

A
  • Cause cancer when insertion of the LTR causes overexpression of a cellular proto-oncogene
  • Leads to cancer only some of the time, and does so slowly in infected animals;
25
Q

Human T cell lymphotropic virus type 1 (HTLV-1)

A
  • Linked to adult cutaneous T-cell lymphoma and HTLV associated myelopathy
  • Oncogenic properties caused by two proteins (Tax and HBZ) encoded in the provirus
  • Neither protein has a known homolog among normal cellular genes.
26
Q

HTLV-1 Tax

A
  • Transcription regulator
  • In addition to activating viral genes, also activates many host genes, including those that
    promote host cell proliferation and resistance to apoptosis.
27
Q

HBZ

A
  • Can interact with pRB, therefore promoting cell cycling
  • Tax may be essential for starting the process of oncogenesis, but HBZ may be responsible
    for maintaining it
  • Active at different times over course of persistent oncogenic infections
28
Q

Rb

A
  • Tumour suppressor gene that shuts off cell proliferation by binding to E2F (transcription factor)
  • If conditions are not right for cell division, cell cycle pauses at restriction point (no DNA synthesis)
  • R point is controlled by cellular protein Rb
  • Oncogenic DNA viruses (also HCV) put cells into S phase (so they can replicate DNA) by blocking Rb
29
Q

HCV NS5B protein

A
  • Interacts with Rb in the cytoplasm and recruits the E3-ubiquitin ligase E6AP to facilitate ubiquitinylation of Rb
  • This targets Rb for degradation in proteasome
30
Q

Loss of Rb

A

Results in dysregulation of many Rb controlled process including comprised cell cycle checkpoints that guard against p53 dependent apoptosis

31
Q

How do viruses cause transformation

A

Via inactivation of tumour suppressor p53

32
Q

p53

A
  • Arrests cell cycle in presence of damaged DNA and leads to apoptosis of cells whose DNA is irreversibly damaged
  • Virus infection causes DNA damage and hypoxia (activated p53)
  • MAny viruses alter p53 activity
33
Q

SV40 large T antigen

A

Stabilises p53 in inactive state

34
Q

HPV E6

A

Triggers degradation of p53

35
Q

Adeno E1B

A

Blocks transcriptional activation function of p53

MICR3320 (25 decks)

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