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Virology 21-30 > #26 oncogenic viruses > Flashcards

#26 oncogenic viruses Flashcards

1
Q

transformation can be defined as

A

the introduction of a inheritable change in a cell that causes changes in growth phenotype and immortalisation (change is passed from mother to daughter)

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2
Q

are cancers monoclonal or clonal

A

cancers are clonal
meaning they are produced from a single cell that has been transformed
one cell undergoes a transformation and that cell will pass the change on to its daughters

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3
Q

how do transformed cells differ from normal cells?

A
  • lack inhibition of growth
  • lack dependence on exogenous growth factors
  • lack anchorage dependence
  • not all oncogenic viruses can transform cells in culture
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4
Q

what are the 5 phases of the cell cycle and what occurs in them

A

G0 phase - the quiescent resting phase

G1 phase - synthesis of proteins required for DNA synthesis occurs (enzymes are synthesised)

s phase: DNA synthesis occurs

G2 phase: synthesis of proteins for daughter cells occurs

M phase - mitosis occurs / cell will enter the G0 phase or go back into G1 and begin division again

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5
Q

what are go and stop signals required for

A

Go signals: growth factors, oncogenes, cyclins, CDKs
- required to make to make the switch from the G0 to the G1 phase

Stop signals

  • used for control
  • can inhibit go signals
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6
Q

where is the point of no return and how do you get there

A

between the G0 and restriction point the cell is paused and waiting in response to environmental signals (go signals/stop signals)
when there is enough go signal in the g1 phase the cell will reach a point of no return where the cell will not be able to turn back
it will divide - DNA synthesis will occur in s phase and so on

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7
Q

what are genes encoding go signals called

A

proto-oncogenes

or c-onc (cellular oncogenes)

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8
Q

how do oncogenic viruses cause cancer

A

they affect the expression or function of proteins that play roles in cell growth and division

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9
Q

what are tumor suppressor genes

A

they are genes encoding proteins that are involved in negative regulation of cell growth (they’re stop signals)
i.e. P53 and rb

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10
Q

what are the 4 classes of oncogene
give examples of each

what can viruses do to these c-onc genes

A

Growth factors - EGF
growth factor receptors - EGF receptor
intracellular signal transducers - Elk, raf, Mek, Ras
transcription factors - Elk-1, SRF

they all assist in cell growth and division (c-onc)

virus can mutate all of these genes

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11
Q

name the 6 viruses that can induce cancer

A

DNA

  • Epstein barr virus EBV (herpesviridae)
  • HPV (papovaviridae)
  • human polyomavirus (papovaviridae)
  • hepatitis B virus (hepadnaviridae)

RNA

  • HTLV-1
  • Hepatitis C (Flaviviridae)
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12
Q

what are the features of RNA tumor viruses

A
  • they are a non-lytic infection
  • integration is essential part of the replication cycle
  • they may bring a v-onc however it will have a cellular counterpart (it uses a cellular oncogene as a viral oncogene)
  • transformation involves stimulating the activators of the cell cycle (c-onc’s) - they will do this by mutating it or activating it
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13
Q

what are the features of the DNA tumor viruses

A
  • often lytic infection
  • integration is not an essential part of the virus cycle but may occur in transformed cells
  • the v-onc’s they bring are usually unique viral gene products - they do not have a cellular counterpart. they bring their own v-onc
  • transformation involves inactivation of inhibitors of the cell cycle (inhibition of tumor suppressor genes)
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14
Q

what are the two categories of oncogenic retroviruses divided into?
what are their features

A

Endogenous retrovirus

  • integrated provirus
  • transmitted in the germline to every cell
  • will be passed from mother to her child
  • the virus is usually totally silent
  • only become a problem in response to stimuli such as irradiation, chemicals etc. virions will be produced

Exogenous retrovirus

  • typical virus infection
  • acquire the infection after birth
  • virions will be produced - most will be replication competent
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15
Q

what are the features of a defective retrovirus - how does it work

A
  • a defective retrovirus will encode a oncogene
  • the onc will have replaced a viral gene i.e. pol gene
  • therefore the virus is missing a gene segement
  • the virus will be defective and will not be able to replicate on its own
  • it can only replicate with a helper virus present (normal virus)
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16
Q

what is unique about rous sarcoma virus?

A

it is a retrovirus
it has picked up a oncogene, but is not defective
it is replication competent
when it picked up an oncogene it didnt replace any genes - it still has all of its genes hence can replicate

17
Q

what are the 3 mechanisms in which an exogenous retrovirus can cause tumor production

how?

A
  1. transducing retroviruses
    - introduce themselves into the host with a v-onc
    - LTR will act as the promoter for the oncogene
  2. cis-activating retroviruses
    - dont have an oncogene
    - the LTR of the virus drives the transcription of a nearby c-oncogene
    - called insertional mutagenesis
  3. trans-activating retroviruses
    - contain a gene regulation protein or a gene activating RNA
    - they will both act to activate a c-oncogene
18
Q

how do transactivating (acute) retroviruses work?

A
  • they induce a v-onc under LTR transcriptional control into the host genome
  • the these viruses are mostly defective except for Rous sarcoma virus
  • these viruses will not produce any infectious virus unless they have the help from a helper virus (normal virus)
  • these viruses cause tumors in weeks
  • tumors may be polyclonal as multiple cells can be infected and acquire a c-onc
19
Q

describe how cis-activating (non-acute) retroviruses work

A
  • perform insertational mutagenesis
  • they do not encode a v-onc
  • they insert into host near a c-onc
  • the LTR from the virus drives transcription of the c-onc

Can occur in 2 ways
1. land next to a c-onc and the 5’LTR drives transcription of the virus and the 3’ LTR drives transcription of the c-onc

  1. long range: they land far away from the c-onc however the 3’ enhancer will drive transcription of the c-onc
20
Q

how is Koala Retrovirus causing Leukaemia in koalas

A
  • the virus is an exogenous retrovirus
  • it is causing cancer via insertational mutagenesis
  • where the virus inserts into the genome and the LTR drives transcription of a c-onc
21
Q

how do trans-activating retroviruses work?

what is an example

A
  • it is a virus that contains a gene regulation proteins
  • HTLV-1 is a transactivating retrovirus -its exogenous
  • causes ATL
  • it transcribes two regulatory proteins that drive proliferation of the infected cell: Tax and Hbz
22
Q

how does Tax and HBZ of HTLV-1 work?

what is this mechanism of cancer induction called?

A

they both act as gene regulation proteins for HTLV-1 to cause cell proliferation
- called transactivating retroviruses

  • Tax: is a gene regulation protein, it binds to the LTR of the virus to up-regulate expression of Gag, pol and env but it also it activates many cellular interleukins (IL2 and IL-2R) to drive proliferation of the cell

HBZ: down-regulates the expression of Tax protein
but HBZ mRNA also drives proliferation of the cell

23
Q

explain the regulation of HTLV1 expression and replication for HBZ and Tax protein

A
  • initially most infected cells only produce HBZ mRNA and HBZ protein
  • HBZ protein drives proliferation of the cell
  • HBZ mRNA can cause bursts of Tax protein
  • Bursts of tax will cause virion production and cell proliferation via activating cellular interleukins
  • tax bursts can also be induced by cell stress, hypoxia, t-cell activation
  • HBZ protein will act on tax to down-regulate it
24
Q

how does Leukeamia from HTLV-1 develop

A
  • occurs mainly through the expression of viral proteins HBZ, Hbz mRNA and Tax
  • also can occur through insertional mutagenesis where virus inserts into host DNA and drives long range transcription of a c-onc
  • the viral enhancer drives transcription of a c-onc
25
Q

explain the features of tumor induction by DNA viruses

A
  • DNA viruses transform cells as a consequence of their replication strategy
  • they undergo lytic growth
  • they require host enzymes to replicate their DNA which are produced in the S phase of the cell cycle
  • it is in favour for the virus to push the cell to the s phase
  • they use viral proteins to push the cell into the s phase of the cycle
  • they often encode proteins that inactivate tumor suppressor proteins -they eliminate the stop signal
  • the tumors need to have persistent expression of the viral oncogenes either as an episome or intergrated into the viral genome
  • the virus is often the indirect cause of cancer - tumor formation is often multi-factorial
26
Q

what are the two tumor supressor genes and what do they do

A

Rb and P53 gene
cellular genes that inhibit cell cycle
Rb protein controls the transition from G0 to G1 - it will activate and associate with ELF transcription factors to put a break on the cell cycle
P53 protein is a transcription factor that induces expression of proteins that arrest cell growth
lot of tumors have mutations in P53 gene

27
Q

explain how some strains of HPV causes tumors

A
  • DNA virus
  • in benign warts the genome is kept as a circular episome. however in malignant cells the HPV genome randomly integrates into the genome resulting in the loss of the E2 gene
  • E2 negatively represses the transcription of E6 and E7 proteins
  • when E2 is lost E6 and E7 will be transcribed
  • E6 and E7 will stop p53 and Rb proteins
  • HPV targets p53 for degradation
28
Q

explain how Hep.B causes cancer

A
  • DNA virus
  • usually a part of the genome will integrate into the host chromosome randomly
  • when Hep. B integrates it will retain its X gene and its promoter. However it will become non-infectious (this is not advantageous for the virus)
  • the X gene encodes a transactivating gene that may activate a nearby c-onc (Src tyrosine kinase) - insertional mutagenesis
  • it has an indirect role in cancer as its a combination of the viral proteins and the international mutagenesis which causes cancer from HBV
29
Q

How does Polyomavirus (SV40) cause cancer

A
  • causes merkel cell cancer
  • virus integrates into the host DNA and produces the large T antigen which has truncation mutations that make the T antigen defective initiating DNA replication
30
Q

what cancers does EBV cause

How does EBV cause cancer

A

causes burkitts lymphoma, nasopharyngeal cancer, B-cell lymphomas, hodgekins lymphoma

In burkitts lymphoma the EBV cells cause cloal expansion of B-cells - enhances the chances of genetic accidents such as the chromosomal translocation of C-myc which encodes a ‘go signal’ (G1 to S signal)
Can cause the c-myc to be under transcriptional control of the Ig heavy chain enhancer which causes the overproduction of c-myc
causes production of tumors

Virology 21-30 (6 decks)

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