Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IMIN 324 > Viruses and cancer > Flashcards

Viruses and cancer Flashcards

1
Q

What is cancer?

A

uncontrolled proliferation of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why does HIV preferentially integrate within genes/transcriptional units?

A

transcriptional units are the most ‘relaxed’ –> usually open and not wound in chromatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is transformation? What is a major characteristic of transformed cells?

A

a change in morphological, biochemical or growth pattern of a cell

major characteristic = immortal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What prevents normal cells from being immortal, how do cancer/transformed cells prevent this?

A
  • normal cells differentiate and proliferate then stop because their telomeres get too short
  • cancer cells can encode tolermerases to make their telomeres longer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does it mean that viruses can cause transformation which is a single hit process?

A

only cells infected will display a transfomed phenotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What phenotypes can transfomed cells display?

A
  1. loss of anchorage dependence
  2. loss of contact inhibition
  3. decreased requirements for GFs
  4. morphological changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How can viruses indirectly cause cancer?

A
  • prolonged inflammation
  • may cause DSBs that are repaired incorrectly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name some types of RNA viruses that cause cancer

A
  • flaviviruses (e.g. HCV)
  • retroviruses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name some types of DNA viruses that cause cancer

A
  • hepadnaviruses
  • papillomoviruses
  • adenovirus
  • herpesvirus
  • poxviruses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What was the first oncogenic virus discovered?

A

rous-sarcoma virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What kind of virus is rous-sarcoma virus, what gene makes it oncogenic?

A

virus = retrovirus
gene = v-src

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the difference between c-src and v-src?

A

v-src cannot be -ve regulated by phosphorylation at the C-term:
- truncated regulatory domain
- always active

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe retrovirus helper virus coinfections

A
  1. retroviruses can package other incomplete retrovirus genomes if the incomplete genome as a psi packaging signal
  2. this way incomplete retrovirus genome like PRC II avian leukosis virus that lacks env can be packaged by a full infectious avian leukosis virus like rous-sarcoma virus –> RSV becomes the helper virus to PRC ll ASV
  3. when a replication defective virus genome is packaged by a different retrovirus it’s called an env pseudotype
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does the psi package signal work? Where is it located in the genome of retroviruses?

A
  • psi package signal lies in front of the 1st splice donor site and just after the 1st LTR in the 1st bit of the gag gene
  • forms an RNA stemloop structure recognized and bound by gag
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how can v-oncogenes be grouped, what are the existing groups? Name an example for each group

A

Grouped based on common biochemical features:
1. GFs (v-sis truncated PDGF)
2. memb Rs (v-erb EGFR)
3. tyr kinases (v-src)
4. G proteins (v-ras)
5. intermediate relay (v-raf)
6. TFs (v-fos)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Do retroviruses have to encode a v-oncogene to mediate cellular transformation?

A

no - retroviruses can cause cellular genes to be disregulated or disrupt important cellular genes depending where they integrate their genomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is cis activation of a proto-oncogene?

A

virus integration induces ts of a proto-oncogne, turning into an oncogene (think integrating in the regulatory region, for example)

18
Q

What is trans activation of a proto-oncogene?

A

virus proteins activate ts of a proto-oncogene (think like how TFs can activate gene ts)

19
Q

Why are IL-2 and IL-2R proto-oncogenes?

A

IL-2 is a GF for T cells –> leukemia

20
Q

what is an oncogene?

A

gene that, when mutated or expressed at high level, helps turn a normal cell into a tumor cell

21
Q

What is a transinducing retrovirus?

A

v-oncogene is present in virus genome

22
Q

what is v-src necessary for?

A

virus-induced cellular transformation and tumorigenesis

23
Q

What are low risk HPV types and what do they cause? What are high risk HPV types and what do they causes?

A
  • low risk (6 and 11) –> genital warts
  • high risk (16 and 18) –> 70% of cervical cancers
24
Q

What are HPV’s oncogene?

A

E6 and E7

25
Q

What are some characterisitics of HPV-induced cancer?

A
  • after infection there is a delay in progression to cervical cancer
  • tumorgenesis is linked to integration of at least the E6 and E7 viral oncogenes into cell DNA
  • progression to cervical cancer is also critically linked to persistent infection
26
Q

What are the proteins that inhibit tumor suppressors in adenovirus and SV40?

A

adenovirus = E1a and E1b
SV40 = large T Ag

27
Q

How does the tumor suppressor Rb work?

A

Rb binds and inhibits E2F - a TF necessary for G1 to S transition –> phosphorylation of Rb causes Rb to be displaced from E2F –> E2F ts genes involved in DNA synthesis

28
Q

How does HPV E7 work? How does the mechanism vary between low risk and high risk HPV?

A

inactivates Rb –> E2F is free –> cell cycle progression –> viral DNA replication

low risk E7 = competitive inhibition of Rb
high risk E7 = targets Rb to the proteosome; binds Rb more efficiently

29
Q

Is HPV E7 sufficient to progress the cell cycle?

A

No - p53 needs to be inhibited

30
Q

How does p53 work?

A

cell stress or DNA damage –> p53 upregulation –> TF –> halt cellular proliferation or apoptosis (both pathways inhibit viral proliferation)

31
Q

How does HPV E6 work? How is high risk E6 different from low risk?

A

binds p53 and inhibits it –> cell cycle progression

high risk E6 –> binds more efficiently and marks p53 for proteasome degradation

32
Q

Why is p53 a key player is oncogenesis?

A
  • p53 inactivation promotes the cell cyle
  • because p53 stalls the cell cycle to allow repair of DNA damage, p53 inactivation promotes more mutation events
33
Q

What is the primary difference between how RNA viruses and DNA viruses cause cancer?

A

RNA viruses encode v-oncogenes

DNA viruses evolved mechanisms to counter tumor-suppressors

34
Q

What is the HPV vaccine: what’s the name, what types does it target, what is it derived from (why?), when is it given?

A

Name = Gardasil
Target = high and low risk HPV
Derived from recombinant viral capsid protein L1 (L1 self aggregates and is highly immunogenic)
Given = prophylactic (best administered before exposure)

35
Q

How can viruses be used in anti-cancer therapy?

A
  • use of a live virus to selectively lyse cancer cells (oncolysis)
  • normal cells left unaffected
  • virus will replicate and spread to uninfected tumor tissue
36
Q

What is an issues with using oncolytic viruses and how is this issue fixed?

A
  • issue = host immune system clears virus faster than tumor cells -> lysis cannot be the only mechanism used
  • fix = virus has to cause immunogenic cell death –> exposes neo-Ag. –> immune system can target tumor cells
37
Q

Why do reoviruses prefer Ras-transfomed cells? What oncogenic gene does it carry

A
  • ras allows growth of cell and inhibits IFN1 production –> good environment for reovirus replication
  • normal cells don’t have much activation of the ras pathway
  • oncogene = v-erbB
38
Q

What are some ideal oncolytic virus attributes?

A
  • causes only mild, well-characterized human disease
  • have a secondary inactivation mech
  • cannot damage normal tissues
  • low mutation freq
  • non-integrating viral genome
  • cannot spread from host to host
39
Q

What is MOI?

A

multiplicity of infection:
- number of productive viral infections per cell
- bigger the MOI = more virus infection

40
Q

What data has shown that myxoma virus can be good candidate as an oncolytic therapy?

A
  • high MOI in cancer cells, low MOI in healthy cells
  • myxoma infections reduce tumors and do not spread (very restricted)

IMIN 324 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions