L06: Viruses And Cancer Flashcards

1
Q

What are the characteristic features of a virus

A

DNA/RNA
Protein capsid
Membrane envelope

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2
Q

Why does viruses require a host cell

A

For translation of viral MRNA
Genome transcription
Genome replication

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3
Q

Give 3 examples of virus that are associated with cancer

A

Adenovirus
Herpes virus
Papillomovirus

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4
Q

In a tumour cell what happens to oncogenes and tumour suppressor genes

A

Oncogene is activated

Tumour suppressor gene is inacitved

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5
Q

What is the normal role of tumour suppressor genes

A

Inhibit cell division

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6
Q

What is the role of proto-oncogenes

A

Drive cell division and cell cycle

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7
Q

Which viruses in the IARC classification are considered to be carcinogenic

A
Epstein Barr virus 
Kaposi sarcoma associated virus 
Hepatitis C
Hepatitis B
Humans T cell lymphotrophic virus type 1 
High risk human papilloma virus types 
Merkel cell polyomavirus 
HIV-1
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8
Q

Which bacteria in the IARC classification is considered to be carcinogenic

A

Helicobacter pylori

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9
Q

In what type of countries are infectious agents that cause cancer higher in

A

Developing countries due to better hygiene and better screening programs

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10
Q

What are the 2 ways viruses can behave as carcinogens

A

Direct

Indirect

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11
Q

What is a direct carcinogen

A

Viral oncogenes when expressed drive cell cycle and proliferation

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12
Q

What are indirect carcinogens

A

Viruses that cause cancer through chronic infection, inflammation and immunosuppression that lead to carcinogenic mutation in host

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13
Q

Is HIV-1 a direct or indirect carcinogen

A

Indirect carcinogen

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14
Q

In HIV what does persistent immune activation lead to in tissues

A

Chronic tissue damage

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15
Q

When there is cytokine release in HIV what happens to the micro-environment

A

Changes

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16
Q

What are the other roles of HIV

A

Increase angiogenesis

Accelerate fibrosis

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17
Q

How is fibrosis accelerated in HIV

A

By stimulation of extracellular matrix

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18
Q

If there is fibrosis what cancer is likely to occur

A

Liver cancer

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19
Q

In people with HIV what risk are they are

A

Increased proliferation of co-existing viruses

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20
Q

What co-existing viruses can occur in HIV patients

A

EBV
KSHV
Herpes
HBV/HCV

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21
Q

What is the Koch’s postulate useful for

A

Identifying an infectious as the cause of a specific disease

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22
Q

List the reasons why the Koch’s postulate fails in viral cancer

A
  • Viral infection have a long latency period between primary and tumour development
  • only small percent of individuals with the virus develop cancer
  • cancer is not only due to the virus because there are other factors involved
  • cancer only contains a part of the viral genome (not the whole)
  • virus is only one part of the chain
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23
Q

Name a viral infection that shows latency

A

Herpes (EBV)

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24
Q

What cancer is herpes virus (EBV) associated with

A

Nasopharyngeal carcinoma

Burkkit lymphoma

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25
Q

Apart from the herpes virus what other factors contribute to burkitt lymphoma

A

Malaria

Chromosome translocation of c-myc (oncogene) to IG enhancer

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26
Q

Apart from herpes virus what others factors contribute to nasopharyngeal carcinoma

A

Salted fish

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27
Q

Why does salted fish contribute to nasopharyngeal carcinoma

A

Salted fish contains nitrosamines that leads to genetic cell changes

28
Q

What cancer is HPV type 16 and 18 (human papillomovirus) associated with

A

Cervical cancer

29
Q

What is HPV 6 and 11 associated with

A

Anogenital warts

30
Q

Is HPV classed as a direct or indirect carcinogen

A

Direct carcinogen

31
Q

What type of cells does HPV affect

A

Epithelial cells

32
Q

What are the 2 viral oncogenes that HPV encodes

A

E6 and E7 viral oncogene

33
Q

Which cancer is HPV most associated with

A

Cervical cancer

34
Q

What is HPV dependent on for replication of viral DNA

A

Host cell i.e epithelial cells

35
Q

Where are epithelial cells mitotically active

A

In the basal layer

36
Q

As epithelial cells begins to migrate up from the basal layer what happens to there mitotic activity

A

Declines

37
Q

Where does viral DNA amplification of HPV occur

A

In the mid layers

38
Q

Where does capsid assembly of HPV occur

A

In the upper layers

39
Q

What does viral dna amplification and capsid assembly occur in the upper layers

A

These layers have poor immune system so it prevents the immune activation that can get rid of the virus

40
Q

If the HPV is affecting the mid layers what type of cells are these in terms of mitosis

A

Mitotically inactive with no replication machinery

41
Q

What happens to the cells in the mid layers to have replication of the virus from occurring

A

Get pushed back to increase cell division

42
Q

What are the viral oncogenes of HPV

A

E6 and E7

43
Q

What does E7 inhibit

A

Rb

44
Q

What is RB

A

A tumour suppressor gene that prevents inappropriate cell cycle

45
Q

If RB is not functioning due to E7 bound to RB what tumour suppressor is induced

A

P53

46
Q

What does p53 lead to

A

Apoptosis

47
Q

What viral oncogene inhibits P53 to stop apoptosis

A

E6

48
Q

In a normal cell if there are positive growth signals what happens to RB to proceed the checkpoint

A

1) positive growth signals activate cyclin D/ CDK4,6
2) cyclin D/cdk4,6 phosphorylates Rb
3) RB results in release of E2F which activates genes to proceed into s phase

49
Q

What type of signals stop rb from functioning.

A

Negative growth signal

Stress signal

50
Q

Describe what happens when there is negative growth signal and stress signal to stop the cell cycle

A

1) negative growth signal causes the release of P16
2) stress signal causes the release of P53
3) p53 activates p21
4) p16 and p21 inhibit cyclin D, CDK4,6 so E2F remains inhibited and cell cycle stops

51
Q

Therefore when E7 binds to RB what happens

A

E2F is released which promotes transcription of genes to proceed into the s phase

52
Q

What other host cell factor does E6 bind to P53 with

A

E6AP

53
Q

When E6 and E6AP binds to P53 what happens to P53

A

Degrades

54
Q

With the use of E7 and E6 what happens to the virus

A

Survives

55
Q

In combination with the virus, genetics, diet what happens

A

Tumour

56
Q

How to we prevent hepatitis b from occurring

A

Hepatitis b vaccine

57
Q

What happened to liver cancers when there hep b vaccine was introduced

A

Liver cancer decreased

58
Q

How do we control cervical cancer due to HPV

A

Cervical screening programmes

59
Q

What does cervical screening involve

A

Cervical smear test

60
Q

What does the cervical smear test look for

A

Cytological abnormalities

61
Q

Apart from cervical smear test what other test is involved in cervical screening

A

HPV dna testing

62
Q

Why is HPV dna testing involved

A

Because some women can be missed with screening

63
Q

What are the other methods of controlling HPV

A

Prophylactic HPV vaccine

64
Q

What are 2 HPV vaccines used in the U.K.

A

Cervarix

Gardasil

65
Q

How does these HPV vaccine work

A

Stimulate the production of neutralising antibodies so it can bind to a real virus upon exposure

66
Q

At what age are people injected with HPV vaccine

A

Young age before they are sexually active