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PATH3309 > 11 - Viral Carcinogenesis > Flashcards

11 - Viral Carcinogenesis Flashcards

1
Q

What causes cancer

A
  • Viruses / bacteria
  • Some chemicals
  • Radiation
  • Influenced by heredity, diet and hormones
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2
Q

How do viruses cause cancer

A

Virus inserts and changes genes for cell growth

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3
Q

Virus replication cycle

A
  • Virus attached to cell
  • Virus penetrates cells membrane and injects nucleic acid into cell
  • Viral nucleic acid replicates using host cellular machinery
  • New viral nucleic acids are packaged into viral particles and released from cell
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4
Q

Viruses

A
  • Non-living
  • Cannot reproduce or produce protein without a host cell
  • Do not undergo cell division
  • Lab growth is only possible in animals, embryonated chicken eggs, or cell/tissue cultures systems
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5
Q

What does a complete virus particle (virion) typically consist of

A
  • Genome and capsid (make up nucleocapsid)
  • Membrane and ligands (makes up envelope)
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6
Q

Capsid

A

Composed of capsomeres

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7
Q

Membrane

A

Host cell derived

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8
Q

Ligands

A

Glycoprotein complex

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9
Q

Features of virus

A
  • Small size (10-300 nm)
  • DNA or RNA genome (ds or ss)
  • Helical, polyhedral or complex shape
  • Envelope or no envelope
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10
Q

Helical Viruses

A

Nucleic acid core is surrounded by hollow cylinder of protein (capsid) that is wrapped around it for form helical

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11
Q

Polyhedral Viruses

A

The nucleic acid core is
surrounded by a polyhedral (usually icosahedral) capsid

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12
Q

Binal / Complex Viruses

A

Capsid is irregularly shaped or complex in structure

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13
Q

Oncovirus

A
  • Virus that can cause cancer
  • Currently 7
  • ~12% of human cancers are caused by infections
  • Second most important risk factor for cancer development after tobacco
  • FIrst human oncovirus identified was EBV
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14
Q

Examples of oncoviruses

A
  • HBV
  • HCV
  • HPV
  • EBV
  • Herpes virus 8 (Karposi’s sarcoma)
  • HIV-1
  • HTLV-1
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15
Q

Where do DNA tumour viruses replicate

A

Nucleus

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16
Q

Where do RNA tumour viruses replicate

A

Cytoplasm

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17
Q

Main difference between normal viruses and oncoviruses

A
  • Normal virus cycle is lytic
  • Oncovirus cycle is latent
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18
Q

Lytic cycle

A

Once virus has invaded the cell, they replicate their genome and package into protein, then lyse the cells to release progeny to continue their infectious life cycle

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19
Q

Steps of latent life cycle

A

Virus infects cell –> Viral genome integration into host genome –> transformation

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20
Q

Latent life cycle

A
  • Some virus-specific proteins expressed (early functions) but no mature virus formed
  • Viral structural proteins are not expressed
  • Sometimes latency may terminate (cells must be infected by complete viurs
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21
Q

Transformation

A
  • Ability to form tumours
  • Viral genes interfere with control of cell replication and other aspects of cell phenotype
  • Both DNA and RNA tumor viruses can transform cells
  • Similar mechanisms of transformation by each type of tumor virus
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22
Q

Other aspects of cell phenotype viral genes interfere with

A
  • Loss of growth control
  • Reduced adhesion
  • Motility
  • Invasion
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23
Q

Life cycle of viruses with dsDNA genomes

A
  • Introduction of nucleocapsid into cell
  • Uncoating of viral DNA
  • Translocation into nucleus
  • Replication by cellular DNA polymerases OR transcription by cellular RNA polymerase 2
  • Encapsidation of progeny DNA in viral proteins OR translation by cellular ribosomes
24
Q

Proto-oncogenes

A
  • Positive growth regulators present in normal, healthy cells
  • 803 human proto-oncogenes have been identified
25
Q

Oncogenes

A
  • Gene that has the potential to transform a normal cell into a malignant cell
  • Has been altered or mutated from its original form (the proto-oncogene)
  • Oncogene transmitted by virus is known as viral oncogene
26
Q

Examples of oncogenes

A
  • MYC
  • TRK
  • ERK
  • Bcr-Abl
27
Q

Oncogene activation

A
  • Activation of endogenous retroviral (ERV) genomes
  • Proto-oncogenes can be activated by genetic changes
    affecting either protein expression or structure (e.g. gene amplification, viral insertion, chromosomal translocations)
  • ERVs also activated by environmental mutagens
28
Q

How much of the human genome derives from endogenous retroviral genomes

A

8%

29
Q

Tumour suppressor genes

A
  • Controllers of cellular proliferation
  • Responsible for maintaining a healthy cell
  • Regulate cell cycle, apoptosis and genomic stability
  • Negative growth regulator (proto-oncogene is positive growth regulator)
30
Q

Examples of tumour suppressor genes

A
  • p53
  • Retinoblastoma protein
31
Q

p53

A
  • In a normal cell p53 is inactivated by its negative regulator, mdm2.
  • Upon DNA damage or other
    stresses, p53 will induce cell
    cycle arrest to allow either
    repair and survival of the cell
    or apoptosis to discard the
    damaged cell
32
Q

Which virus caused 10% of human cancer

A

HPV (cervical, vulval, uterine)

33
Q

HPV

A
  • 150+ HPV serotypes known to infect humans (skin and mucosa)
  • Transmitted by sexual or close contact
  • Infect skin epithelial cells and mucous membranes
  • Non-enveloped, icosahedral circular dsDNA viruses
34
Q

HPV 6 & 11

A

Warts (benign)

35
Q

HPV 16 & 18

A

Cancer

36
Q

E5, E6, E7

A
  • Oncoproteins
  • E6 and E7 genes code for proteins that inactivate p53 and Rb)
  • E5 onco-protein interacts with EGF-R1 signaling pathways and pro-apoptotic proteins to affect cellular transformation
37
Q

L1 gene

A
  • Codes for a protein that self assembles into capsid of virus
  • Empty L1 capsid form VLPs which are used in vaccines
38
Q

LCR

A
  • Long control region
  • Early E non structural genes and late structural capsid genes
39
Q

EGF-R1 signalling pathways

A

MAP kinase and PI3K/Akt

40
Q

HPV genome

A
  • 8 kb, encoding 9 genes
  • E1, E2, E4, E5, E6, E7, L1, L2, LCR
41
Q

L2

A
  • Minor capsid component and lacks the capacity to form VLPs
  • Co-assembles with L1 into VLPs, enhancing their assembly.
42
Q

HPV life cycle

A
  • Infects the keratinocytes in basal layers of a stratified squamous epithelium
  • Tightly regulated by keratinocyte differentiation
43
Q

Disease progression of HPV

A
  • Persistent infection can cause irreversible changes leading to invasive cancer
  • Other co factors important in progression (e.g. smoking, age at first intercourse, genetics, contraception use)
44
Q

L/GSIL

A

Low/High grade squamous intraepthielial lesion

45
Q

CIN

A

Cervical intra-epithelial neoplasia

46
Q

Main way of preventing cervical cancer

A

Regular screening (instead of pap test)

47
Q

Examples of HPV Vaccines

A
  • Cervirax (bivalent)
  • Gardasil (quad-valent)
  • Both protec against HPV 16, 18)
48
Q

What does gardasil 9 protect against

A
  • Serotypes 16 and 18 (two types that cause the majority of HPV-related cancers)
  • The five next most common HPV types associated with cervical cancer (serotypes 31,
    33, 45, 52 and 58)
  • Two non-cancer-causing HPV types (serotypes 6 and 11), which cause 90% of genital warts.
49
Q

Epstein Barr Virus (EBV)

A
  • Virus of herpes family (herpesvirus 4)
  • One of the most common viruses in humans (glandular fever / mononucleosis)
  • Infects B cells and epithelial cells
  • Infection occurs by oral transfer of saliva
  • Complex virus
50
Q

Diseases associated with EBV

A
  • Burkitt’s lymphoma
  • Hodgkin’s lymphoma
  • Nasopharyngeal carcinoma
  • B cell lymphoma
  • Duncans syndrome
51
Q

How is EBV diagnosed

A

EBER in situ hybridisation in formalin fixed tissue section

52
Q

Burkitt’s lymphoma

A
  • EBV induces chromosomal translocation of chromosome 8 and 14
  • Break in chromosome 14 at q32
53
Q

Theory 1 of malarial infection and EBV

A
  • BL correlates roughly with malaria infection in Africa
  • Malaria infection induces B-cell activation, predisposing B cells to acquisition of IG/MYC translocations.
54
Q

Theory 2 of malarial infection and EBV

A
  • Malaria infection reactivates latent (endemic) EBV infection in memory B cells.
  • Inducing proliferation of B cells and increase probability of IG/MYC translocations
  • EBV inhibits the apoptosis of
    premalignant tumor cells,
    allowing transforming events to occur
55
Q

TCF-3

A

Rendered constitutively active in Burkitt lymphoma by two related mechanisms

56
Q

Two related mechanism of TCF-3

A
  1. Somatic mutations that inactivate its negative regulator ID3,
  2. Somatic mutations
    in TCF-3 that block the ability of ID3 to bind and interfere with its activity as a transcription factor.
57
Q
A

PATH3309 (12 decks)

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