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Microbiology > Viral Oncogenesis > Flashcards

Viral Oncogenesis Flashcards

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Biology 101 flashcards
1
Q

percentage of the association of virus with a given cancer

A

15% to 100%

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2
Q

what human cancer arises as an acute consequence of an infection

A

none – latency period between first infection and cancer development can be range from 15 - 40 years

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3
Q

how common are viral infections that are linked to human cancers

A

extremely common - ubiquitous

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4
Q

is there synthesis of the viral agent within the cancer cells

A

no

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5
Q

what is mandatory for malignant conversion of a cell in relation to a virus

A

the virus must act on the host chromosome to cause mutation or the mutation must be within the viral genome

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6
Q

what does it mean for some infectious agents to be indirect carcinogen

A

they play a role in cells becoming cancerous without actually persistence of their genes within the respective cancer cells

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7
Q

what does it mean for chemical and physical carcinogens to act as mutagens

A

they cause genetic mutation (usually synergistically with carcinogenic infectious agents)

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8
Q

what are the officially designated human carcinogens by DHHS and what cancers do they lead to?

A

Hep C - hepatocellular carcinoma
Hep B - hepatocellular carcinoma
HPVs - cervical, anal, and oral carcinomas and maybe non melanoma skin cancers

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9
Q

18.6% of total cancer incidence is due to what 5 viral infections

A 
HBV
HCV
HPV
EBV
Helicobacter Pylori
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10
Q

what are some mechanisms done differently in tumor viruses

A

aberrant cell cycle, block apoptosis, cellular transcription development, chromatin remodeling, inflammation, metastasis, modulating signaling

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11
Q

why is it thought that cancer development by viruses is an accident

A

it is not smart for virus to produce cancer because the cells in which they transform cannot make more viruses and release them

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12
Q

in cells in which virus transform, what are the hallmarks causing cancer

A

loss of growth control, reduced adhesion, motility, invasion, ability to form tumors

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13
Q

what do transformed cells (those transformed by virus) usually exhibit

A

chromosomal aberrations

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14
Q

what type of viruses can transform cells

A

both DNA and RNA tumor viruses

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15
Q

what happens when tumor viruses integrate their viral genome into the host chromosome?

A

production of more viruses by host diminishes or becomes absent

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16
Q

what are human oncovirus replication and persistence strategies (hallmarks of cancer)

A
  • find/create conditions for replication (induce the cell cycle, metabolic programming, inducing angiogenesis)
  • ensure correct replication (recruit or inhibit DDR)
  • maximize virus production (prevent apoptosis until virion matures, immune evasion)
  • multiply latent episomes or provirus (cell survival, cell immortalization, cell proliferation)
17
Q

viral oncoprotein in EBV

A

EBNA-1

18
Q

viral oncoprotein in HPV

A

E6 and E7

19
Q

viral oncoprotein in HBV

A

HBx (important because it hits all pathways)

20
Q

viral oncoprotein in HTLV-1

A

Tax

21
Q

pathways that most tumor viruses go through

A

p53 and Rb

22
Q

proteins involved in papilloma and polyoma respectively (DNA tumor virus)

A

papilloma - E6 and E7

polyoma - Large T and small T antigen

23
Q

proteins involved in adenovirus and BK virus (DNA tumor virus)

A

adenovirus - E1A and E1B

BK - Large T

24
Q

proteins involved in SV-40 (DNA tumor virus)

A

large T

25
Q

what do DNA Tumor Viruses have in common

A

have sequences in common –> mutations in these regions abolish transformation capacity

26
Q

properties of DNA Tumor Viruses

A
  • can transform cells or have lytic life cycle
  • often integrate into host genome
  • in transformation, often ONLY early genes are transcribed
  • these are genes that are also necessary for a PRODUCTIVE infection
27
Q

1 virus associated STD

A

HPV

28
Q

how does HPV cause cancer

A

HPV infection (0-1yrs) –> low grade dysplasia (1-5 years) –> high grade dysplasia ( 1- 40 years) –> invasive cervical cancer

29
Q

mechanism of HPV associated carcinogenesis

A

HPV infection –> viral clearance –> type specific immunity

HPV infection –> viral persistence –> viral clearance –> type specific immunity

HPV infection –> viral persistence –>episomal or integration of viral DNA (overexpression of E6 and E7) –> increased in cell proliferation, decrease in repair –> mutation –> CIN –> invasive cervical cancer

30
Q

what does E6 and E7 target

A

p53 and pRb respectively

31
Q

ultimate B lymphocyte parasite

A

EBV (HHV4)

32
Q

symptoms of EBV

A

greater than 90% of those infected are asymptomatic but do shed for life

33
Q

what does EBV do

A

stimulate growth and immortalizes B cells in culture

34
Q

what carcinomas are EBV associated with

A

AfBL (african burkitt lymphoma), hodgkins disease, NPC, B cell lymphomas in patients with acquired or congenital immunodeficiencies

35
Q

what is the virus associated with Kaposi’s Sarcoma

A

HHV-8 aka KSHV

36
Q

what is kaposi’s sarcoma

A

tumor of the blood vessel walls that is usually common in those with HIV – frequently detected in those with AIDS

37
Q

how does kaposi’s sarcoma present

A

pink, red, or purple lesions on the skin or mouth

Microbiology (39 decks)

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