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Flashcards in Viral Oncogenesis Deck (37)
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1

percentage of the association of virus with a given cancer

15% to 100%

2

what human cancer arises as an acute consequence of an infection

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

3

how common are viral infections that are linked to human cancers

extremely common - ubiquitous

4

is there synthesis of the viral agent within the cancer cells

no

5

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

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

6

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

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

7

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

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

8

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

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

9

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

HBV
HCV
HPV
EBV
Helicobacter Pylori

10

what are some mechanisms done differently in tumor viruses

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

11

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

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

12

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

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

13

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

chromosomal aberrations

14

what type of viruses can transform cells

both DNA and RNA tumor viruses

15

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

production of more viruses by host diminishes or becomes absent

16

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

-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

viral oncoprotein in EBV

EBNA-1

18

viral oncoprotein in HPV

E6 and E7

19

viral oncoprotein in HBV

HBx (important because it hits all pathways)

20

viral oncoprotein in HTLV-1

Tax

21

pathways that most tumor viruses go through

p53 and Rb

22

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

papilloma - E6 and E7
polyoma - Large T and small T antigen

23

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

adenovirus - E1A and E1B
BK - Large T

24

proteins involved in SV-40 (DNA tumor virus)

large T

25

what do DNA Tumor Viruses have in common

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

26

properties of DNA Tumor Viruses

• 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

#1 virus associated STD

HPV

28

how does HPV cause cancer

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

29

mechanism of HPV associated carcinogenesis

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

what does E6 and E7 target

p53 and pRb respectively